§Renal Dosing & Dialyzability
Creatinine-clearance thresholds and dialyzability for 290 agents: does the dose change in renal impairment, and is the drug removed by dialysis? Switch to Needs a renal change for the 76 agents with a curated renal rule (70 with a defined reduction, hold or GFR-based dose; the rest flagged for caution without a banded threshold), or Dialysis to filter by hemodialysis removal, peritoneal-dialysis and CRRT guidance, dose-adjustment, and the 29 agents contraindicated in dialysis. Or work a single patient with the Dosing Assistant (enter an eGFR) and the Carboplatin Calculator. Every row links to its profile.
290 of 290 agents
| Agent | Renal dose adjustment | Dialyzable |
|---|---|---|
| 5-Fluorouracil TMA Pyrimidine analog | No standard CrCl-based dose adjustment for IV 5-FU (catabolism is enzymatic via DPD, not renal); dose by toxicity and consider DPYD-genotype-guided reduction. In significant renal impairment, monitor closely but renal clearance is a minor pathway. | — 5-FU has a very short half-life and is enzymatically catabolized; it is not managed by dialysis. Its catabolite fluoro-beta-alanine is renally excreted and can accumulate in renal failure but is not the toxic species. |
| Abemaciclib PSEUDO CDK4/6 inhibitor | No dose adjustment for mild-to-moderate renal impairment; severe renal impairment and ESKD are not well characterized (hepatic, not renal, impairment drives reduction). Critically, the drug-induced serum-creatinine rise should NOT trigger dose reduction by itself — verify true GFR first. | — Not characterized; abemaciclib is highly protein-bound and hepatically (CYP3A4) metabolized, so it is unlikely to be appreciably dialyzed. No ESKD dosing guidance exists. |
| Abiraterone LYTE CYP17 inhibitor | No formal renal dose adjustment for mild–moderate impairment (not studied in severe CKD/ESKD). Hepatic impairment requires dose reduction. The actionable adjustment is glucocorticoid coverage and potassium/BP management, not renal dosing. | Yes Highly protein-bound (>99%) and hepatically metabolized (CYP3A4/SULT2A1); not meaningfully dialyzable. No specific ESKD dosing established — manage electrolytes clinically. |
| Acalabrutinib HTN BTK inhibitor | No dose adjustment for mild-to-moderate renal impairment (CrCl ≥30 mL/min); severe impairment (CrCl <30) and dialysis are not well studied. <2% renal excretion; hepatic (CYP3A) clearance dominates. Acid-reducing agents alter absorption of the original capsule (a key non-renal interaction). | Yes Not meaningfully dialyzable — highly protein-bound, hepatically cleared small molecule. No post-HD supplemental dosing needed. |
| Adagrasib PRE KRAS G12C inhibitor | No dedicated renal dose adjustment is established; standard is 600 mg orally twice daily, modified for GI/QTc/hepatic toxicity. A measured (rather than creatinine-estimated) GFR is preferred when dosing renally cleared co-medications, because adagrasib inflates serum creatinine. | — Not characterized; highly protein-bound, hepatically metabolized (CYP3A4) small molecule, unlikely to be appreciably dialyzed. No ESKD dosing guidance exists. |
| Afamitresgene autoleucel (Afami-cel) PRE MAGE-A4 TCR-T cell therapy | Not applicable in the conventional sense - this is a one-time autologous cell product, not a renally cleared small molecule, so there are no CrCl-based dose thresholds. No renal dose adjustment is established; lymphodepleting chemotherapy given before infusion may itself require attention to renal function. | No Not applicable. As a living-cell therapy, afami-cel is not dialyzable; dialysis is used only to support severe AKI, not to clear the product. |
| Afatinib PRE EGFR TKI | No initial renal dose reduction for mild-moderate impairment; for severe renal impairment (eGFR ~15-29) a reduced starting dose (30 mg daily) is advised per labeling, with titration as tolerated. The practical priority is holding/reducing for grade >=2-3 diarrhea to prevent prerenal AKI. | Yes Not appreciably dialyzable—highly protein-bound (~95%), lipophilic, with predominantly fecal/biliary excretion and minimal renal clearance; hemodialysis is not expected to remove meaningful amounts. |
| Alectinib PSEUDO ALK TKI | No starting-dose change for mild-to-moderate renal impairment; data in severe impairment/ESKD are limited (alectinib is hepatically metabolized with <1% renal excretion), so no PK-based renal adjustment is mandated. Hepatic impairment requires dose reduction. | No Highly protein-bound (>99%) and hepatically cleared; not dialyzable and no supplemental dosing expected in ESKD. |
| Alpelisib PRE PI3Kα inhibitor | No dose adjustment for mild-moderate renal impairment; not studied in severe impairment (CrCl <30) or ESKD. Dose modification is driven by hyperglycemia and rash, not by baseline GFR. | Yes Highly protein-bound small molecule; not expected to be meaningfully dialyzable and no ESKD dosing established. |
| Altretamine (hexamethylmelamine) PRE Alkylating agent (methylmelamine) | No established renal-specific dosing algorithm; altretamine is extensively hepatically metabolized with low urinary excretion of unchanged drug. Dose reductions and interruptions are primarily for GI, neurologic and hematologic toxicity. | Yes Not characterized as dialyzable; high lipid solubility, extensive hepatic metabolism and tissue distribution make significant dialytic removal unlikely. Dialysis is not used for drug clearance. |
| Amivantamab LYTE EGFR-MET bispecific antibody | No established renal dose adjustment (monoclonal antibody, not renally cleared). Manage by electrolyte repletion and infusion-rate modification; hold for suspected AIN rather than dose-reduce. | No Large IgG bispecific antibody — not dialyzable and cleared by reticuloendothelial proteolysis; no ESKD dose change expected. Electrolyte management is the renal priority in advanced CKD. |
| Amsacrine LYTE Topoisomerase II inhibitor (acridine) | The pharmacokinetic study recommends an initial dose reduction of 30-40% in severe hepatic or renal impairment or documented impaired drug clearance, since elimination is predominantly hepatobiliary and prolonged in organ dysfunction; compute the absolute dose from the protocol's own baseline rather than a fixed range. Patients with impaired amsacrine clearance experienced the most severe toxicity in that study. | — Unlikely to be efficiently dialyzed given very high plasma protein binding (~96-98%) and hepatobiliary elimination; dialysis is reserved for managing TLS metabolic complications rather than drug removal. |
| Arsenic trioxide PRE Differentiating agent | No formal CrCl-based dose schedule is established, but because arsenic is largely renally excreted, dose reduction and intensified monitoring are advised in significant renal impairment; the label notes caution and reduced clearance in renal dysfunction. Standard induction is 0.15 mg/kg/day. | Yes Arsenic is partially dialyzable, and case experience supports continuing arsenic trioxide with dosing around hemodialysis sessions in ESKD; given renal excretion, careful exposure/QT monitoring is essential. |
| Asciminib HTN BCR-ABL STAMP inhibitor | No dose adjustment required for renal impairment in labeling (renal clearance is minor); use general caution in advanced CKD. Hepatic metabolism predominates. | Yes Highly protein-bound; not expected to be dialyzable. No specific ESKD dosing required given minimal renal clearance. |
| Asparaginase PRE Enzyme | Large protein cleared by reticuloendothelial proteolysis, not renal filtration - no renal dose adjustment. Management is toxicity-driven (hold/switch for pancreatitis, severe hypersensitivity, or thrombosis). | No Large enzyme; not dialyzable. Dialysis/CRRT is used to support AKI or refractory hyperammonemia, not to clear the drug. |
| Atezolizumab AIN Anti-PD-L1 antibody | No baseline renal dose adjustment (fixed-dose antibody not renally cleared). The relevant 'adjustment' is immune-toxicity grading: per consensus guidance, withhold for grade 2 (creatinine 2-3x baseline) and treat with steroids, and permanently discontinue for grade 3-4 or recurrent severe nephritis. | No Not dialyzable—an IgG1 monoclonal antibody cleared by reticuloendothelial catabolism; not removed by hemodialysis and no dose supplementation needed. ESKD patients can receive standard dosing. |
| Avapritinib PRE KIT / PDGFRA inhibitor | No dose adjustment for mild-moderate renal impairment; severe impairment/ESKD not well studied (hepatic CYP3A4 metabolism). Modifications driven by edema, CNS effects and cytopenias. | Yes Highly protein-bound; not expected to be dialyzable. No established ESKD dosing. |
| Avelumab AIN Anti-PD-L1 antibody | No baseline renal dose adjustment (fixed-dose antibody, not renally cleared). Toxicity-based modification follows irAE grading: withhold for grade 2 nephritis with steroids; permanently discontinue for grade 3-4 or recurrent severe nephritis. Avelumab requires premedication to prevent infusion reactions (unrelated to renal dosing). | No Not dialyzable—IgG1 monoclonal antibody cleared by reticuloendothelial catabolism; not removed by hemodialysis, no supplemental dosing, standard dosing in ESKD. |
| Avutometinib LYTE RAF/MEK inhibitor | No dedicated renal-impairment dosing has been established for this 2025 first-in-class agent; formal data in moderate-to-severe impairment and dialysis are lacking. Avutometinib is cleared mainly by hepatic (CYP3A4) metabolism with limited renal elimination, so dose modification is driven by toxicity — chiefly CPK elevation, diarrhea, and myopathy — rather than by eGFR. The approved schedule is avutometinib 3.2 mg orally twice weekly with defactinib 200 mg twice daily, dosed 3 weeks on / 1 week off; the label prescribes stepwise interruptions and reductions for grade >=3 CPK elevation, rhabdomyolysis, and severe diarrhea. Avoid strong CYP3A inhibitors/inducers. | Yes Not characterized. As a small-molecule, predominantly hepatically cleared oral agent expected to be substantially protein-bound with a large volume of distribution, avutometinib is unlikely to be meaningfully removed by hemodialysis; specific dialysis-removal data are not available. Dialysis in this setting supports severe AKI rather than clearing the drug. |
| Axitinib HTN VEGFR TKI | No renal dose adjustment is generally required across the range of baseline renal function studied, and patients with mild-to-severe renal impairment have been treated, though data in end-stage renal disease are very limited. Less than 1% of an administered dose is excreted unchanged in urine (axitinib is cleared primarily by hepatic CYP3A4/1A2 metabolism), so renal clearance is not a major elimination route. Dose modification in practice is driven by toxicity (e.g., uncontrolled hypertension, proteinuria) rather than by creatinine clearance, using protocol-based interruptions and reductions. | — Not well characterized. Axitinib is a small-molecule, highly protein-bound (>99%) oral TKI with predominantly hepatic clearance and minimal (<1%) urinary excretion of unchanged drug, so meaningful removal by hemodialysis is considered unlikely; specific dialysis-removal data are lacking. |
| Azacitidine FANC Hypomethylating agent | No starting-dose adjustment is required for baseline renal impairment, but the label mandates a 50% dose reduction of the next cycle if unexplained serum bicarbonate <20 mEq/L or a rise in BUN/creatinine occurs, with resumption only after recovery to baseline. Use with caution and closer monitoring in CKD. | — Azacitidine and its metabolites are partly renally cleared; specific hemodialysis removal data are limited. It is given to dialysis patients in practice with careful monitoring, but no validated supplemental dosing exists. |
| Belantamab mafodotin GLOM Antibody-drug conjugate (BCMA/MMAF) | No renal dose adjustment defined; pharmacokinetics are not expected to depend on renal clearance for an IgG-MMAF conjugate. Dosing modifications are driven by ocular findings, not renal function. | No Not dialyzable (large ADC; non-cleavable linker, internalization-dependent MMAF). No supplemental dosing for HD/PD. |
| Belzutifan PRE HIF-2α inhibitor | No baseline renal dose change per the FDA label, including ESKD; in severe impairment (eGFR 15-29, MDRD) the label directs monitoring for increased adverse reactions and modifying the dose accordingly. Standard 120 mg once daily; modifications are driven by anemia and hypoxia rather than CrCl. | Yes Not characterized; belzutifan is highly protein-bound and primarily metabolized by UGT2B17/CYP2C19, so it is unlikely to be substantially removed by dialysis. No ESKD dosing guidance exists. |
| Bendamustine XTAL Alkylator | Do not use if CrCl <30 mL/min - PK in severe impairment is unknown. At CrCl >=30 the label specifies no dosage adjustment and carries no reduced-dose band at any clearance, population PK having shown no clinically meaningful effect of mild-to-moderate impairment. (A CrCl <40 mL/min floor appears in older references: that was the US label until it moved to <30 in 2017, and it is superseded.) Active metabolites contribute little to overall effect, but exposure data in advanced CKD are sparse - individualize with pharmacy. | Yes Parent drug is rapidly hydrolyzed/metabolized with short half-life, so it is not meaningfully dialyzable; reported ESKD/HD cases dosed bendamustine successfully with careful timing rather than relying on dialytic removal. |
| Bevacizumab GLOM Anti-VEGF antibody | No renal dose adjustment is defined by the FDA label, as bevacizumab is a monoclonal antibody cleared by proteolytic catabolism rather than renal excretion, and pharmacokinetics are not meaningfully altered in renal impairment. Management is toxicity-driven, not level-driven: per label, interrupt for moderate-to-severe proteinuria pending resolution to <2 g/24 h, and discontinue permanently for nephrotic syndrome, biopsy-proven thrombotic microangiopathy, or hypertensive crisis. | No As a ~149 kDa IgG1 monoclonal antibody, bevacizumab is not removed by conventional or high-flux hemodialysis; HD does not mitigate its renal vascular toxicity. There are no special dosing recommendations for patients on dialysis, and clinical experience in ESKD/HD is limited to small reports. |
| Bicalutamide AIN Nonsteroidal antiandrogen | No dose adjustment for renal impairment. Dose with caution in severe hepatic impairment (slower (R)-enantiomer elimination). | Yes Not expected to be meaningfully dialyzable given high protein binding and hepatic clearance; not clinically relevant to dosing. |
| Binimetinib ATN MEK inhibitor | No dedicated renal dose adjustment; no change recommended for mild-moderate impairment, and severe impairment/dialysis are not studied. Modifications are driven by CK, LVEF, retinopathy, and hepatic toxicity. | — Highly protein-bound oral small molecule; not expected to be appreciably dialyzed. No validated ESKD dosing. |
| Bleomycin PRE Antitumor antibiotic | Reduce dose in renal impairment; common guidance reduces by ~25% for CrCl 40-50 mL/min and progressively more (up to ~50-60%) for CrCl 10-40 mL/min, reflecting the exponential rise in half-life below ~25-35 mL/min. Verify against local protocol. | — Low-molecular-weight and water-soluble, so some dialytic removal is plausible and case-level reports suggest it, but it has not been formally characterized and is not relied upon clinically. Dosing in dialysis patients should be conservative and individualized. |
| Blinatumomab PRE BiTE (CD19×CD3) | No specific renal dose adjustment for CrCl >=30 mL/min; pharmacokinetic data in severe impairment (CrCl <30) and dialysis are limited, so use with monitoring. The practical levers are step-up dosing and interruption for severe CRS/TLS rather than renal dose modification of the continuous infusion. | No Not dialyzable as a therapeutic—a ~54 kDa bispecific protein given by continuous infusion with a very short half-life (~2 hours), cleared by catabolism; renal replacement therapy is used to treat TLS/AKI, not to remove the drug, and no supplemental dosing is needed. |
| Bortezomib TMA Proteasome inhibitor | No renal dose adjustment required at any level of renal function, including dialysis (bortezomib is hepatically metabolized via CYP-mediated deboronation). This renal-sparing profile is a key reason it anchors regimens for myeloma with kidney involvement. | — Not appreciably dialyzed; on dialysis days, administer after the HD session per label. No supplemental dose required. |
| Bosutinib PSEUDO BCR-ABL TKI | Per labeling, reduce the starting dose in baseline renal impairment: CrCl 30-50 mL/min use a reduced starting dose (e.g., 400 mg in the resistant/intolerant setting), and CrCl <30 mL/min use a further-reduced dose (e.g., 300 mg). Titrate per response and tolerability. | — Highly protein-bound and hepatically metabolized; not expected to be appreciably dialyzed and no supplemental post-dialysis dosing is established. Use clinical judgment in ESKD. |
| BRAF / MEK Inhibitors ATN BRAF/MEK inhibitor | No CrCl-based dose adjustment is established for the BRAF inhibitors (vemurafenib, dabrafenib, encorafenib) or MEK inhibitors (trametinib, cobimetinib, binimetinib) — all are hepatically metabolized small molecules with low renal elimination, so mild-to-moderate impairment is not expected to require change. Manage emergent AKI by holding the drug and treating the precipitant (pyrexia/volume loss) rather than by reducing dose for GFR; data in severe impairment/dialysis are limited (class-level guidance). | Yes Not appreciably dialyzable as a class — these agents are highly protein-bound, non-renally cleared small molecules, so hemodialysis is not expected to remove meaningful drug. No ESKD-specific dosing guidance exists; standard dosing with clinical monitoring is reasonable (limited data). |
| Brentuximab vedotin PRE Antibody-drug conjugate (CD30/MMAE) | Per label, severe renal impairment (CrCl <30) increases MMAE exposure and adverse events - use with caution and avoid where alternatives exist; no adjustment needed for mild-moderate impairment. MMAE is a CYP3A4 substrate. | — Not appreciably dialyzed (large ADC; protein-bound MMAE). No supplemental dosing guidance for HD/PD. |
| Brigatinib PSEUDO ALK TKI | Reduce the dose for severe renal impairment (eGFR <30 mL/min/1.73 m2) - e.g., decrease the maintenance dose by ~50% per labeling. No adjustment is needed for mild-to-moderate impairment. Hepatic impairment also warrants reduction. | — Highly protein-bound (~91%) and hepatically metabolized; not expected to be meaningfully dialyzed. ESKD data are limited - monitor clinically. |
| Busulfan TMA Alkylator | Busulfan clearance is largely hepatic (GST-mediated); no formal renal CrCl dose banding, but AUC-targeted (therapeutic-drug-monitoring) dosing is standard to avoid the high exposures linked to TMA and VOD. Reduced clearance at high doses warrants level monitoring. | No Busulfan is moderately dialyzable in principle, but TDM-guided dosing (not dialysis) is the control strategy; dialysis is reserved for managing TA-TMA-related renal failure rather than for drug removal. |
| Cabazitaxel PRE Taxane | Hepatically (CYP3A) metabolized with minimal renal excretion - no formal renal dose adjustment for mild-moderate impairment; use caution in severe impairment/ESKD given limited data. Reduce dose for hepatic impairment and with strong CYP3A inhibitors. | No Highly protein-bound and non-renally cleared; not dialyzable. No HD-timed dosing established. |
| Cabozantinib HTN VEGFR/MET TKI | No dose adjustment for mild-to-moderate renal impairment; cabozantinib has not been studied in severe renal impairment or ESKD, so use is cautious there. It is hepatically metabolized (CYP3A4), and dose reduction is recommended for hepatic impairment. | Yes Highly protein-bound (~99.7%) and hepatically cleared, so it is not meaningfully dialyzable; no supplemental dosing rationale for HD, and data in dialysis patients are sparse. |
| Capecitabine PRE Pyrimidine analog (oral 5-FU) | Per labeling/PK data: no adjustment for mild impairment (CrCl 51-80); reduce to 75% of starting dose for moderate impairment (CrCl 30-50). Below CrCl 30 the current XELODA label does NOT contraindicate - section 4 lists only severe hypersensitivity to fluorouracil or capecitabine - but states that experience is limited and a dosage has not been established, permitting administration on an individual basis if no treatment alternative exists, at a reduced starting dose with close clinical and biochemical monitoring. Treat that band as avoid-unless-no-alternative rather than an absolute bar: every patient with severe impairment in the PK study experienced grade 3-4 toxicity, and legacy pre-PLR generic labels still carry an outright CrCl <30 contraindication. | — Capecitabine and 5-FU have short half-lives and are not managed by dialysis; the renally cleared catabolites (e.g., fluoro-beta-alanine) accumulate in renal failure, which is why severe impairment is avoided rather than dialysis-supported - no dialysis dosing has been established. |
| Capivasertib PRE AKT inhibitor | No dedicated renal dose adjustment for mild–moderate impairment; severe impairment/ESKD not well studied. Dose modification is driven by GI/metabolic toxicity grade. Capivasertib is given on an intermittent (4-days-on/3-days-off) schedule. | — Hepatically metabolized small molecule (CYP3A4); dialyzability not well characterized and unlikely to be the management lever. In advanced CKD, focus on volume/glucose management. |
| Capmatinib PSEUDO MET inhibitor | No starting-dose adjustment for mild-moderate renal impairment; severe impairment and dialysis are not well studied (use with caution). Dose modifications are driven by edema, ILD/pneumonitis, and hepatotoxicity rather than a CrCl rule. | — Highly protein-bound oral small molecule; not expected to be appreciably dialyzed. No validated ESKD dosing. |
| CAR-T Cell Therapy PRE CAR-T cell therapy | CAR-T is a one-time autologous cell infusion, not a dose-titrated drug, so there is no renal dose adjustment for the cells themselves; however, the lymphodepleting chemotherapy given beforehand (fludarabine/cyclophosphamide) IS renally cleared, and fludarabine should be dose-reduced in renal impairment to limit neuro/marrow toxicity. Baseline renal impairment does not preclude CAR-T but raises CRS/AKI supportive-care stakes. | No Not applicable to the cell product; AKI is driven by cytokine-release-syndrome hemodynamics and tumor lysis and is managed supportively, with continuous renal replacement therapy (CRRT) used for severe AKI in the ICU. Tocilizumab and corticosteroids used for CRS are not removed by dialysis. |
| Carboplatin ATN Platinum agent | Dosed by target AUC using the Calvert formula (dose mg = AUC x [GFR + 25]), so renal function is built directly into the prescription rather than handled by a separate adjustment. Capping the GFR estimate at 125 mL/min guards against overdosing when a creatinine-based estimate runs spuriously high — a consequence of IDMS standardization of creatinine assays, which lowered reported creatinine and so inflated Cockcroft-Gault GFR (McLean et al., Gynecol Oncol 2020, PMID 32220419). The cap is a dosing convention rather than a physiologic ceiling, and it is not unanimous: it is endorsed by the FDA, ASCO and GOG (Fehr et al., ESMO Open 2018, PMID 29531843) and attributed to a 2010 NCI recommendation (Morrow et al., J Oncol Pharm Pract 2019, PMID 30336729), but that same analysis concludes that capping a genuinely high GFR delivers a lower AUC than intended, and ADDIKD 2025 instead treats an eGFR above 125 mL/min/1.73 m2 as the trigger to obtain a directly measured GFR. Lower target AUCs are used as GFR falls; in severe impairment or dialysis-dependent patients, dose individually with pharmacy/onco-nephrology input. | Yes Carboplatin (and its reactive aquated/platinum species) is partially removed by hemodialysis, particularly the unbound platinum fraction; protein-bound platinum that accumulates over days is not efficiently cleared. In dialysis-dependent patients it is dosed to a reduced target AUC with chemotherapy timed relative to HD sessions (commonly drug given a few hours before dialysis), though optimal timing rests on limited pharmacokinetic data. |
| Carfilzomib TMA Proteasome inhibitor | Per label no starting-dose adjustment is required across renal function including dialysis (carfilzomib is rapidly metabolized by peptidase/epoxide hydrolase, not renally cleared); however, given the high rate of renal events, monitor closely and hold for TMA/AKI rather than adjusting prophylactically. | Yes On hemodialysis days, administer carfilzomib after the HD session (per label) for theoretical dialytic clearance; the parent drug is largely cleared by non-renal metabolism. Dialysis is otherwise used to support TMA/AKI. |
| Carmofur (HCFU) TMA Antimetabolite (oral 5-FU prodrug) | No validated renal nomogram; use caution and consider reduction in significant renal impairment given renal elimination of 5-FU metabolites, per regional labeling. | — Not well characterized; dialysis is supportive for AKI rather than for drug removal. |
| Carmustine (BCNU) CIN Nitrosourea alkylator | No precise CrCl-banded schema; reduce or avoid in baseline renal impairment and cap cumulative lifetime dose. Hold subsequent courses for a sustained creatinine rise rather than waiting for symptomatic CKD. | Yes Highly lipophilic, rapidly metabolized parent drug; not meaningfully removed by dialysis and dialysis is not a management strategy. ESKD use is essentially limited to individualized conditioning protocols. |
| Casdatifan PRE HIF-2α inhibitor (investigational) | Not established (investigational). HIF-2α inhibitors are hepatically metabolized; meaningful renal-clearance dependence is not expected, but formal renal-impairment dosing has not been published. Many ccRCC patients have reduced nephron mass after nephrectomy, which is relevant to baseline GFR interpretation. | — Not characterized; a protein-bound, hepatically cleared small molecule is unlikely to be appreciably dialyzed. No ESKD dosing data. |
| Catumaxomab PRE Trifunctional bispecific (EpCAM×CD3) | No renal dose adjustment defined; the agent is given intraperitoneally as an antibody and is not renally cleared. The actionable interventions are hemodynamic/supportive rather than renal dosing. | No A large trifunctional antibody — not dialyzable and cleared by proteolysis; no ESKD dosing guidance. Renal management is volume- and electrolyte-focused. |
| Cemiplimab AIN Anti-PD-1 antibody | No baseline renal dose adjustment (fixed-dose antibody, not renally cleared). Toxicity-based modification follows irAE grading: withhold for grade 2 nephritis with steroids; permanently discontinue for grade 3-4 or recurrent severe nephritis. | No Not dialyzable—IgG4 monoclonal antibody cleared by reticuloendothelial catabolism; not removed by hemodialysis, no supplemental dosing, standard dosing in ESKD. |
| Ceritinib PRE ALK TKI | No starting-dose change for mild-to-moderate renal impairment (negligible renal excretion); severe-impairment/ESKD data are limited, so use clinical monitoring. The practical 'renal' adjustment is interruption/reduction when GI toxicity threatens volume status. Hepatic impairment requires dose reduction. | — Highly protein-bound (~97%) and hepatically metabolized; not expected to be dialyzed and no supplemental dosing established. |
| Cetuximab LYTE Anti-EGFR antibody | No renal dose adjustment. Cetuximab is a ~152 kDa IgG1 antibody cleared by reticuloendothelial catabolism, not glomerular filtration, so kidney function does not change its exposure and no reduction is needed in CKD. The management problem is electrolyte monitoring and repletion, not dosing. | No Not dialyzable — an IgG1 monoclonal antibody is far too large to cross dialysis membranes and stays confined to the vascular compartment. Hemodialysis neither removes cetuximab nor corrects the underlying tubular defect; note that dialysis can itself remove magnesium, so Mg status still needs attention in dialysis patients. |
| Chlorambucil SIADH Alkylating agent (nitrogen mustard) | No formal renal dose-adjustment scheme is established; chlorambucil is extensively hepatically metabolized to phenylacetic acid mustard with limited unchanged renal excretion. Dosing is guided mainly by hematologic tolerance. | Yes Not characterized as dialyzable and unlikely to be efficiently removed given rapid metabolism and protein binding; dialysis is not used for drug clearance. |
| Ciltacabtagene autoleucel PRE BCMA CAR-T cell therapy | A fixed cell product with no renal dose adjustment; renal dosing applies to the lymphodepleting fludarabine. | — Not applicable (a living-cell product). Dialysis supports AKI/tumor lysis rather than removing the therapy. |
| Cisplatin ATN Platinum agent | No fixed CrCl-banded schedule in the FDA label, and two different conventions circulate that must not be blended. Many centers treat CrCl as an eligibility floor: avoid or withhold cisplatin when baseline CrCl is below ~50-60 mL/min and substitute carboplatin (AUC-dosed by GFR). Renal-dosing tables instead continue treatment into that range at a reduced dose (~25% reduction for CrCl 46-60, ~50% for CrCl 30-45) with intensified hydration and CrCl reassessment every cycle. Because the reduction bands sit entirely inside the range the eligibility floor excludes, confirm which rule the treating protocol uses before dosing below ~60 mL/min. High single doses (e.g., >=100 mg/m2) per cycle and short cycle intervals raise nephrotoxicity risk; cumulative platinum dose drives chronic injury, so respect a defined cumulative ceiling and reassess renal function before each cycle. | No Free (unbound, ultrafilterable) platinum is small and dialyzable, but cisplatin binds plasma proteins irreversibly within hours and that bound fraction is not removed by hemodialysis, so dialysis does not reliably rescue overdose once binding has occurred. In ESKD/HD, free platinum accumulates because renal elimination is lost; if cisplatin is used, give reduced doses and time HD relative to infusion in coordination with pharmacy (limited data). |
| Cladribine XTAL Purine analog | Substantially renally eliminated; the label advises caution and consideration of dose reduction with close monitoring in renal impairment. No firmly validated CrCl bands exist; published practice uses reduced/spaced (e.g. every-other-week) dosing in severe CKD, where complete remission is still achievable. | Yes Not reliably characterized and not considered readily dialyzable for drug removal; dialysis is used to manage tumor-lysis metabolic derangements. |
| Clofarabine PRE Purine analog | Limited renal pharmacokinetic data; the label advises starting at a reduced dose and monitoring closely when CrCl is 30-60 mL/min, and clofarabine is not recommended (avoid) when CrCl is below 30 mL/min. Renal clearance accounts for a substantial fraction of elimination, so impaired clearance raises systemic exposure. | — Not formally characterized; no established supplemental dosing for hemodialysis. Given its small size and renal elimination, removal is theoretical, but it is not used in dialysis-dependent patients and HD is employed only to manage AKI complications, not to dose the drug. |
| Cobimetinib ATN MEK inhibitor | No renal dose adjustment recommended for mild-moderate impairment; severe impairment and dialysis are not studied. Dose modification is driven mainly by CK elevation, retinopathy, LVEF, and photosensitivity. | — Highly protein-bound oral small molecule; not expected to be meaningfully dialyzed. No validated ESKD dosing. |
| Copanlisib HTN Pan-PI3K inhibitor | No specific dose adjustment for renal impairment in labeling; hepatic metabolism predominates. Dose modification is driven by hypertension, hyperglycemia and cytopenias rather than GFR. | Yes Protein-bound IV agent given intermittently; not expected to be dialyzable, and ESKD dosing is not established. |
| Cosibelimab AIN PD-L1 immune checkpoint inhibitor | No starting-dose adjustment for renal impairment is established; as a ~150 kDa IgG1 monoclonal antibody, cosibelimab is not cleared by the kidney, and mild-to-moderate renal impairment is not expected to alter exposure. Dosing is a fixed flat regimen (1200 mg IV every 3 weeks). Management of nephrotoxicity is by holding or discontinuing the drug and immunosuppression rather than dose reduction. Data in severe renal impairment or dialysis are lacking. | No Not dialyzable. Large therapeutic monoclonal antibodies are not removed by hemodialysis or peritoneal dialysis owing to their size; no dosing change is anticipated for patients on dialysis, though formal data are absent. |
| Crizotinib RCYST ALK/ROS1/MET TKI | No starting-dose change for mild-to-moderate renal impairment (CrCl >=30). For severe renal impairment not on dialysis (CrCl <30), reduce the dose (e.g., to 250 mg once daily) per labeling. Hepatic impairment also requires adjustment. | — Highly protein-bound (~91%) and hepatically metabolized; not appreciably dialyzed. ESKD dosing data are limited - use clinical monitoring. |
| Cyclophosphamide SIADH Oxazaphosphorine alkylator | Cyclophosphamide itself is not classically considered intrinsically nephrotoxic and the FDA label does not specify creatinine-clearance-based cutpoints; however, parent drug and active metabolites are partly renally cleared, so clinical practice and onco-nephrology references suggest dose attenuation (often roughly 25% reduction) for severe impairment (CrCl <10-25 mL/min) and caution in advanced CKD to limit accumulation and exaggerated toxicity. Adequate hydration with high IV doses is the key renal-safety measure, more so than empiric dose cuts. | Yes Cyclophosphamide and its metabolites are appreciably dialyzable (the parent is a small, water-soluble, minimally protein-bound molecule), with reported clearance during hemodialysis; on HD days it is conventionally administered after dialysis, or dosing is timed to avoid removing drug before it is bioactivated. Data are limited and largely pharmacokinetic/case-level rather than from prospective ESKD dosing studies. |
| Cytarabine XTAL Nucleoside analog | Standard-dose cytarabine needs little renal adjustment; for HIGH-dose cytarabine, reduced renal function (and age) increase the risk of neurotoxicity (cerebellar) so dose reduction is advised when creatinine/CrCl worsens. Renal handling is a high-dose neurotoxicity concern more than a nephrotoxicity one. | — Cytarabine is rapidly deaminated to inactive ara-U with a short half-life; it is not primarily managed by dialysis, though dialysis is used to treat TLS-related renal failure and electrolyte derangements. |
| Dabrafenib AIN BRAF inhibitor | No dedicated renal dose adjustment is specified in the FDA label. Dabrafenib is cleared predominantly by hepatobiliary metabolism (CYP2C8/CYP3A4) and fecal excretion with a minority renal route, so no adjustment is recommended for mild-to-moderate renal impairment. It has not been formally studied in severe renal impairment or ESRD — use with caution and monitor. In practice, dose interruptions/reductions are driven by pyrexia, transaminitis, and other toxicities rather than by eGFR. | Yes Not expected to be removed by dialysis and not established as dialyzable. Dabrafenib is highly protein-bound (~99.7%) with a large volume of distribution and hepatic metabolism, so hemodialysis is unlikely to clear meaningful drug; no data support supplemental dosing around dialysis. |
| Dacarbazine PRE Alkylator | No established renal CrCl dose modification; dacarbazine is partly renally excreted but dose adjustment is driven mainly by hematologic toxicity and hepatic function. Use general caution and maintain hydration in renal impairment. | — Short-lived parent prodrug undergoing hepatic activation; not a drug managed by dialysis. ESKD data are minimal. |
| Dactinomycin (actinomycin D) LYTE Antitumor antibiotic | No well-established renal dose-adjustment scheme; dactinomycin is largely excreted in bile/feces with minor renal elimination. Dose modification is generally driven by hepatic toxicity and myelosuppression rather than kidney function. | Yes Not meaningfully dialyzable; high tissue binding and predominantly biliary/fecal elimination. Dialysis is used only for TLS-related metabolic derangements, not drug removal. |
| Daratumumab PRE Anti-CD38 antibody | No renal dose adjustment; antibody clearance is target-mediated/reticuloendothelial, not renal. Standard IV or subcutaneous dosing is used regardless of CrCl, including in dialysis-dependent patients per trial and case data. | No Not dialyzed — a large IgG1 antibody not removed by HD/PD; full standard dosing in ESKD. Renal recovery off dialysis has been reported with daratumumab-based therapy. |
| Darolutamide LYTE Androgen receptor inhibitor (ARSI) | Reduce the starting dose to 300 mg twice daily in severe renal impairment (eGFR 15-29 mL/min/1.73 m2, not on hemodialysis) and in moderate hepatic impairment, because systemic exposure is increased; standard 600 mg twice daily otherwise. | — Dialyzability not formally established; darolutamide is substantially protein-bound and hepatically metabolized, so dialysis is unlikely to be a primary management consideration. Use clinical judgment and labeling in dialysis patients. |
| Dasatinib GLOM BCR-ABL TKI | No formal renal dose adjustment is specified (dasatinib is extensively hepatically metabolized with <4% renal excretion); however, the practical 'renal' adjustment is dose reduction or drug switch when treatment-emergent proteinuria appears. | — Dasatinib is highly protein-bound and extensively metabolized; it is not appreciably dialyzed and needs no supplemental post-dialysis dose. Standard dosing applies in ESKD with clinical monitoring. |
| Datopotamab deruxtecan (Dato-DXd) ATN Antibody-drug conjugate (TROP2/DXd) | No dosage adjustment is recommended for CLcr 30 to <90 mL/min; however, the label reports a higher incidence of ILD/pneumonitis in that band, so monitor those patients more closely for respiratory and other adverse reactions. Pharmacokinetics of the ADC and of DXd below CLcr 30 are unknown and ESKD is unstudied. Modify dose/hold for toxicity per label. The antibody component is not renally cleared; small-molecule payload exposure in advanced CKD is not well defined. | No The IgG–ADC is not dialyzable; the released small-molecule DXd payload's dialyzability is not characterized. No ESKD dosing guidance — use clinical judgment and close monitoring. |
| Decitabine XTAL Hypomethylating agent | No formal renal dose adjustment is established in the label; decitabine is largely metabolized by deamination (cytidine deaminase) rather than renal excretion. Use caution in significant renal impairment given limited data and monitor renal function closely. | — Not well characterized; the short plasma half-life and rapid deamination limit the rationale for dialytic dosing. Hemodialysis is used to treat AKI/metabolic complications, not to adjust drug levels. |
| Denileukin diftitox PRE Immunotoxin (IL-2–diphtheria) | Weight-based dosing (9 micrograms/kg/day for 5 days every 21 days); modification is driven by toxicity (albumin, organ function), not by CrCl. No CrCl-based dose thresholds are defined. | — Not established — a large fusion protein; AKI here is managed hemodynamically rather than by dialytic drug removal. |
| Denosumab LYTE Anti-RANKL antibody | No dose reduction for renal function (cleared by the reticuloendothelial system, independent of GFR), but in CKD stage 4-5/dialysis the hazard is hypocalcemia - intensify calcium/vitamin D and monitoring rather than altering the dose. Avoid concurrent same-indication dosing of Xgeva and Prolia. | No Monoclonal antibody (IgG2); not dialyzable and pharmacokinetics are unaffected by dialysis. Hemodialysis is used to manage the metabolic consequences, not to remove the drug. |
| Dinutuximab PRE Anti-GD2 antibody | No specific renal dose adjustment in labeling (a monoclonal antibody); manage infusion rate and interruptions for capillary leak, pain and hemodynamic instability. | No A monoclonal antibody; not dialyzable. ESKD dosing is not established (used in pediatric neuroblastoma). |
| Docetaxel PRE Taxane | Hepatically (CYP3A4) metabolized and biliary excreted - no renal dose adjustment; reduce dose (or avoid) with significant hepatic dysfunction/elevated bilirubin and transaminases, which raise toxicity risk. | No Highly protein-bound, large volume of distribution, non-renally cleared; not dialyzable. Tolerated in dialysis and transplant patients with standard dosing and supportive care. |
| Dordaviprone PRE Imipridone (ONC201; DRD2/ClpP) | No renal-impairment dose adjustment is established; dordaviprone is an orally administered small molecule given on an intermittent schedule and is not primarily renally cleared. Dose interruption/modification is driven by tolerability and by QT/cardiac considerations rather than by GFR. | Yes Not characterized as dialyzable and not clinically relevant: dordaviprone is not primarily renally eliminated, and there is no renal-clearance or drug-removal scenario in which dialysis is relevant. Renal replacement therapy would only ever address an unrelated AKI. |
| Dostarlimab AIN Anti-PD-1 antibody | No baseline renal dose adjustment (fixed-dose antibody, not renally cleared). Toxicity-based modification follows irAE grading: withhold for grade 2 nephritis with steroids; permanently discontinue for grade 3-4 or recurrent severe nephritis. | No Not dialyzable—IgG4 monoclonal antibody cleared by reticuloendothelial catabolism; not removed by hemodialysis, no supplemental dosing, standard dosing in ESKD. |
| Doxifluridine TMA Antimetabolite (oral 5-FU prodrug) | No validated renal nomogram. Given a documented renal clearance component for doxifluridine and renal elimination of 5-FU metabolites, consider caution/dose reduction in significant renal impairment per regional labeling. | — Not well characterized; dialysis is supportive for AKI rather than established for drug removal. |
| Doxorubicin GLOM Anthracycline | No renal dose adjustment is required — doxorubicin is hepatically metabolized and biliary-excreted, so dosing is guided by hepatic function and bilirubin rather than renal function. Renal impairment does not mandate dose reduction. | No Not dialyzable to any clinically meaningful extent; doxorubicin is large, highly protein- and tissue-bound, with a very large volume of distribution, so hemodialysis does not remove it and no supplemental dosing is needed in ESKD. |
| Durvalumab AIN Anti-PD-L1 antibody | No baseline renal dose adjustment (fixed-dose antibody, not renally cleared). Toxicity-based modification follows irAE grading: withhold for grade 2 nephritis with steroids; permanently discontinue for grade 3-4 or recurrent severe nephritis. | No Not dialyzable—IgG1 monoclonal antibody cleared by reticuloendothelial catabolism; not removed by hemodialysis, no supplemental dosing, standard dosing in ESKD. |
| Duvelisib PRE PI3Kδ/γ inhibitor | No renal dose adjustment specified (hepatic CYP3A4 metabolism); use caution in CKD. Dose modifications are driven by colitis, hepatotoxicity, infection and cytopenias. | Yes Highly protein-bound; not expected to be dialyzable. No ESKD dosing established. |
| Elacestrant PRE Oral selective estrogen-receptor degrader (SERD) | No renal dose adjustment is established for mild–moderate impairment; severe impairment/ESKD are not well studied. Dose reductions per label are driven by hepatic impairment and CYP3A4 interactions, not renal function. | Yes Highly protein-bound and hepatically metabolized; not expected to be dialyzable. No ESKD dosing guidance exists. |
| Elotuzumab PRE Anti-SLAMF7 mAb | No dose adjustment for any degree of renal impairment, including severe impairment and end-stage renal disease on dialysis (Berdeja 2015). The actionable renal adjustment is to the partner immunomodulator, not to elotuzumab. | No A ~150 kDa IgG1 antibody — not removed by hemodialysis and cleared by proteolysis; pharmacokinetics are unchanged in dialysis patients, so no peri-dialysis timing change is needed. |
| Elranatamab PRE Bispecific (BCMA×CD3) | No specific renal dose adjustment is established; elranatamab pharmacokinetics are not meaningfully renally dependent. Two-step priming dosing and holds for severe CRS, plus TLS prophylaxis, are the operative levers rather than renal dose modification. | No Not dialyzable—an IgG-based bispecific antibody cleared by catabolism; not removed by hemodialysis and no supplemental dosing needed. Renal replacement therapy treats AKI/TLS, not drug clearance. |
| Enasidenib PRE IDH2 inhibitor | No dedicated renal dose adjustment is established; enasidenib was not studied in severe renal impairment/ESKD. Standard dose is 100 mg orally once daily, modified for toxicity (including differentiation syndrome and indirect hyperbilirubinemia), not for CrCl. | Yes Not characterized; enasidenib is highly protein-bound and hepatically metabolized, so it is not expected to be appreciably removed by hemodialysis. No HD-specific dosing guidance exists. |
| Encorafenib ATN BRAF inhibitor | No dedicated renal dose adjustment established; no change recommended for mild-moderate impairment, and severe impairment/dialysis are not studied (use with caution). Dose modifications are driven mainly by CK, hepatic, and cardiac (QT) toxicity. | Yes Highly protein-bound oral small molecule; not expected to be appreciably removed by dialysis. No validated ESKD dosing. |
| Enfortumab vedotin ATN Antibody-drug conjugate (Nectin-4/MMAE) | No starting-dose adjustment for mild-moderate renal impairment; per label, the recommended dose has been administered to patients with CrCl >=15 mL/min, and the drug is used in real-world practice at eGFR <30. Limited data in ESKD/dialysis. The cytotoxic exposure is the released MMAE (hepatically metabolized via CYP3A4), not renally cleared parent ADC. | — The intact ADC and protein-bound MMAE are not meaningfully dialyzed; HD is used to support AKI/metabolic complications, not to remove the drug. Terminal half-life ~3.4 days guides how long toxicity (e.g., refractory hyperglycemia) may persist. |
| Ensartinib PSEUDO ALK TKI | No CrCl-based renal-impairment dose thresholds are established in the cited literature; consult current product labeling. A benign transporter-mediated creatinine rise should not by itself prompt CrCl-based dose modification. | — Not characterized. As a highly protein-bound small-molecule oral TKI, substantial dialytic removal is unlikely, but drug-specific data are lacking. |
| Entrectinib PSEUDO TRK/ROS1 TKI | No renal dose adjustment for mild-to-moderate impairment; entrectinib is hepatically (CYP3A4) metabolized with low renal clearance. The creatinine rise should not be misread as AKI requiring dose reduction. Limited data in severe impairment/dialysis. | — Not characterized; highly protein-bound, lipophilic, non-renally cleared — unlikely to be appreciably dialyzed. No ESKD dosing guidance. |
| Enzalutamide HTN Androgen-receptor inhibitor | No dose adjustment for mild–moderate renal impairment; severe impairment and ESKD have not been formally studied. Reduce dose (to 80 mg once daily) with concomitant strong CYP2C8 inhibitors; no dose adjustment is required for hepatic impairment (Child-Pugh A-C) per label. | Yes Highly protein-bound and hepatically metabolized; not expected to be dialyzable. No established ESKD dosing — use clinical judgment and blood-pressure-directed care. |
| Epcoritamab PRE Bispecific (CD20×CD3) | No specific renal dose adjustment defined; IgG bispecific exposure is not expected to depend on renal clearance. No dedicated data in severe impairment/ESKD. | No Not dialyzable (large IgG, reticuloendothelial catabolism). No supplemental dosing for HD/PD. |
| Erdafitinib LYTE FGFR inhibitor | No starting-dose change for mild-moderate renal impairment; severe impairment and dialysis are not well studied (use with caution). The principal 'dose adjustment' is phosphate-guided titration/interruption rather than a CrCl-based rule. | — Highly protein-bound oral small molecule; not expected to be appreciably dialyzed. No validated ESKD dosing — phosphate handling is also altered in ESKD, complicating the pharmacodynamic phosphate biomarker. |
| Eribulin PRE Microtubule inhibitor | Reduce dose to 1.1 mg/m2 across CrCl 15-49 mL/min (moderate or severe impairment) per the label; no adjustment for mild impairment (CrCl 50-79). PK data support 1.1 mg/m2 matching the exposure seen at 1.4 mg/m2 with normal function. | Yes Highly protein-bound with a large volume of distribution and predominantly hepatobiliary elimination; not expected to be dialyzable. No HD-timed dosing established. |
| Erlotinib GLOM EGFR TKI | No specific dose reduction is established for renal impairment (erlotinib is hepatically metabolized via CYP3A4/1A2 and biliary-excreted); use caution in severe impairment as renal data are sparse, and manage GI-driven volume depletion proactively. The pancreatic-cancer regimen pairs it with gemcitabine, which has its own renal considerations. | Yes Not appreciably dialyzable—highly protein-bound (~93%), lipophilic, with predominantly hepatic clearance and minimal renal elimination; hemodialysis is not expected to remove meaningful drug. |
| Estramustine PRE Hormonal–alkylating conjugate | No established CrCl-based dose algorithm; use caution with cardiovascular/cerebrovascular disease and in heart failure. It is contraindicated with active thromboembolic disorders. | — Not characterized/not relevant (highly protein-bound and lipophilic). |
| Etoposide XTAL Topoisomerase II inhibitor | Reduce dose for renal impairment: roughly 75% of dose for CrCl 15-50 mL/min and consider further reduction below 15 mL/min, because renal clearance contributes meaningfully and hypoalbuminemia raises free drug. | Yes Highly protein-bound (~95%) and not cleared by hemodialysis: in the PK-guided dialysis study that dosed carboplatin and etoposide together, carboplatin was cleared by hemodialysis and etoposide was not, and peritoneal dialysis removed neither. There is therefore no post-HD supplemental dose to give. Dialysis is used for TLS-related metabolic complications, not to clear etoposide; reduce dose in renal impairment and target exposure by pharmacokinetic monitoring. |
| Everolimus GLOM mTOR inhibitor | No renal-function-based dose adjustment is defined — everolimus is hepatically metabolized (CYP3A4/P-glycoprotein) and its pharmacokinetics are not meaningfully altered by renal impairment, so dosing is instead adjusted for hepatic impairment, CYP3A drug interactions, and toxicity. When nephrotoxicity (heavy proteinuria or TMA) develops, dose interruption/reduction or discontinuation is the lever, not a renal-clearance-based reduction. | Yes Not meaningfully dialyzable and no supplemental post-dialysis dosing is defined: everolimus has a large apparent volume of distribution, is substantially protein-bound (~74%), and is extensively metabolized, so hemodialysis is not expected to remove significant drug. Data in dialysis patients are limited. |
| Fedratinib LYTE JAK2 inhibitor | Mild renal impairment (CrCl 60-89 mL/min): no dose adjustment. Moderate impairment (CrCl 30-59 mL/min): the standard 400 mg once-daily dose may be used but with monitoring and dose reduction as needed, since exposure is ~37% higher on population PK. Severe impairment (CrCl 15-29 mL/min): reduce to 200 mg once daily — a dedicated phase 1 study found ~1.9-fold higher AUC. End-stage renal disease was included in that same phase 1 study, but it yielded no ESRD dosing recommendation, so no ESRD/dialysis dose is defined. Separately, reduce the dose (or avoid) with concomitant strong CYP3A4 inhibitors. | Yes Not established and unlikely to be meaningfully dialyzable. Fedratinib is extensively protein-bound with a large volume of distribution and a long (~41 h) effective half-life; the dedicated impairment study did not identify hemodialysis as a clearance route, and no dosing recommendation exists for dialysis patients. Dosing is driven by exposure and tolerability, not by dialytic removal. |
| Fludarabine XTAL Purine analog | Per PK/labeling: reduce dose for CrCl 30-70 mL/min (commonly ~20% reduction) and avoid for CrCl <30 mL/min. Prospective dose-adjustment studies show CrCl-banded dosing yields equivalent exposure and acceptable safety; full dosing in unrecognized impairment risks severe (even fatal neuro-) toxicity. | — 2-F-ara-A is renally cleared, so ESKD markedly prolongs exposure, and hemodialysis does remove it: in an anuric patient extended daily dialysis achieved a dialysis clearance of 33.85 mL/min, about 25% of the clearance seen without renal failure. The label still advises avoiding CrCl <30, but that case concluded fludarabine can be given on dialysis where dose reduction and adequate dialytic removal are provided. In conditioning protocols, PK-guided/reduced dosing is used. |
| Fotemustine CIN Nitrosourea (alkylating) | Use caution and consider dose reduction or avoidance in significant renal impairment; specific renal dosing thresholds are not well established for fotemustine. Withhold for evolving renal dysfunction and reassess cumulative exposure. | — Dialyzability is not well characterized; nitrosoureas are lipophilic and rapidly metabolized, so dialysis is not a relied-upon removal strategy. Manage by dose limitation and monitoring rather than dialysis timing. |
| Fruquintinib HTN VEGFR TKI | No specific renal dose adjustment for mild–moderate impairment; not adequately studied in severe renal impairment/ESKD. Modify dose for grade of hypertension/proteinuria per label rather than for GFR alone. | — Highly protein-bound small molecule with hepatic metabolism; not expected to be appreciably dialyzed. No established ESKD dosing — monitor blood pressure and proteinuria closely. |
| Futibatinib LYTE FGFR inhibitor | No starting-dose change for mild-moderate renal impairment; severe impairment/dialysis not well studied. Phosphate-guided modification, not a CrCl rule, governs dosing. | — Highly protein-bound oral small molecule; not expected to be appreciably dialyzed. No validated ESKD dosing; phosphate-based pharmacodynamic monitoring is confounded in ESKD. |
| Gallium nitrate ATN Antineoplastic metal salt | A threshold contraindication rather than a graded reduction: do not initiate if serum creatinine is above ~2.5 mg/dL, and discontinue therapy if creatinine rises to ~2.5 mg/dL (or shows a significant increase) during treatment. Ensure the patient is well hydrated with adequate urine output before and throughout the 5-day course, and give by slow continuous IV infusion. No validated dosing exists for dialysis-dependent patients. | Yes Not well characterized. Gallium circulates largely bound to transferrin and plasma proteins and redistributes into bone with a long terminal elimination, so it is not expected to be efficiently cleared by conventional hemodialysis, and there is no established role for dialysis in managing its toxicity. Data are limited — treat as probably not meaningfully dialyzable. |
| Gedatolisib LYTE Pan-PI3K inhibitor | No renal dose adjustment is established for eGFR >=45 mL/min/1.73 m2 — the range in which the label reports no clinically significant pharmacokinetic differences (MDRD equation); the label states the effect of eGFR <45, or dialysis, on gedatolisib pharmacokinetics is unknown, so use below that threshold is uncharted rather than dose-banded. Dose modifications are driven by hyperglycemia, stomatitis and hematologic toxicity, not by GFR. | Yes Not characterized as dialyzable and not clinically relevant: no dialysis-based removal scenario applies, and patients on dialysis fall below the eGFR range in which the drug's pharmacokinetics have been studied at all. |
| Gefitinib GLOM EGFR TKI | No defined renal dose adjustment (hepatic CYP3A4 metabolism, biliary excretion; <4% renal elimination); caution in severe impairment given limited data. The intervention for glomerular toxicity is drug discontinuation, not dose titration. | Yes Not appreciably dialyzable—highly protein-bound (~90%), lipophilic, large volume of distribution with predominantly hepatic clearance; hemodialysis is not expected to remove meaningful amounts. |
| Gemcitabine TMA Nucleoside analog | No formal renal dose adjustment is specified in the FDA label, which advises caution in renal impairment given limited data; many centers use gemcitabine cautiously at standard or modestly reduced doses with close monitoring rather than a fixed CrCl-based reduction. Critically, dose reduction does not prevent gemcitabine-associated TMA, which is a cumulative-dose/duration phenomenon — once TMA is suspected, the drug must be permanently discontinued rather than dose-reduced. | Yes Gemcitabine and its active metabolite dFdU are renally cleared, and dFdU accumulates markedly in severe renal impairment; the parent drug has a short half-life and is partly cleared by intermittent hemodialysis, but pharmacokinetic data in HD are limited. When gemcitabine is given to dialysis patients (rare, individualized), some protocols administer it 6-12 hours before HD to limit dFdU accumulation; supportive data are sparse and this remains expert-opinion rather than label-driven. |
| Gemtuzumab ozogamicin PRE Antibody-drug conjugate (CD33/calicheamicin) | No specific renal dose adjustment; dose decisions are driven by hepatic function and VOD risk, not renal clearance. Calicheamicin is hepatically handled. | — Not appreciably dialyzed (large ADC; protein-bound calicheamicin). HD/CRRT in VOD is for fluid/AKI support, not drug removal. |
| Gilteritinib PRE FLT3 inhibitor | No dose adjustment for mild-moderate renal impairment; severe impairment/ESKD not well studied (predominantly hepatic CYP3A4 metabolism). Manage interruptions for differentiation syndrome/TLS/PRES rather than by GFR. | Yes Highly protein-bound; not appreciably dialyzable. Dialysis is used for TLS metabolic complications, not drug removal. |
| Glasdegib PRE Hedgehog (SMO) inhibitor | No dose adjustment recommended for mild-moderate renal impairment; safety/PK in severe renal impairment were not established at approval (labeled limitation; post-marketing study required). Hepatic CYP3A4 metabolism predominates. | Yes Highly protein-bound small molecule; not expected to be appreciably dialyzable, and ESKD dosing is not established. |
| Glofitamab PRE Bispecific (CD20×CD3) | No specific renal dose adjustment defined; IgG bispecific exposure is not expected to be renally dependent. No dedicated data in severe impairment/ESKD. | No Not dialyzable (large IgG, reticuloendothelial clearance). No supplemental dosing for HD/PD. |
| Hydroxyurea XTAL Ribonucleotide reductase inhibitor | Hydroxyurea is predominantly renally excreted. The label and pharmacokinetic data support reducing the starting dose in renal impairment (commonly halving the dose when CrCl < 60 mL/min and using marked reductions or avoidance in ESKD) to prevent excessive myelosuppression; titrate to blood counts. | Yes Yes — hydroxyurea is a small (76 Da), water-soluble molecule that is readily removed by hemodialysis. In dialysis-dependent patients, dosing is commonly given after the HD session and reduced; counts must be followed closely. |
| Ibandronate ATN Bisphosphonate | Oral/IV for osteoporosis: no adjustment for CrCl ≥30 mL/min; not recommended (or use with caution) below 30 mL/min. Oncology IV dosing should be reduced and infused slowly in renal impairment; withhold for acute decline in renal function and reassess. | — Negligible plasma drug at steady state due to rapid bone uptake; not meaningfully dialyzed. In hemodialysis patients a reduced IV dose (e.g., 2 mg) given after dialysis achieves equivalent bone binding (Bergner 2005). |
| Iberdomide PRE Cereblon E3 ligase modulator (CELMoD) | The label sets exactly one renal threshold, and it has a deliberate exception in the middle of it. At eGFR below 30 mL/min/1.73 m2 NOT receiving dialysis, reduce to 0.75 mg once daily on Days 1 to 21 of a 28-day cycle; if a further reduction is needed for adverse events, 1 mg every other day on the same schedule. At eGFR 30 or above - and also at eGFR below 30 WITH intermittent hemodialysis - no dose adjustment is recommended. Dose modifications for CYP3A inhibitors are separate and can be the more frequent trigger: strong inhibitors are to be avoided, and if unavoidable the dose drops to 1 mg every other day; moderate inhibitors drop it to 0.75 mg once daily. | — Partially removed, with no dose consequence. Dialysis clearance measured 3.07 L/hr, about 16% of total clearance in patients with kidney failure on intermittent hemodialysis - real but small, and total clearance and exposure on hemodialysis were comparable to subjects with normal renal function. The label therefore recommends no dose adjustment for these patients and directs no post-dialysis timing or supplemental dose, which is why dialysis patients are the one group below eGFR 30 who stay on the full 1 mg. Iberdomide is 75% plasma protein bound with a 415 L apparent volume of distribution and a 37-hour terminal half-life, which is why removal stays partial. Peritoneal dialysis and CRRT are not characterized. |
| Ibritumomab tiuxetan PRE Radioimmunotherapy (Y-90 anti-CD20) | Administered activity is capped by platelet count (e.g. reduced to 0.3 mCi/kg if platelets 100,000-149,000/uL; contraindicated if platelets <100,000/uL or >25% lymphomatous marrow involvement) — a hematologic threshold. No renal CrCl-based dose adjustment is defined; the kidney does not drive dosing. | No The radioimmunoconjugate is not dialyzable. Dialysis is relevant only for managing TLS metabolic derangements, not for removing the drug. |
| Ibrutinib HTN BTK inhibitor | No dose adjustment for mild-to-moderate renal impairment (CrCl ≥30 mL/min); severe impairment (CrCl <30) and dialysis are not well studied — use with caution. Ibrutinib is hepatically (CYP3A) cleared, so hepatic impairment, not renal, drives dose reduction; <10% renal excretion of metabolites. | Yes Not meaningfully dialyzable — highly protein-bound (~97%) small molecule with hepatic clearance. No supplemental dosing after HD is needed. |
| Idarubicin XTAL Anthracycline | Primarily hepatobiliary elimination; reduce in hepatic dysfunction. The current label defines a GFR-based algorithm: reduce the dose by 33% for GFR <30 mL/min or hemodialysis (no adjustment at GFR >=30 mL/min); clinical trials excluded serum creatinine >2 mg/dL. Cumulative anthracycline cardiotoxicity also limits dosing. | Yes Not appreciably dialyzable (large volume of distribution and tissue binding); dialysis manages tumor-lysis derangements. |
| Idecabtagene vicleucel PRE BCMA CAR-T cell therapy | No CAR-T dose adjustment for renal function (it is a fixed cell product); the renal-relevant lever is the conditioning regimen, where fludarabine requires renal dose consideration. Cohort data show CAR-T is feasible even with reduced renal function or on dialysis. | — Not applicable — a living-cell product. Dialysis is used to support AKI/tumor lysis, not to remove the therapy. |
| Idelalisib PRE PI3Kδ inhibitor | No specific renal dose adjustment is defined; metabolism is hepatic (CYP3A/aldehyde oxidase). Caution and monitor in CKD; dose changes are driven by colitis, hepatotoxicity and cytopenias. | Yes Extensively protein-bound; not meaningfully dialyzable. No established ESKD dosing. |
| Ifosfamide FANC Oxazaphosphorine alkylator | No specific renal dose-adjustment thresholds are given in the FDA label, but ifosfamide is used cautiously in pre-existing renal impairment and dose should be individualized; some clinicians reduce or avoid it when CrCl falls below ~30-50 mL/min given accumulation of neurotoxic and nephrotoxic metabolites (chloroacetaldehyde). A reduced renal reserve, prior cisplatin, young age (<5 yr), and high cumulative dose (>60-100 g/m2) all raise tubulopathy risk and warrant a more conservative dose. Mesna does NOT prevent tubular nephrotoxicity (only hemorrhagic cystitis), so it is not protective against the Fanconi signature. | Yes Limited data on dialytic removal in routine practice; ifosfamide and its metabolites are partly removed by hemodialysis given low molecular weight and modest protein binding, but it is rarely dosed against HD. Hemodialysis is used as salvage for life-threatening encephalopathy/overdose and to clear toxic metabolites rather than as scheduled supplemental dosing, so timing relative to HD is not standardized. |
| Imatinib LYTE BCR-ABL TKI | Decrease the starting dose by ~50% for moderate renal impairment (CrCl 20-39 mL/min; doses >400 mg not recommended), with further reduction (e.g. 100 mg) and added caution in severe impairment (CrCl <20 mL/min); mild impairment (CrCl 40-59) tolerates up to standard/600 mg. Adjust for tolerability rather than by a strict eGFR algorithm. | Yes Imatinib is highly protein-bound (~95%) with a large volume of distribution and is not appreciably removed by hemodialysis; supplemental post-dialysis dosing is not required. |
| Imetelstat PRE Telomerase inhibitor | No dedicated renal dose adjustment is established in lower-risk MDS labeling. As an oligonucleotide, elimination is largely via nuclease metabolism/tissue distribution rather than glomerular filtration; mild-moderate renal impairment is not expected to require change. No data in severe impairment or dialysis. | Yes Not characterized; large protein-bound oligonucleotides are generally not appreciably removed by hemodialysis. No ESKD dosing guidance. |
| Imlunestrant PSEUDO Oral selective estrogen-receptor degrader (SERD) | No renal-impairment dose adjustment is established for imlunestrant; it is an orally administered, hepatically handled SERD and EMBER-3 required adequate organ function. GFR does not drive its exposure, and dose modification is based on tolerability (GI, hepatic) rather than kidney function. The main renal caveat is interpretive — do not down-titrate for the benign abemaciclib creatinine rise. | Yes Not characterized as dialyzable and not clinically relevant: as a protein-bound, hepatically metabolized oral SERD, imlunestrant is not expected to be removed by hemodialysis, and there is no renal-elimination or drug-removal scenario in which dialysis matters for this agent. |
| Immune Checkpoint Inhibitors AIN Immune checkpoint inhibitor | As large monoclonal antibodies (anti-PD-1, anti-PD-L1, anti-CTLA-4) cleared by reticuloendothelial proteolysis rather than the kidney, ICIs require no dose adjustment for renal impairment and the labels specify no CrCl-based modification. Management of nephrotoxicity is immunologic, not pharmacokinetic: per ASCO/NCCN/KDIGO, hold the drug for grade 2+ AKI and start corticosteroids (typically prednisone ~0.5-1 mg/kg/day, higher for severe cases), with permanent discontinuation for grade 3-4 or recurrent nephritis. | No Not dialyzable — IgG-class antibodies are far too large to cross dialysis membranes, and renal replacement does not alter exposure, so no peri-HD timing adjustment is needed. ICIs have been used in patients on hemodialysis without PK-based dose changes, though outcome data are limited; ICI-AIN itself can progress to dialysis-requiring AKI in a minority, which is often reversible with timely steroids. |
| Inavolisib LYTE PI3Kα inhibitor | Per the FDA label: no change for mild impairment (eGFR 60-89 mL/min, CKD-EPI); reduce from the 9 mg once-daily standard to 6 mg once daily for moderate (eGFR 30-59) and 3 mg once daily for severe (eGFR <30) impairment. Additional dose modification in practice is driven by hyperglycemia and GI toxicity. | — Not characterized. As a small-molecule oral agent, dialytic clearance data are not available; management of hyperglycemic emergencies follows standard metabolic principles. |
| Infigratinib LYTE FGFR inhibitor | Standard 125 mg daily for 21 of 28 days. No dedicated adjustment is established for mild-moderate renal impairment, but reduced GFR raises hyperphosphatemia risk and warrants closer monitoring; severe-impairment data are limited. | Yes Not established; highly protein-bound and CYP3A4-metabolized, so it is not expected to be meaningfully dialyzable. |
| Inotuzumab ozogamicin PRE Antibody-drug conjugate (CD22/calicheamicin) | No specific renal dose adjustment; decisions are driven by hepatic function/VOD risk rather than renal clearance. Calicheamicin is hepatically handled. | — Not appreciably dialyzed (large ADC; protein-bound calicheamicin). HD/CRRT in VOD supports AKI, not drug removal. |
| Interferon-α GLOM Cytokine | No renal dose threshold is established for the glomerular injury itself, which is an immune-mediated, idiosyncratic reaction rather than a dose-dependent toxicity. However, pegylated interferon-α formulations accumulate in renal impairment and each carries its own banding: peginterferon alfa-2b (Sylatron) is reduced 25% at CrCl 30-50 and 50% at CrCl <30 or ESRD on dialysis, while peginterferon alfa-2a (Pegasys) keeps the full 180 mcg weekly at CrCl 30-50 and drops to 135 mcg only below 30 including hemodialysis, with caution advised at CrCl ≤50. Neither label directs avoidance. Discontinuation, not dose reduction, is the management when nephrotic-range proteinuria, rising creatinine, or TMA emerges. | Yes Limited data; standard interferon-α is a ~19 kDa protein cleared largely by renal catabolism and tubular reabsorption, and is not meaningfully removed by conventional hemodialysis. Pegylation further reduces clearance and dialyzability, so accumulation in dialysis-dependent patients is expected and supports reduced/avoided dosing rather than reliance on dialytic removal. |
| Interleukin-2 (high-dose) PRE Cytokine | No formal CrCl-based dose reduction is defined; high-dose aldesleukin (600,000 IU/kg IV q8h x up to 14 doses per cycle) is dosed by weight, but the label mandates withholding doses for nephrotoxicity. Treatment is contraindicated/should not be initiated with significant baseline renal impairment, and a held dose is generally not made up. In practice individual doses are skipped (not reduced) when serum creatinine rises (commonly >4-4.5 mg/dL) or oliguria/hypotension develops, with the next cycle deferred until renal function recovers. | — Not applicable in the usual sense — high-dose IL-2 nephrotoxicity is a transient prerenal/hemodynamic AKI that resolves with drug discontinuation and volume resupport, so renal replacement therapy is rarely required. Dialyzability of aldesleukin itself is not clinically relevant given its short half-life and the reversible nature of the injury; data in established ESKD/hemodialysis patients are essentially absent and high-dose IL-2 is generally avoided in dialysis-dependent patients. |
| Iobenguane I-131 ATN Radiopharmaceutical (¹³¹I-MIBG) | The therapeutic activity is weight-based (~18.5 GBq / 500 mCi, capped) preceded by an imaging/dosimetric dose. Because clearance is renal and the kidney is a dose-limiting non-target organ, the prescribing information recommends a reduced therapeutic activity in patients with moderate renal impairment (eGFR ~30 to <60 mL/min/1.73m2). The prescribing information carries no studied dose for severe renal impairment (eGFR <30) or for dialysis-dependent patients, but published experience is not absent: dosimetry-guided, activity-reduced treatment of HD-dependent patients has been reported. Activity should be individualized by measured GFR and/or dosimetry with expert nuclear-medicine input; the broader radiopharmaceutical CKD-dosing evidence remains limited (Schreuder 2021). | Yes The 2008 EANM guidelines list dialysis-requiring renal insufficiency as a contraindication, but that is not evidence-based: dosimetry-guided [131I]MIBG has since been delivered safely to hemodialysis-dependent patients (metastatic paraganglioma and neuroendocrine-tumor cases) with acceptable normal-organ doses and staff exposures within limits. The catch is that [131I]MIBG is NOT effectively cleared by hemodialysis, so an anuric patient retains it longer and the cumulative whole-body/renal absorbed dose runs higher — the key adaptation is dosimetry-guided activity reduction, not relying on dialysis to strip the radioligand. Radiation-safety and radioactive-dialysate handling still apply, and dialysis does not treat or reverse the delivered renal absorbed dose. |
| Ipilimumab AIN CTLA-4 checkpoint inhibitor | No pharmacokinetic dose adjustment for renal impairment. Ipilimumab is dosed by body weight (e.g., 3 mg/kg in melanoma monotherapy; 1 mg/kg every 3 or 6 weeks in nivolumab combinations) and, as a ~150 kDa IgG1 antibody, is cleared by reticuloendothelial proteolysis rather than the kidney, so mild-to-moderate renal impairment does not meaningfully alter exposure. Data in severe impairment and dialysis are limited. Dose modification is event-driven: hold for grade 2-3 nephritis and permanently discontinue for grade 3-4 or recurrent immune-mediated nephritis. | No Not dialyzable. Large IgG1 monoclonal antibodies are not removed by hemodialysis or peritoneal dialysis; dosing timing relative to dialysis is irrelevant. Dialysis is used to support patients with severe ICI-AKI, not to clear the drug. |
| Irinotecan PRE Topoisomerase I inhibitor | Largely hepatic/biliary elimination, so no formal eGFR-based renal dose table — but the FDA label advises caution in renal impairment and directs not using irinotecan in patients on dialysis. UGT1A1 poor metabolizers warrant a ~30% starting-dose reduction. Caution and possible reduction in significant hepatic dysfunction (hyperbilirubinemia). | Yes Irinotecan and SN-38 are protein-bound and hepatically/biliary cleared; not effectively removed by dialysis, and the FDA label directs not using irinotecan in patients on dialysis. |
| Isatuximab PRE Anti-CD38 antibody | No renal dose adjustment; antibody clearance is target-mediated/reticuloendothelial, not renal. Standard weight-based dosing (10 mg/kg) is used across renal-function strata; ICARIA-MM and IKEMA included patients with renal impairment. | No Not dialyzed — a large IgG1 antibody not removed by HD/PD; standard dosing in ESKD. Dialysis treats TLS complications, not drug levels. |
| Ivonescimab GLOM PD-1 x VEGF bispecific antibody | Dosed by weight (20 mg/kg IV every 3 weeks) as a monoclonal antibody; no pharmacokinetic renal dose adjustment is defined, and antibodies are not cleared by the kidney. Management is by holding/modifying for renal toxicity (proteinuria, hypertension, AIN) rather than by GFR-based dose reduction. No data in dialysis or severe CKD; use with nephrology input. | No Not dialyzable. As a ~150+ kDa IgG bispecific antibody, it is not removed by hemodialysis or peritoneal dialysis; timing of dosing around dialysis is irrelevant. |
| Ivosidenib PRE IDH1 inhibitor | No dedicated renal dose adjustment established; no change recommended for mild-moderate impairment, and severe impairment/dialysis are not well studied. Dose interruption is driven by differentiation syndrome, QTc prolongation, and other toxicities rather than a CrCl rule. | — Highly protein-bound oral small molecule; not meaningfully dialyzed. Renal replacement therapy is used to manage AKI/TLS metabolic derangements, not to clear the drug. |
| Ixazomib TMA Proteasome inhibitor | No starting-dose change for mild renal impairment (CrCl >=30). For severe renal impairment (CrCl <30) or ESRD requiring dialysis, reduce the ixazomib dose from 4 mg to 3 mg. Hepatic impairment also requires reduction. | Yes Ixazomib is not meaningfully dialyzable (highly protein-bound, large volume of distribution); it may be given without regard to dialysis timing. Use the reduced 3 mg dose in dialysis-dependent patients. |
| Lanreotide LYTE Somatostatin analog | Exposure increases with the degree of renal impairment; some labeling recommends a reduced starting dose in moderate-to-severe renal impairment for certain indications. Consult product information for the specific formulation and indication. | Yes Not established as meaningfully dialyzable for supplemental dosing; depot peptide pharmacology and case experience suggest cautious use in hemodialysis without routine post-dialysis supplementation. |
| Larotrectinib PSEUDO TRK inhibitor | No dose adjustment is required for mild/moderate renal impairment (no change to the starting dose). Adults 100 mg PO twice daily; children 100 mg/m2 (max 100 mg) twice daily. Moderate-to-severe hepatic impairment does require dose reduction — a useful contrast, since the creatinine bump can be mistaken for a renal-dosing trigger. | Yes Not established; a small-molecule, lipophilic, highly protein-bound drug not expected to be meaningfully dialyzable. |
| Lazertinib SIADH EGFR TKI (3rd-gen) | No established renal dose adjustment (not renally cleared to a significant degree); severe impairment/ESKD not well studied. Manage by sodium/electrolyte correction and drug hold for severe hyponatremia rather than GFR-based dosing. | — Highly protein-bound, hepatically metabolized small molecule; not expected to be appreciably dialyzed. No specific ESKD dosing — focus on sodium and electrolyte management. |
| Lenalidomide ATN Immunomodulatory drug (IMiD) | Per pharmacokinetic data, adjust the starting dose when CrCl <60 mL/min (myeloma labeling): CrCl 30-60 use ~10 mg daily; CrCl <30 not on dialysis use 15 mg every other day; on dialysis use 5 mg once daily, given after dialysis on dialysis days. Disease-specific labels differ; titrate to tolerance. | Yes Yes, lenalidomide is removed by hemodialysis - a 4-hour session cleared ~31% of body drug content. Administer the daily dose after the dialysis session on dialysis days. |
| Lenvatinib HTN VEGFR TKI | Reduce the starting dose for severe renal impairment (CrCl < 30 mL/min) per label (e.g., a lower mg starting dose in thyroid/RCC indications); no adjustment for mild-moderate impairment. Lenvatinib is mainly hepatically metabolized (CYP3A and aldehyde oxidase), so hepatic impairment also drives dose reduction. | Yes Highly protein-bound (~98-99%) and hepatically cleared, so it is not appreciably removed by hemodialysis; dosing in ESKD follows the severe-renal-impairment reduction with toxicity-guided titration. |
| Leuprolide HTN GnRH agonist | No renal dose adjustment; leuprolide is a peptide cleared by peptidase/tissue metabolism and is dosed by depot interval, not renal function. | — Peptide depot formulation; not relevant to dialyzability and no ESKD dose change needed. The clinical focus in ESKD is cardiometabolic and bone management. |
| Lifileucel PRE Tumor-infiltrating lymphocyte (TIL) therapy | Lifileucel itself is a one-time cell infusion with no renal dose adjustment. The renal-relevant levers are the conditioning regimen: fludarabine requires dose reduction in renal impairment (it is renally cleared and accumulates), and high-dose IL-2 dosing is governed by real-time hemodynamic/organ tolerance rather than a fixed CrCl threshold. | No The TIL product is not dialyzable. Among conditioning agents, fludarabine's active metabolite is partly dialyzable but timing is not standardized; IL-2 management is hemodynamic. No established protocol exists for the regimen in dialysis-dependent patients, who are generally excluded. |
| Linvoseltamab PRE BCMA×CD3 bispecific T-cell engager | No renal dose adjustment is established. Pharmacokinetics of large IgG bispecific antibodies are not meaningfully governed by renal clearance, and the registrational program did not define renal cutoffs; patients with significant renal impairment were under-represented. Dose modification in practice is driven by CRS/ICANS and hematologic/infectious toxicity, not by creatinine. | No Not dialyzable. As a ~150 kDa IgG4-based bispecific antibody, linvoseltamab is eliminated by reticuloendothelial catabolism, not renal filtration, and is not removed by hemodialysis. No supplemental dosing around dialysis is indicated. |
| Lisocabtagene maraleucel PRE CD19 CAR-T cell therapy | Liso-cel is a one-time, per-kilogram CAR+ T-cell dose with no renal dose adjustment for the cell product itself and no CrCl threshold on the label. The renal-relevant lever is the lymphodepletion regimen: fludarabine is renally cleared and should be dose-reduced in kidney impairment to limit accumulation and tubular toxicity. CAR-T has been delivered feasibly in patients with reduced renal function and even end-stage renal disease with careful lymphodepletion planning, and baseline renal impairment did not worsen renal or efficacy outcomes in a matched cohort (Wood, Transplant Cell Ther 2022). | No Not applicable to the living CAR-T cells, which are not removed by dialysis. Circulating cytokines are only partially cleared by extracorporeal modalities and this is not standard therapy. Fludarabine's active metabolite (in the conditioning regimen) is partly dialyzable but timing is not standardized. CAR-T therapy has been administered successfully to dialysis-dependent patients, so ESRD is not an absolute contraindication (Wood, Transplant Cell Ther 2022; Khan, Clin Hematol Int 2023). |
| Lomustine (CCNU) CIN Nitrosourea alkylator | Reduce or avoid in baseline renal impairment; the oral dose is given at long (~6-week) intervals partly to limit cumulative marrow and organ toxicity. Cap lifetime cumulative dose and hold for a sustained creatinine rise. | Yes Lipophilic, rapidly metabolized; not meaningfully dialyzable and dialysis is not a rescue strategy. ESKD experience is anecdotal. |
| Loncastuximab tesirine PRE Antibody-drug conjugate (CD19/PBD) | No dose adjustment for mild-moderate renal impairment; severe impairment/ESKD not well studied. As an ADC, clearance is not primarily renal. | No A large antibody-drug conjugate; not dialyzable. ESKD dosing is not established. |
| Lorlatinib PSEUDO ALK TKI | No starting-dose change for mild-to-moderate renal impairment. For severe renal impairment (eGFR <30 mL/min not on dialysis), reduce the dose (e.g., from 100 mg to 75 mg once daily) per labeling. Avoid strong CYP3A inducers/inhibitors. | — Hepatically metabolized and protein-bound; not expected to be meaningfully dialyzed, and ESKD data are limited - monitor clinically. |
| Lurbinectedin ATN Marine alkylating agent | Standard 3.2 mg/m2 IV over 1 h every 3 weeks; dose reductions to 2.6 then 2.0 mg/m2 for toxicity. No dedicated renal adjustment for mild-moderate impairment; severe renal/hepatic impairment has not been studied, so CrCl cutoffs are not established. | — Not characterized; high protein binding and a large volume of distribution make significant dialytic removal unlikely. Dialysis would be used to support AKI, not to clear drug. |
| Lutetium-177 Dotatate CIN Radioligand therapy (PRRT) | Standard course is 7.4 GBq IV every 8 weeks for 4 cycles. There is no simple CrCl-based dose table; instead activity is governed by the renal radiation-tolerance threshold (classically ~23 Gy absorbed dose; a renal BED cap of ~37-40 Gy is used in dosimetry-guided practice). Baseline CrCl <30 mL/min or rapidly declining renal function is a contraindication/caution; reduce or omit cycles for grade >=2-3 renal toxicity. | — Dialysis does not treat the toxicity itself — established radiation nephropathy is structural, not a removable circulating drug. But treating a hemodialysis-dependent (ESKD) patient is feasible and reported, not off-limits: because the radiopeptide is predominantly renally excreted, an anuric patient cannot excrete it, so reported protocols schedule hemodialysis after initial tumor uptake to strip circulating Lu-177 and limit whole-body/marrow dose. Removal is real but partial, and how much comes off differs sharply between reports: a two-cycle case that cut administered activity 33% then 45% and began postdilution hemodiafiltration 6 h and 5 h after dosing saw whole-body activity fall 40% and 47%, reproducing normal-clearance retention curves, while a separate dotatate patient lost 4.9% of total-body radioactivity per session averaged across his dialysis course. Activity already taken up by tumor, kidney, marrow and salivary tissue is beyond the membrane's reach at any timing. Amino-acid renoprotection is pointless in an anuric patient; the concern shifts to marrow dose and radioactive-dialysate handling, which can stay above release limits for weeks of later sessions. A 2024 ESKD treatment algorithm and case reports (including a completed 4-cycle course with sustained remission) describe safe delivery under hemodialysis. |
| Lutetium-177 PSMA-617 (vipivotide) CIN Radioligand therapy (PSMA) | Standard 7.4 GBq IV every 6 weeks for up to 6 cycles. No simple CrCl-based table; the same ~23 Gy renal radiation-tolerance principle applies (renal dose ~0.4-0.55 Gy/GBq in dosimetry series). Hold/reduce for grade >=3 renal or hematologic toxicity; caution with significantly impaired baseline GFR. | — Dialysis does not treat the toxicity (a structural radiation effect, not a removable drug), but hemodialysis-dependent patients CAN be treated — the earlier 'not a candidate' stance is outdated. One hemodialysis patient received all 6 Lu-177 PSMA-617 cycles with dialysis during each and a strong PSA response (298 to 7.1 ng/mL); another completed 5 cycles of PSMA-I&T at the standard 7.4 GBq activity. Dialysis is scheduled after the dose — within about 24 h across the reported series, with a second session near 72 h in one report — to take off the renally-excreted radioligand, with dialysate collected and handled as radioactive waste and measured staff exposure in that report low (2-19 microSv accumulated). Removal is real but partial: blood activity fell 32% over a 3 h session and then partly rebounded, activity already bound in tumor and organs is beyond reach, and bone-marrow dose still ran about twice the non-dialysis literature. Radiation-nephropathy risk is moot in an already-failed kidney; the real issues are blood/marrow dose from slowed clearance and radiation-safety logistics. |
| Mechlorethamine LYTE Alkylating agent (nitrogen mustard) | No validated renal dose-adjustment algorithm for systemic use; the drug is rapidly chemically hydrolyzed with very short plasma half-life. Topical gel requires no renal adjustment given absent systemic absorption. | — Not relevant for drug removal given near-instantaneous chemical degradation in plasma; dialysis is used only to manage TLS metabolic complications. |
| Melphalan SIADH Alkylator | For high-dose conditioning, 140 mg/m2 is commonly used as a conservative dose in significant renal impairment / dialysis dependence and in AL amyloidosis. Melphalan pharmacokinetics are NOT adversely affected by impaired renal function (Tricot), so renal impairment is not itself a barrier to high-dose conditioning; that study nonetheless found renal insufficiency associated with longer fever and hospitalization, and the same group later reported that the more pronounced toxicity of the 200 mg/m2 regimen is why 140 mg/m2 became the standard of care. | Yes Melphalan is short-lived (rapid chemical hydrolysis) so it is not reliably removed by dialysis as a rescue; however, high-dose autotransplant has been performed safely in dialysis-dependent patients using the reduced 140 mg/m2 dose with attention to mucositis. |
| Melphalan flufenamide (melflufen) ATN Peptide-conjugated alkylator | Reduced dose (30 mg) recommended for moderate renal impairment (eGFR ~30 to <45 mL/min/1.73 m2) based on the BRIDGE PK study; data in severe impairment are limited (a 20 mg dose was studied). Recalculate eGFR before dosing. | — Released melphalan is a small molecule with limited published dialyzability data for the conjugate; no established dosing in dialysis-dependent patients. Use with caution and close monitoring in advanced CKD. |
| Methotrexate (high-dose) XTAL Antifolate | High-dose MTX (>500 mg/m2) is predominantly renally cleared, so it is contraindicated or sharply dose-reduced when CrCl/eGFR is low and is generally withheld until any prior AKI resolves; nephrotoxicity itself is the chief driver of toxic exposure because delayed clearance prolongs systemic MTX and amplifies marrow/mucosal/hepatic toxicity. Rather than a single fixed CrCl band, practice is to confirm adequate baseline renal function, intensify hydration and urinary alkalinization, and titrate leucovorin rescue against serial MTX levels (Bleyer-type nomogram). | — Conventional intermittent hemodialysis clears MTX inefficiently and is followed by substantial post-dialysis rebound from tissue redistribution, so it is not a reliable rescue for MTX overexposure; high-flux/high-efficiency HD and continuous modalities (CVVHD) remove somewhat more but still lag far behind enzymatic clearance. Glucarpidase (carboxypeptidase-G2), which cleaves circulating MTX to inactive metabolites within minutes, is the definitive intervention for MTX-induced AKI with toxic levels and largely supplants dialysis. |
| Midostaurin PRE FLT3 / multikinase inhibitor | No specific renal dose adjustment for mild-moderate impairment; severe impairment/ESKD not well characterized (extensive hepatic CYP3A4 metabolism, highly protein-bound). Modifications driven by hematologic/GI toxicity and QT. | Yes Highly protein-bound; not expected to be dialyzable. Dialysis is used for TLS metabolic complications, not drug clearance. |
| Mirdametinib PRE MEK inhibitor | No established renal dose adjustment; mirdametinib is hepatically metabolized with low renal elimination, so reduced GFR is not expected to require modification. Dosing is BSA-based in children. No data in severe impairment or dialysis. | — Not characterized; a small, protein-bound, non-renally cleared molecule is unlikely to be appreciably dialyzed. No ESKD dosing guidance. |
| Mirvetuximab soravtansine PRE Antibody-drug conjugate (FRα/DM4) | No renal dose adjustment defined for mild-moderate impairment; data are limited in severe impairment/ESKD. DM4 is hepatically metabolized rather than renally cleared. | — Not appreciably dialyzed (large ADC; protein-bound maytansinoid payload). |
| Mitomycin C TMA Antitumor antibiotic | No validated CrCl-based renal dosing algorithm exists; the FDA label gives no creatinine-clearance thresholds, but mitomycin is generally avoided or used cautiously when serum creatinine exceeds roughly 1.7 mg/dL. The dominant renal hazard is cumulative-exposure-dependent thrombotic microangiopathy (TMA): in the 85-case national C-HUS registry all but nine mitomycin-treated patients had received a cumulative total dose above 60 mg, so capping total lifetime exposure is the key protective measure rather than per-cycle renal adjustment. | — Mitomycin undergoes rapid hepatic/tissue metabolism with a short plasma half-life (~10-20 min), so hemodialysis is not expected to meaningfully remove parent drug and is not a strategy to mitigate acute exposure (limited formal PK data in HD). Dialysis is relevant chiefly as renal-replacement support for the ESKD that frequently follows mitomycin-induced TMA. |
| Mitotane LYTE Adrenolytic | Mitotane has no standardized CrCl-band renal dose reduction; dosing is guided by plasma-level monitoring and tolerability. Per the FDA label, mitotane is not recommended in severe renal impairment; in mild-to-moderate impairment, monitor plasma levels frequently and modify the dose as needed. In EDP-M with mild renal impairment, cisplatin scheduling (e.g., continuous infusion) is also modified to mitigate nephrotoxicity. | — Dialyzability not characterized/clinically relevant; mitotane is highly lipophilic and tissue-distributed, making dialysis removal unlikely to be useful. |
| Mitoxantrone XTAL Anthracenedione | No well-defined renal CrCl thresholds (minimal renal elimination — predominantly hepatobiliary clearance); reduce/monitor in hepatic impairment. Cumulative dose is limited by cardiotoxicity rather than renal function. | Yes Not appreciably dialyzable (large volume of distribution and high tissue/protein binding); dialysis is used for tumor-lysis metabolic management. |
| Mobocertinib PRE EGFR exon20 TKI | Standard 160 mg PO daily. No fully established renal dose-adjustment scheme; renal management is mainly diarrhea/volume control plus dose interruption/reduction. | Yes Not characterized; a small-molecule TKI that is highly protein-bound and hepatically metabolized, so it is unlikely to be dialyzable. |
| Mogamulizumab PRE Anti-CCR4 antibody | No dose adjustment for renal impairment (a monoclonal antibody, not renally cleared); interruptions are driven by rash and infusion reactions. | No A monoclonal antibody; not dialyzable. Dialysis is used for TLS metabolic complications, not drug removal. |
| Momelotinib PSEUDO JAK/ACVR1 inhibitor | No dose adjustment is needed for mild-to-severe renal impairment per the registrational program; momelotinib is hepatically metabolized (with an active metabolite). Data in dialysis are limited. Dose modification is driven primarily by cytopenias rather than renal function. | — Not characterized; highly protein-bound, hepatically cleared. Not expected to be meaningfully dialyzed. No ESKD-specific dosing guidance. |
| Mosunetuzumab PRE Bispecific (CD20×CD3) | No specific renal dose adjustment is defined; mild-to-moderate renal impairment is not expected to alter exposure of an IgG bispecific. No data in severe impairment/ESKD — dose on clinical grounds. | No Not dialyzable (~145 kDa IgG cleared by reticuloendothelial catabolism, not renal filtration). No supplemental dosing needed for HD/PD. |
| Moxetumomab pasudotox TMA Immunotoxin (anti-CD22 PE38) | Do not initiate if CrCl <30 mL/min. Hold for serious CLS or HUS; permanently discontinue for HUS or recurrent serious CLS. No simple CrCl-based dose scaling otherwise. | — Not characterized — dialysis supports AKI/HUS rather than clearing the immunotoxin. |
| mTOR Inhibitors GLOM mTOR inhibitor | No mandatory renal dose adjustment for sirolimus, everolimus, or temsirolimus by CrCl — these are hepatically (CYP3A4) metabolized, and renal excretion of parent drug is minimal, so labels do not specify creatinine-based reductions. Dosing is instead driven by trough levels (sirolimus/everolimus in transplant) or fixed mg dosing (oncology). In practice, dose is reduced or the drug held when proteinuria worsens or new-onset TMA appears, since toxicity is not a clearance problem but a podocyte/endothelial effect. | Yes Not appreciably dialyzable — large molecules with very high protein binding (~92% sirolimus, ~74% everolimus) and very large volumes of distribution, so hemodialysis does not meaningfully remove them and no post-HD supplemental dose is needed. There is no separate ESKD dose recommendation; level-guided or standard fixed dosing applies, with limited formal pharmacokinetic data in dialysis patients. |
| Naxitamab PRE Anti-GD2 antibody | No pharmacokinetic renal dose adjustment is defined: as a ~150 kDa IgG1 monoclonal antibody, naxitamab is cleared by reticuloendothelial catabolism, not renal excretion, so creatinine clearance does not drive dosing. Dose modifications are triggered by infusion reactions and hemodynamic toxicity — slowing the rate, interrupting, reducing the dose, or giving a half-dose for a given day (as has been done for infusion-associated hypotension), with subsequent full doses usually tolerated. There is no established creatinine- or eGFR-based dose reduction. | No Not dialyzable. Naxitamab is a large (~150 kDa) IgG1 monoclonal antibody with a large-molecule volume of distribution and reticuloendothelial clearance; it is not removed by hemodialysis or peritoneal dialysis, and dialysis has no role in enhancing its elimination. |
| Necitumumab LYTE Anti-EGFR antibody | No renal dose adjustment of the antibody is defined; necitumumab is not renally cleared. Management is electrolyte repletion and dose holds for severe hypomagnesemia rather than mg/kg reduction. Concurrent cisplatin requires its own CrCl-based dosing/hydration. | No Not dialyzable—a ~145 kDa IgG1 monoclonal antibody cleared by reticuloendothelial catabolism, not removed by hemodialysis; no supplemental dosing after HD. (Magnesium itself is small and dialyzable, but the toxicity is renal wasting, not retention.) |
| Nedaplatin ATN Platinum agent | No formally validated CrCl-banded schema in Western labeling; in practice dose is reduced and free-platinum AUC monitored when CrCl is low. Reduce dose / extend interval for baseline renal impairment and avoid stacking with cisplatin-level cumulative platinum. | Yes Free (unbound) platinum is dialyzable like other small-molecule platinums; protein-bound platinum is not. Timing of any platinum agent around hemodialysis should be individualized with pharmacy. Renal clearance is a major elimination route, so ESKD prolongs exposure. |
| Nelarabine XTAL Purine analog | No specific renal dose adjustment is defined in the label, but exposure is higher and clearance lower in renal impairment, so the FDA label advises monitoring patients with CrCl < 50 mL/min closely for increased toxicity. Ara-G is renally cleared. | — Not formally established; ara-G is a small renally excreted molecule with theoretical dialytic removal, but no validated supplemental dosing exists and HD is used only to manage AKI complications. |
| Neratinib PRE HER2 / pan-EGFR TKI | No dose adjustment for mild-moderate renal impairment; severe impairment/ESKD not well studied (hepatic CYP3A4 metabolism). Dose changes are driven by diarrhea and hepatotoxicity. | Yes Highly protein-bound; not expected to be dialyzable. No established ESKD dosing. |
| Nilotinib PRE BCR-ABL TKI | No renal dose adjustment is required across renal-function categories (negligible renal excretion). Note the QT-prolongation black-box warning and the need to take it on an empty stomach. | No Highly protein-bound and hepatically cleared; not dialyzable and no supplemental dosing needed in ESKD. |
| Nimustine (ACNU) CIN Nitrosourea (alkylating) | Use caution in renal impairment; nimustine-specific renal dose thresholds are not well defined. Limit cumulative exposure and withhold for evolving renal dysfunction; individualize per protocol. | — Not well characterized. Although nimustine is comparatively water-soluble, it is rapidly metabolized with a short plasma half-life, so dialysis is not an established removal strategy; manage by dose limitation and monitoring. |
| Nintedanib HTN VEGFR/FGFR/PDGFR TKI | No dose adjustment for mild-to-moderate renal impairment; <1% is excreted renally and nintedanib is predominantly cleared by hydrolytic ester cleavage and biliary/fecal excretion. It has not been studied in severe renal impairment (CrCl < 30 mL/min). Dose reduction is driven by hepatotoxicity (transaminitis) more than by renal function. | Yes Highly protein-bound (~98%) with biliary/fecal elimination, so it is not meaningfully dialyzable; no supplemental dosing for HD. ESKD data are essentially absent. |
| Niraparib HTN PARP inhibitor | No formal renal dose adjustment for mild-moderate impairment; not studied in CrCl <30 mL/min or on dialysis (use with caution). Individualized starting dose (200 mg) is recommended by weight (<77 kg) and platelet count (<150,000/µL) for hematologic, not renal, safety. | Yes Small molecule but highly protein-bound (~83%) with a large volume of distribution; not expected to be meaningfully removed by hemodialysis. No validated ESKD dosing — extrapolate cautiously and prioritize cytopenia monitoring. |
| Nirogacestat LYTE Gamma-secretase inhibitor | No established renal dose adjustment; not studied in significant renal impairment. Modify dose for GI/dermatologic toxicity per label rather than for GFR. CYP3A interactions apply. | — Hepatically metabolized small molecule; dialyzability not characterized and not the management focus. In advanced CKD, monitor and replete electrolytes/phosphate. |
| Nivolumab AIN PD-1 checkpoint inhibitor | As a monoclonal antibody, nivolumab requires no baseline renal dose adjustment; pharmacokinetics are not meaningfully altered by mild-to-moderate renal impairment and it is dosed as a flat or weight-based IV regimen. The relevant adjustment is immunologic, not pharmacokinetic: hold or permanently discontinue based on AKI grade per immune-related adverse event protocols rather than CrCl banding. | No Not dialyzable. As a ~146 kDa IgG4 antibody it is not removed by hemodialysis, and ESKD/dialysis does not require dose change. Patients on dialysis or with a kidney transplant can receive nivolumab, though transplant recipients carry a substantial risk of allograft rejection from checkpoint blockade. |
| Obecabtagene autoleucel (Obe-cel) PRE CD19 CAR-T cell therapy | Not applicable in the small-molecule sense - obe-cel is a one-time autologous cell product with no CrCl-based dose thresholds. No renal dose adjustment is established; attention to renal function is warranted for the lymphodepleting chemotherapy and supportive medications given around infusion. | No Not applicable. The CAR-T product is a living-cell therapy and is not dialyzable; dialysis serves only to support severe AKI or tumor-lysis metabolic derangements. |
| Obinutuzumab XTAL Anti-CD20 antibody | No renal dose adjustment; antibody clearance is target-mediated/reticuloendothelial, not renal. CLL11 specifically included patients with CrCl 30–69 mL/min, supporting use in moderate renal impairment with appropriate TLS precautions. | No Not dialyzed — a large IgG1 antibody not removed by HD/PD; usable in ESKD at standard dosing. Dialysis treats TLS complications, not drug levels. |
| Octreotide LYTE Somatostatin analog | No adjustment for mild-to-moderate renal impairment is generally mandated, but clearance is reduced in severe impairment and in dialysis patients, where lower or less frequent dosing and closer monitoring are prudent; consult product labeling for the specific formulation. | Yes Not meaningfully removed by dialysis as a basis for supplemental dosing; the peptide is partly renally eliminated, and case experience supports cautious use in hemodialysis patients without routine post-dialysis supplementation. |
| Odronextamab XTAL Bispecific (CD20×CD3) | No pharmacokinetic renal dose adjustment is defined: odronextamab is a ~150 kDa IgG4 antibody cleared by reticuloendothelial catabolism, not glomerular filtration, so creatinine clearance does not change drug exposure, and dedicated data in severe renal impairment or dialysis are limited. The clinically important dose lever is instead the cycle-1 step-up schedule (e.g., 0.7/4/20 mg), which exists to control CRS/TLS magnitude; dosing is interrupted, delayed, or re-escalated based on CRS/TLS severity and organ toxicity rather than on baseline GFR. | No Not dialyzable — a full-size IgG4 monoclonal antibody vastly exceeds any dialysis-membrane cutoff and stays in the vascular/interstitial compartment, so hemodialysis does not remove the drug. This is distinct from treating its complications: renal replacement therapy is a legitimate and sometimes necessary tool for the TLS metabolites (potassium, phosphate, uric acid) and for oliguric AKI, but it clears the metabolic consequences, not the antibody. |
| Olaparib PSEUDO PARP inhibitor | No starting-dose change for mild renal impairment (CrCl 51-80). For moderate impairment (CrCl 31-50), reduce the dose (e.g., to 200 mg twice daily) per labeling. Severe impairment/ESKD (CrCl <30) is not recommended due to limited data; if used, monitor closely. | — Olaparib is protein-bound and predominantly hepatically metabolized (CYP3A); dialyzability is not well characterized and it is not relied upon for clearance. Avoid in dialysis-dependent ESKD given sparse data. |
| Olutasidenib PRE IDH1 inhibitor | No dose adjustment for mild-moderate renal impairment; severe impairment/ESKD not well characterized (hepatic metabolism). Interruptions are driven by differentiation syndrome/TLS rather than GFR. | Yes Highly protein-bound; not appreciably dialyzable. Dialysis is used for TLS metabolic complications, not drug removal. |
| Olverembatinib GLOM BCR-ABL1 tyrosine kinase inhibitor (3rd generation) | Standard dosing is 30-40 mg orally every other day (30 mg for non-T315I per the phase 1b recommended dose; 40 mg the RP2D in the Chinese program). No validated renal-impairment dose adjustment has been published; pharmacokinetics support alternate-day dosing, and a high-fat meal substantially increases exposure (Cmax +106%, AUC +70%), so administration relative to food should be consistent. Use clinical caution in significant renal impairment given limited data. | Yes Not appreciably dialyzable (no formal data). As a small-molecule TKI that is highly protein-bound and lipophilic with a large apparent volume of distribution, it is unlikely to be appreciably removed by hemodialysis. |
| Osimertinib SIADH EGFR TKI | No osimertinib dose adjustment is required for mild-to-moderate renal impairment; data in severe impairment/ESKD are limited (hepatic CYP3A metabolism predominates). Management of SIADH is fluid restriction and dose hold, not renal dose modification. | Yes Not appreciably dialyzable—a small but highly lipophilic, extensively protein-bound molecule with a very large volume of distribution; minimal renal excretion of parent drug, so hemodialysis is not expected to remove clinically relevant amounts. |
| Oxaliplatin TMA Platinum agent | No dose reduction is required for mild-to-moderate impairment; the FDA label permits the standard 85 mg/m2 starting dose down to CrCl ~30 mL/min, with reduction to 65 mg/m2 advised for severe impairment (CrCl <30 mL/min). Unlike cisplatin, oxaliplatin is not directly tubulotoxic, so renal dosing is driven by accumulation of the renally-cleared platinum moiety rather than by nephrotoxicity risk. Hold or reduce for an acute rise in creatinine and reassess before re-exposure. | Yes Ultrafilterable (protein-unbound) platinum is dialyzable, but the large fraction irreversibly bound to plasma proteins and erythrocytes is not, so hemodialysis removes only a minor portion of total platinum; data are limited to case reports. Scheduling chemotherapy a few hours before an HD session has been used pragmatically in dialysis-dependent patients, but no validated protocol exists. |
| Paclitaxel PRE Taxane | Hepatically (CYP2C8/CYP3A4) metabolized and biliary excreted - no renal dose adjustment; reduce dose for significant hepatic impairment. Renal impairment does not require dose change. | No Highly protein-bound, large volume of distribution, and non-renally cleared; not dialyzable. Can be given without regard to dialysis timing. |
| Pacritinib PRE JAK2/ACVR1 inhibitor | There is no filtration-based renal dose rule for the kidney injury itself — the actionable lever is holding or reducing pacritinib for severe diarrhea (grade 3-4) or clinically significant volume/electrolyte depletion, then resuming at a reduced dose per the label. Pharmacokinetically, pacritinib is cleared predominantly by hepatic CYP3A4 metabolism with limited renal excretion, so no dose reduction is required for mild-to-moderate renal impairment; the label directs avoiding pacritinib in severe renal impairment (eGFR <30 mL/min), where PK and safety data are lacking. Avoid strong CYP3A4 inhibitors and inducers. Confirm all thresholds against the current prescribing information. | — Not established. Pacritinib is a highly protein-bound, hepatically (CYP3A4) metabolized small molecule, so meaningful removal by hemodialysis is unlikely and no formal dialysis-clearance data are available — and the label directs avoiding use at eGFR <30 mL/min, so ESKD dosing does not arise. If AKI develops on therapy, manage it by treating the diarrhea and the volume/electrolyte disturbance rather than by timing doses around dialysis sessions. |
| Palbociclib PSEUDO CDK4/6 inhibitor | No renal dose adjustment is specified for mild-to-moderate impairment; pharmacokinetic data in severe impairment/ESKD are limited. Do not dose-reduce for an isolated creatinine rise that is actually pseudo-AKI. | Yes Highly protein-bound, large volume of distribution, and hepatically (CYP3A4) metabolized; not meaningfully removed by hemodialysis. No HD-timed dosing established. |
| Pamidronate GLOM Bisphosphonate | No formal renal-function dosing algorithm exists for the oncology (hypercalcemia/myeloma/bone-metastasis) indications because pamidronate was not adequately studied in renal impairment; the label advises against use in severe renal impairment and recommends holding therapy if renal function deteriorates. Nephrotoxicity is dose-dependent — in the landmark collapsing-FSGS series five of the seven patients had been escalated above the approved dose (180 mg monthly in two, 360 mg in three), and at the recommended 90 mg monthly renal toxicity is infrequent — so adhere to the labeled 90 mg over no less than 2-4 hours, not exceeding 90 mg per dose. | Yes Pamidronate is not meaningfully dialyzable — roughly half of an absorbed dose is rapidly taken up and sequestered in bone, and the remainder is renally excreted unchanged, so it is not given to "treat" with HD removal in mind. There are limited data to guide dosing in dialysis-dependent ESKD; given the severity of the glomerular lesion at presentation and the lack of renal clearance, use in advanced CKD/ESKD is generally avoided in favor of denosumab. |
| Panitumumab LYTE Anti-EGFR antibody | No renal dose adjustment. Panitumumab is an IgG2 monoclonal antibody cleared by target-mediated and reticuloendothelial catabolism, not renal excretion, and GFR is preserved, so eligibility and dosing are unchanged in CKD. The clinical challenge is magnesium (and secondary calcium/potassium) repletion, not adjusting the antibody dose. | No Not dialyzable. At roughly 147 kDa the IgG2 antibody vastly exceeds any dialysis membrane cutoff and is not removed by hemodialysis (the repleted magnesium is dialyzable, but the drug is not). |
| Pazopanib GLOM VEGFR TKI | No starting-dose adjustment is generally required for mild-to-moderate renal impairment; data in patients with CrCl <30 mL/min are limited. Pazopanib undergoes predominantly hepatic metabolism (CYP3A4) with minimal renal excretion, so renal impairment is not the principal pharmacokinetic driver; dose modification is guided more by hepatic function and toxicity (including proteinuria) than by GFR. | Yes Not meaningfully dialyzable — pazopanib is highly protein-bound (>99%) and largely hepatically cleared, so hemodialysis is not expected to remove appreciable drug. |
| Pegaspargase PRE Enzyme (asparaginase) | The enzyme is cleared by reticuloendothelial/proteolytic mechanisms, not renally excreted, so no renal dose adjustment is required. Hold or adjust for pancreatitis, serious thrombosis/hemorrhage, or severe hypersensitivity — not for creatinine. | Yes Not meaningfully dialyzable (a large PEGylated protein); hemodialysis is not used for removal. |
| Pembrolizumab AIN PD-1 checkpoint inhibitor | No pharmacokinetic renal dose adjustment is required — pembrolizumab is a monoclonal antibody cleared by catabolism, not renal excretion, so none is needed across the spectrum of renal impairment. Management is immunologic (hold drug, grade the irAE, treat) rather than dose-based: per standard irAE grading, grade 2 nephritis prompts holding the drug and corticosteroids, and grade 3-4 prompts permanent discontinuation. | No Not dialyzable — as a ~149 kDa IgG4 monoclonal antibody it is not removed by hemodialysis. Patients on dialysis can receive pembrolizumab without dose change; dialysis does not mitigate the immune-mediated nephritis. |
| Pemetrexed CIN Antifolate | Pemetrexed is predominantly renally cleared, and the FDA label contraindicates initiation when CrCl is below 45 mL/min (Cockcroft-Gault) because reduced clearance drives severe myelosuppression and mucositis; there is no validated reduced-dose regimen below this threshold. In patients with CrCl 45-79 mL/min no dose reduction is specified, but avoid NSAIDs around dosing (hold short-half-life NSAIDs 2 days before to 2 days after, longer-half-life agents ~5 days) since they impair tubular clearance and amplify toxicity. Mandatory folic acid (350-1000 mcg/day starting ~1 week pre-treatment) and IM vitamin B12 (1 mg every ~9 weeks) supplementation is required to blunt overall toxicity. | Yes Limited data; pemetrexed is moderately protein-bound (~81%) with a low molecular weight, so it is theoretically partly dialyzable, but it is not used in dialysis-dependent patients and no established schedule exists. Because the drug is contraindicated below CrCl 45 mL/min, dosing in ESKD/HD is essentially uncharacterized and should be avoided outside specialist judgment. |
| Pemigatinib LYTE FGFR inhibitor | No starting-dose change for mild or moderate renal impairment (eGFR 30-89). Severe impairment (eGFR 15-29) carries a specific label reduction: 9 mg on whichever schedule the indication designates, down from 13.5 mg. ESRD on intermittent hemodialysis needs no adjustment per label. Beyond those bands, dosing is driven by the phosphate-guided algorithm (and the intermittent 14-days-on/7-days-off schedule) rather than a CrCl rule. | Yes Highly protein-bound oral small molecule; not expected to be appreciably dialyzed. The label carries a dedicated ESRD-on-intermittent-hemodialysis cohort and recommends no dosage adjustment there — which is also the strongest support for the non-dialyzable verdict. The phosphate biomarker, however, is confounded in ESKD. |
| Penpulimab AIN PD-1 immune checkpoint inhibitor | No pharmacokinetic dose adjustment for renal impairment: penpulimab is a ~150 kDa IgG1 monoclonal antibody eliminated by reticuloendothelial catabolism, not by glomerular filtration or tubular secretion. Dosing is fixed (200 mg IV every 2 or 3 weeks depending on regimen). Modifications are driven by immune-related toxicity grade (hold/discontinue and add steroids) rather than by eGFR. The cisplatin component of the combination regimen does require renal dosing/eligibility consideration, and carboplatin substitution is used for patients unable to tolerate cisplatin. | No Not dialyzable. As a large IgG monoclonal antibody, penpulimab is not removed by hemodialysis or peritoneal dialysis; timing relative to dialysis sessions is irrelevant. No data establish its use in dialysis-dependent patients, but pharmacokinetics are not expected to be altered by renal replacement therapy. |
| Pentostatin ATN Purine analog (ADA inhibitor) | Renally adjusted: CrCl >60 mL/min ~4 mg/m2 every 14 days (standard); CrCl 41-60 ~3 mg/m2; CrCl 21-40 ~2 mg/m2; CrCl <20-30/severe generally avoid (insufficient data). Even these reductions may overexpose critically ill patients (Cockcroft-Gault overestimates function) — interpret cautiously. | Yes Dialyzable — deliberate post-infusion hemodialysis has been used to limit exposure and permit cautious dosing in ESKD. |
| Pexidartinib PRE CSF1R inhibitor | The label recommends a reduced starting dose for mild-to-severe renal impairment (CrCl 15-89 mL/min); the other critical dose modifications are for hepatotoxicity, which predominates in hepatic metabolism. | Yes Highly protein-bound; not expected to be dialyzable. No established ESKD dosing. |
| Pirtobrutinib XTAL Non-covalent BTK inhibitor | No dosage adjustment for mild (eGFR 60-89) or moderate (eGFR 30-59) renal impairment; per label, reduce the dose in severe impairment (eGFR 15-29), where pirtobrutinib exposure rises. ESKD/dialysis data are limited. Hepatic and drug-interaction adjustments apply. | — Small molecule, highly protein-bound, hepatically metabolized; dialyzability not well characterized and removal unlikely to be clinically significant. Renal replacement therapy in this setting treats TLS, not drug levels. |
| Pivekimab sunirine PRE CD123 antibody-drug conjugate | No pharmacokinetic renal dose adjustment is defined. Pivekimab sunirine is an antibody-drug conjugate whose antibody scaffold is cleared by reticuloendothelial/lysosomal catabolism rather than glomerular filtration, so creatinine clearance is not expected to change drug exposure, and dedicated data in severe renal impairment or dialysis are limited. Dose modification is driven by hematologic and organ toxicity (notably the veno-occlusive-disease and infusion-reaction signals) and by tumor-lysis/capillary-leak events, not by baseline GFR. Pre-existing CKD raises the risk of tumor-lysis and hemodynamic AKI and warrants intensified prophylaxis and monitoring rather than a milligram-level renal dose change. | No Not dialyzable — a full-size antibody-drug conjugate vastly exceeds any dialysis-membrane cutoff and stays in the vascular/interstitial compartment, so hemodialysis does not remove the drug. As with other large biologics, renal replacement therapy remains a legitimate tool for the metabolic consequences (tumor-lysis potassium, phosphate, uric acid) and for oliguric AKI or volume overload — it clears the complications, not the conjugate. |
| Plicamycin (mithramycin) ATN Antitumor antibiotic | Contraindicated/avoided in significant renal impairment because nephrotoxicity is cumulative and dose-related; lower doses are used for hypercalcemia than for antitumor effect. No validated renal dose-adjustment schema exists given its obsolescence — the practical guidance is avoidance when renal function is impaired. | — Not characterized; dialysis is not used for dosing. Hemodialysis would be employed only to manage AKI complications, not to remove the drug. |
| Polatuzumab vedotin PRE Antibody-drug conjugate (CD79b/MMAE) | No starting-dose adjustment for CrCl >=30; data are insufficient below CrCl 30. MMAE is hepatically (CYP3A4) metabolized rather than renally cleared. | — Not appreciably dialyzed (large ADC; protein-bound MMAE). No supplemental dosing guidance for HD/PD. |
| Pomalidomide PRE Immunomodulatory drug (IMiD) | No starting-dose change is required for renal impairment short of dialysis (extensive hepatic metabolism). For severe renal impairment REQUIRING DIALYSIS the label directs a reduced starting dose: 3 mg daily in multiple myeloma, 4 mg daily in Kaposi sarcoma, since AUC rises about 38% and the rate of serious adverse events about 64% relative to normal renal function. On hemodialysis days give the dose after the session completes, because exposure falls significantly during dialysis. Reduce dose for hepatic impairment and for hematologic toxicity. | — Exposure falls significantly during hemodialysis, which is why the daily dose is given after the session rather than before it — not because the drug is unaffected by dialysis. Patients on dialysis also start lower (3 mg daily in multiple myeloma, 4 mg in Kaposi sarcoma), since AUC runs about 38% higher and serious adverse events about 64% more frequent than with normal renal function. |
| Ponatinib HTN BCR-ABL TKI | No specific renal dose adjustment is established (minimal renal excretion); dosing is driven instead by response and by mitigation of vascular toxicity (e.g., reduce to 15 mg on achieving response). Use caution in renal impairment given the vascular risk profile. | — Highly protein-bound and hepatically metabolized; not appreciably dialyzed and no supplemental dosing required in ESKD. |
| Pralatrexate XTAL Antifolate | In the dedicated renal-impairment PK study, severe renal impairment (eGFR 15-29) requires dose reduction to 15 mg/m2 owing to reduced clearance and higher exposure, while ESRD (eGFR <15, with or without dialysis) is best avoided given serious adverse reactions (reduce only if benefit justifies risk); mild-moderate impairment (eGFR 30-59) is tolerated near standard dosing with monitoring. Hold/reduce for grade 3-4 mucositis or cytopenias. | — Pralatrexate is partly renally handled, so some dialytic removal is expected pharmacologically, but no study has characterized it and no post-HD supplemental dose is defined; the dedicated renal-impairment study enrolled no ESRD or dialysis cohort, and the label advises avoiding ESRD (eGFR <15, with or without dialysis) unless the benefit justifies the risk, reserving the reduced 15 mg/m2 dose for severe impairment (eGFR 15-29). |
| Pralsetinib HTN RET inhibitor | No dose adjustment for mild-moderate renal impairment; severe impairment is not well characterized and dialysis is not studied (use with caution). Modifications are driven by hypertension, pneumonitis, cytopenias, and hepatotoxicity. | — Highly protein-bound oral small molecule; not expected to be appreciably dialyzed. No validated ESKD dosing. |
| Procarbazine ATN Hydrazine alkylating agent | No well-validated renal dosing algorithm; use caution in renal impairment given active metabolite handling, and consider dose reduction with close monitoring. Hepatic impairment and MAO-inhibitor drug/dietary interactions are the better-defined dosing concerns. | — Dialyzability not well characterized; the parent drug is short-lived and extensively metabolized. No established ESKD dosing — manage clinically with attention to active metabolites. |
| Quizartinib PRE FLT3 inhibitor | No renal dose adjustment is specified for mild-moderate impairment; quizartinib is hepatically (CYP3A) metabolized. Strong CYP3A inhibitors (common azole antifungals in neutropenia) raise exposure and require dose reduction, mainly for QT safety. Limited data in severe impairment/dialysis. | — Not characterized; highly protein-bound, hepatically cleared — not expected to be meaningfully dialyzed. No ESKD dosing guidance. |
| Radium-223 dichloride PRE Radiopharmaceutical (alpha-emitter) | Standard 55 kBq/kg IV every 4 weeks for 6 injections. No renal dose adjustment is required given negligible renal clearance and exposure; holds are driven by hematologic parameters (ANC, platelets), not CrCl. | — Not a clinical consideration for toxicity, and — unlike the renally-excreted radioligands — end-stage renal disease causes no drug accumulation because clearance is predominantly fecal. Dialysis patients have been treated safely and need no renal dose adjustment: in reported hemodialysis and peritoneal-dialysis cases only a small fraction of the administered activity reached the dialysate (~1-2% across a peritoneal-dialysis course), so dialysate contamination and staff radiation exposure stay low. Standard hematologic holds still apply. |
| Raltitrexed ATN Antifolate (TS inhibitor) | Dose by creatinine clearance: full dose for CrCl >= 65 mL/min; reduce dose and lengthen the dosing interval for CrCl 25-65 mL/min (e.g., reduced dose every 4 weeks); not recommended for CrCl < 25 mL/min. Always recalculate GFR before each cycle. | Yes Polyglutamated, tissue-retained antifolate cleared largely by the kidney; not characterized as efficiently dialyzable and not recommended in dialysis-dependent patients. |
| Ramucirumab HTN Anti-VEGFR2 antibody | No pharmacokinetic renal dose adjustment is required for a monoclonal antibody, but dosing is modified by toxicity: interrupt/reduce for grade 3 hypertension until controlled and for proteinuria thresholds above. Renal impairment does not alter antibody clearance. | No Not dialyzable — a ~147 kDa IgG1 monoclonal antibody is not removed by hemodialysis or peritoneal dialysis; no dose change is needed for dialysis patients. |
| Regorafenib HTN VEGFR TKI | No dose adjustment for renal impairment is recommended; regorafenib is hepatically metabolized (CYP3A4 and UGT1A9) with biliary excretion, so it carries hepatotoxicity warnings rather than renal dosing rules. | Yes Highly protein-bound (~99.5%) and hepatically/biliary cleared; not appreciably dialyzable, so no supplemental dosing for HD. Data in ESKD are limited. |
| Relacorilant LYTE Selective glucocorticoid-receptor antagonist | No established pharmacokinetic renal dose adjustment. Relacorilant is a hepatically metabolized small molecule and eligibility in ROSELLA required adequate organ function; dedicated data in severe renal impairment or dialysis are limited. The clinically important levers are electrolyte monitoring and MR blockade rather than a GFR-based milligram change. As a strong CYP3A substrate/inhibitor it carries drug-interaction considerations that matter more to dosing than renal function does. | Yes Not characterized as dialyzable and not clinically relevant: relacorilant is a protein-bound, hepatically cleared small molecule, and its principal renal-relevant effect (hypokalemia) is managed by repletion and mineralocorticoid-receptor blockade, not by dialysis. There is no role for dialysis in removing the drug. |
| Relatlimab AIN Immune checkpoint inhibitor (anti-LAG-3) | No renal dose adjustment is established (monoclonal antibody, not renally cleared); mild–moderate impairment does not require change. The actionable step is holding the drug and steroid treatment for immune-mediated AIN rather than dose modification. | No The IgG antibodies are not dialyzable and are cleared by proteolysis; no ESKD dose change is expected. Dialysis supports severe AKI management, not drug removal. |
| Repotrectinib PSEUDO ROS1/TRK TKI | No renal dose adjustment for mild–moderate impairment; severe impairment/ESKD not well studied. Critically, an isolated transporter-mediated creatinine rise should NOT, by itself, trigger renal dose reduction — confirm true GFR first. | — Hepatically metabolized small molecule; dialyzability not characterized and not clinically relevant to the (artifactual) creatinine rise. No established ESKD dosing. |
| Retifanlimab AIN PD-1 immune checkpoint inhibitor | No dose adjustment for mild-to-moderate renal impairment; retifanlimab is a monoclonal antibody cleared by reticuloendothelial catabolism, not renal excretion. No studied data in severe impairment or dialysis. Dosing is flat (500 mg IV every 4 weeks), not weight- or GFR-based. Renal management is toxicity-driven (withhold/discontinue) rather than pharmacokinetic dose reduction. | No Not dialyzable. As a ~150 kDa IgG4 monoclonal antibody it is not removed by hemodialysis or peritoneal dialysis; no supplemental dosing needed around dialysis sessions. |
| Revumenib PRE Menin inhibitor | Dosed with a strong CYP3A4 inhibitor co-administration strategy in the label; no well-established renal dose adjustment. Manage TLS/differentiation syndrome rather than adjust for GFR; hold for severe differentiation syndrome. | — Small molecule, but renal dialyzability not formally characterized; clinically, renal replacement therapy is used for TLS-driven AKI/refractory hyperkalemia, not for drug removal. |
| Ribociclib PSEUDO CDK4/6 inhibitor | No adjustment for mild-moderate renal impairment; the label provides a reduced starting dose (e.g. 200 mg) for severe impairment. Avoid strong CYP3A4 inhibitors or reduce dose accordingly. | Yes Extensively hepatically metabolized (CYP3A4), highly protein-bound; not expected to be removed by hemodialysis. No HD-timed dosing established. |
| Ripretinib HTN KIT switch-control inhibitor | No dose adjustment for mild-moderate renal impairment in labeling; severe impairment/ESKD not characterized (hepatic CYP3A4 metabolism). Modifications driven by hypertension, PPE and cardiac effects. | Yes Highly protein-bound; not expected to be dialyzable. No established ESKD dosing. |
| Rituximab XTAL Anti-CD20 antibody | No renal dose adjustment; as a monoclonal antibody it is cleared by reticuloendothelial/target-mediated mechanisms, not the kidney, and is dosed by BSA/flat dose regardless of CrCl. Renal function changes are driven by the tumor-lysis risk it provokes, not by drug accumulation. | No Not dialyzed — a ~145 kDa IgG1 antibody is not removed by hemodialysis or peritoneal dialysis. No supplemental dosing around dialysis; usable in ESKD at standard doses. Dialysis is used to treat TLS metabolic complications. |
| Rucaparib PSEUDO PARP inhibitor | No starting-dose adjustment for mild-moderate renal impairment (CrCl >=30 mL/min); not studied in CrCl <30 mL/min or dialysis — use with caution. Modest exposure increases occur with moderate impairment but rarely require dose change. | — Highly protein-bound small molecule; not expected to be appreciably dialyzed. No established ESKD dosing. |
| Ruxolitinib PRE JAK1/2 inhibitor | Renal dosing is required: the starting dose is reduced in moderate-to-severe renal impairment and in ESKD. In myelofibrosis/PV with platelets 100-150 x10^9/L and moderate-to-severe impairment (CrCl 15-59), and in dialysis-dependent ESKD, the label specifies reduced starting doses; in ESKD on hemodialysis, give a single reduced dose after dialysis on dialysis days. Avoid initiating if CrCl <15 mL/min and not on dialysis. Always titrate to platelets and response. | No Ruxolitinib itself is not removed by hemodialysis - dialysate recovery of the parent drug was negligible - but removal of some ACTIVE METABOLITES cannot be ruled out, which matters because ESKD raises the combined parent-plus-active-metabolite exposure about 1.6-fold. Dose AFTER dialysis on hemodialysis days. Highly protein-bound, hepatically (CYP3A4) metabolized small molecule. |
| Sacituzumab govitecan PRE Antibody-drug conjugate (Trop-2/SN-38) | No established renal dose adjustment; pivotal trials did not define renal cutoffs and the active SN-38 is hepatically glucuronidated (UGT1A1), not renally cleared. Use clinical judgment in advanced CKD/ESKD given limited data. | — The intact ADC and protein-bound SN-38 are not appreciably dialyzed; HD in reported cases was for AKI support, not drug removal. |
| Samarium-153 lexidronam ATN Bone-seeking radiopharmaceutical (153Sm-EDTMP) | Renal impairment reduces clearance and increases marrow radiation exposure; administer with caution and assess renal function before dosing. Follow product labeling/nuclear-medicine guidance for impaired renal function. | — Not established as a removal modality; clinical role of dialysis is supportive only. |
| Selinexor SIADH XPO1 (nuclear export) inhibitor | Limited renal data; no dedicated adjustment for mild-moderate renal impairment is established, and severe CKD/dialysis are not well studied — individualize with onconephrology input. Dose is otherwise modified for hyponatremia and cytopenias. | Yes Not established; highly protein-bound and not expected to be meaningfully dialyzable. |
| Selpercatinib HTN RET inhibitor | Per label, no dosage modification is recommended across mild to severe renal impairment (eGFR 15-89 mL/min/1.73 m2, MDRD); the recommended dosage has not been established in end-stage renal disease, and dialysis is not studied. Weight-based dosing; modifications are driven by hypertension, QTc, hepatotoxicity, and hemorrhage. | — Highly protein-bound oral small molecule; not expected to be appreciably dialyzed. No validated ESKD dosing. |
| Selumetinib PRE MEK inhibitor | Weight/BSA-based pediatric dosing; no specific renal adjustment established (renal-impairment data are limited in this young population). Hepatic impairment, not renal, carries label dose guidance. | — Highly protein-bound oral small molecule; dialyzability not characterized and not clinically relevant in this indication. No ESKD dosing data. |
| Sevabertinib PRE HER2/EGFR TKI | No validated pharmacokinetic renal dose adjustment is established; SOHO-01 required adequate organ function and dedicated data in severe renal impairment or dialysis are limited. Sevabertinib is a hepatically metabolized small molecule, so GFR is not the primary determinant of exposure. The practical dose levers are interruption and reduction for diarrhea (and other toxicity) per label, not a GFR-based change; pre-existing CKD raises the stakes of diarrheal volume depletion and warrants closer monitoring and earlier fluid/electrolyte support. | Yes Not characterized as dialyzable and not clinically relevant: as a protein-bound, hepatically cleared small molecule, sevabertinib is unlikely to be appreciably removed by hemodialysis, and there is no role for dialysis in managing the drug. Renal replacement therapy would only be relevant to support severe AKI, which in this setting is prerenal/volume-depletion physiology best treated by rehydration and diarrhea control. |
| Sirolimus GLOM mTOR inhibitor | No mandatory dose reduction for renal impairment (sirolimus is hepatically metabolized via CYP3A4), but keep troughs toward the lower end and monitor proteinuria when GFR is reduced. Avoid initiating or escalating with significant proteinuria or progressive glomerular disease. | Yes Not meaningfully dialyzable—sirolimus is large, highly lipophilic, extensively (~92%) protein/erythrocyte bound with a very large volume of distribution; hemodialysis does not remove clinically relevant amounts and no supplemental dosing is needed after HD. |
| Sonidegib ATN Hedgehog (SMO) inhibitor | No specific renal dose adjustment in labeling for mild-moderate impairment; not studied in severe impairment/ESKD. Dosing is fixed (200 mg daily); modifications are driven by musculoskeletal toxicity/CK. | Yes Highly protein-bound; not meaningfully dialyzable. Hemodialysis is used for the metabolic complications of pigment-induced ATN, not to remove the drug. |
| Sonrotoclax XTAL BCL-2 inhibitor | No validated pharmacokinetic renal dose adjustment is established. Sonrotoclax is cleared predominantly by hepatic metabolism and biliary/fecal excretion rather than renal elimination (Cai, Cancer Chemother Pharmacol 2025), so creatinine clearance is not the primary determinant of exposure, and dedicated data in severe renal impairment or dialysis are limited. The clinically decisive dose lever is instead the mandated stepwise ramp-up, which controls tumor-lysis magnitude; dosing is interrupted, delayed, or re-escalated based on tumor-lysis and organ toxicity rather than on baseline GFR. Pre-existing CKD raises tumor-lysis-AKI risk and warrants intensified prophylaxis and monitoring even though it does not, by itself, mandate a lower milligram dose. | Yes Not meaningfully dialyzable as a therapeutic target: sonrotoclax is a small but highly protein-bound, lipophilic molecule cleared hepatically, so hemodialysis is not a route of drug removal and there is no role for dialysis to reverse an overdose of the parent compound. This is distinct from treating its complications — renal replacement therapy is a legitimate and sometimes necessary tool for the tumor-lysis metabolites (potassium, phosphate, uric acid) and for oliguric AKI; it clears the metabolic consequences, not the drug. |
| Sorafenib HTN VEGFR TKI | No specific renal dose adjustment is established. Sorafenib is cleared predominantly by hepatic metabolism (CYP3A4 oxidation and UGT1A9 glucuronidation) with only a minor fraction of the dose eliminated renally, so mild-to-moderate renal impairment has little effect on exposure and the standard 400 mg twice-daily dose is used. Data in severe impairment and dialysis are limited; modify dose primarily for toxicity (uncontrolled hypertension, nephrotic-range proteinuria, other grade 3-4 events) rather than for eGFR. | Yes Not meaningfully dialyzable. Sorafenib is very highly protein-bound (~99.5%) with a large apparent volume of distribution and minimal renal excretion, so hemodialysis is not expected to remove appreciable drug; small case experience suggests hemodialysis patients can receive standard dosing (started conservatively and titrated), without regard to dialysis timing. |
| Sotorasib PRE KRAS G12C inhibitor | No renal dose adjustment is recommended; sotorasib pharmacokinetics were not meaningfully affected by mild-moderate renal impairment, and severe impairment/ESKD are not well studied. Dose modifications (from 960 mg daily) are driven by hepatotoxicity and GI toxicity, not CrCl. | — Not characterized; as a highly protein-bound, hepatically cleared small molecule it is unlikely to be substantially dialyzed. No ESKD dosing guidance is established. |
| Streptozocin FANC Nitrosourea alkylator | Reduce dose and lengthen interval for impaired renal function; hold for new or worsening proteinuria or rising creatinine. Modern reviews emphasize scheduling (lower per-dose, fractionated) to cap cumulative tubular exposure in pNET. | — Small, renally cleared molecule; specific HD removal data are limited and it is rarely used in ESKD. Avoid in significant renal impairment rather than relying on dialytic clearance. |
| Strontium-89 chloride LYTE Bone-seeking radiopharmaceutical | No standardized renal dose-reduction scheme; instead, renal impairment is a caution/relative contraindication because reduced clearance increases retained activity and marrow exposure. Dosing is activity-based (e.g., ~150 MBq) per protocol with attention to baseline counts and renal function. | Yes Not a standard management consideration; once incorporated into bone mineral, strontium-89 is not meaningfully removed by dialysis. Early circulating/urinary fraction is renally handled, but dialysis is not used as antidotal clearance. |
| Sugemalimab AIN PD-L1 immune checkpoint inhibitor | No pharmacokinetic dose adjustment is required for renal impairment — as a ~150 kDa monoclonal IgG antibody, sugemalimab is cleared by reticuloendothelial proteolysis, not renal excretion, and is dosed as a fixed/flat IV dose (1200 mg every 3 weeks; 500 mg maintenance with pemetrexed in non-squamous disease). Management of nephrotoxicity is by holding or permanently discontinuing the drug per irAE grade, not by dose reduction. | No Not dialyzable. Large therapeutic IgG monoclonal antibodies are not removed by hemodialysis or peritoneal dialysis; no supplemental dosing is needed for patients on renal replacement therapy. |
| Sunitinib HTN VEGFR TKI | No specific renal dose adjustment is established for mild-to-moderate renal impairment; sunitinib pharmacokinetics are not markedly altered by reduced kidney function, and dosing is guided by tolerability/toxicity rather than eGFR. Standard metastatic RCC dosing is 50 mg daily on a 4-weeks-on/2-weeks-off schedule, with reductions (e.g., to 37.5 mg) for toxicity. Hold or reduce dose for severe hypertension, nephrotic-range proteinuria, or significant AKI. | Yes Sunitinib is highly protein-bound and has a large volume of distribution, so it is not expected to be appreciably removed by hemodialysis; supervised use in dialysis patients has been described, with dosing driven by tolerability rather than dialytic clearance. |
| Sunvozertinib LYTE EGFR exon20 TKI | No dedicated renal dose adjustment established; sunvozertinib is hepatically metabolized (CYP3A) with low renal clearance, so mild-moderate impairment is not expected to require change. Limited data in severe impairment/dialysis. | — Not characterized; a highly protein-bound, non-renally cleared small molecule is unlikely to be appreciably dialyzed. No ESKD dosing guidance. |
| Tafasitamab PRE Anti-CD19 antibody | No dose adjustment for renal impairment for the antibody (not renally cleared); the lenalidomide partner does require CrCl-based dose adjustment. Manage tafasitamab interruptions for infusion reactions/cytopenias. | No A monoclonal antibody; not dialyzable. ESKD dosing of the antibody is not specifically established; lenalidomide needs renal dose adjustment. |
| Tagraxofusp PRE IL-3 immunotoxin | No established renal dose adjustment (clearance is proteolytic, not renal). Dosing decisions hinge on albumin, weight, and CLS status rather than eGFR. | No Large fusion protein cleared by proteolysis; not dialyzable. Hemodialysis/CRRT is used to support AKI/volume overload, not to remove the drug. |
| Talazoparib PSEUDO PARP inhibitor | Breast-cancer monotherapy: CrCl 60-89 no change; CrCl 30-59 reduce to 0.75 mg once daily; CrCl 15-29 reduce to 0.5 mg once daily. With enzalutamide in mCRPC, label-specific lower doses apply. Not studied on dialysis or in CrCl <15 mL/min. | — Renally cleared but highly protein-bound; dialyzability not formally established and no validated ESKD dose — avoid or use only with intensive hematologic monitoring. |
| Taletrectinib PSEUDO ROS1 TKI | No dedicated renal-impairment dosing thresholds by CrCl are established in the available literature; refer to current product labeling. A benign transporter-mediated creatinine rise should not by itself trigger CrCl-based dose modification. | — Not characterized. As a small-molecule, highly protein-bound oral TKI, meaningful removal by hemodialysis is unlikely, but drug-specific data are lacking. |
| Talquetamab PRE Bispecific (GPRC5D×CD3) | No specific renal dose adjustment is established; talquetamab pharmacokinetics are not meaningfully renally dependent. Step-up dosing and holds for severe CRS, plus supportive management of oral toxicity, are the operative levers rather than renal dose modification. | No Not dialyzable—an IgG-based bispecific antibody cleared by catabolism; not removed by hemodialysis and no supplemental dosing needed. Renal replacement therapy treats AKI, not drug clearance. |
| Tamoxifen SIADH SERM | No renal dose adjustment required; tamoxifen is hepatically metabolized (CYP2D6/3A4) and not renally cleared. | No Highly protein-bound, large volume of distribution, hepatically cleared — not dialyzable. No special ESKD dosing needed. |
| Tarlatamab PRE Bispecific (DLL3×CD3) | No established renal dose adjustment (T-cell engager, not renally cleared); dosing is by step-up schedule. The renal-relevant action is hemodynamic support during CRS, not dose modification for GFR. | No Bispecific antibody construct — not dialyzable and not renally eliminated; no ESKD dose change expected. Renal replacement therapy is for CRS-driven AKI, not drug clearance. |
| Tasonermin PRE Recombinant TNF-α (cytokine) | No renal dose adjustment. Dosing is fixed by limb volume (roughly ~1 mg for arm and up to ~3-4 mg for leg perfusions per protocol/label) and delivered regionally into the isolated circuit, not titrated to systemic eGFR. The relevant safeguard against renal injury is limiting systemic leakage, not renal-function-based dose reduction. | Yes Not clinically relevant. TNF-alpha is a ~17 kDa cytokine cleared by receptor binding and proteolysis with a short systemic half-life (prolonged to a few hours when bound to shed soluble TNF receptors after leakage). It is administered regionally, and dialysis is not used to remove it; renal replacement therapy is reserved for supporting severe AKI/volume overload, not drug clearance. |
| Tazemetostat PRE EZH2 inhibitor | No specific renal dose adjustment defined for mild-moderate impairment; severe impairment/ESKD not characterized (hepatic CYP3A metabolism). Modifications relate to hematologic toxicity and the secondary-malignancy risk. | Yes Highly protein-bound; not expected to be dialyzable. Dialysis is used for TLS metabolic complications, not drug removal. |
| Tebentafusp PRE Bispecific T-cell engager (gp100×CD3 ImmTAC) | No dedicated renal dose adjustment is established; the fixed weekly step-up schedule is driven by CRS mitigation, not renal function. Manage AKI by hemodynamic support rather than dose change. | Yes The engineered TCR-anti-CD3 fusion protein is not meaningfully dialyzable; no ESKD dose change is defined. Dialysis would support AKI management, not drug removal. |
| Teclistamab PRE Bispecific (BCMA×CD3) | No specific renal dose adjustment is established; teclistamab pharmacokinetics are not meaningfully renally dependent, and patients with renal impairment (including some on dialysis) have been treated. The operative levers are step-up dosing and holds for severe CRS rather than renal dose modification. | No Not dialyzable—an IgG-based bispecific antibody cleared by catabolism; not removed by hemodialysis and no supplemental dosing needed. Renal replacement therapy, if used, treats AKI, not drug clearance. |
| Tegafur-uracil (UFT) TMA Antimetabolite (oral 5-FU prodrug) | No universally validated renal dosing nomogram. Because 5-FU and metabolites have a renal elimination component, use caution and consider dose reduction in significant renal impairment; follow regional product labeling. | — Not well characterized for the tegafur/uracil combination; dialysis is used to support AKI rather than to remove drug. |
| Telisotuzumab vedotin (Teliso-V) ATN c-Met ADC (MMAE) | No dedicated renal dose adjustment is established. The drug has not been formally studied in severe renal impairment or dialysis; mild-to-moderate impairment is not expected to require adjustment based on the antibody-conjugated pharmacology, but data are limited. Follow the current FDA label for dose modifications driven by toxicity. | Yes Not established. As a large antibody-drug conjugate, telisotuzumab vedotin is not expected to be appreciably dialyzable; the small-molecule MMAE payload is highly protein- and tissue-bound, so removal by hemodialysis is unlikely to be clinically meaningful. |
| Temozolomide SIADH Alkylator | No renal dose adjustment is established; temozolomide pharmacokinetics are dominated by non-renal chemical degradation. Standard dosing is used across normal-to-mild renal impairment, with caution and limited data in severe impairment/dialysis. | — Short half-life with predominantly non-renal (spontaneous hydrolysis) elimination; not a drug managed by dialysis. Limited ESKD data, but renal clearance contributes little to total elimination. |
| Temsirolimus GLOM mTOR inhibitor | No specific renal dose adjustment is recommended in the label — temsirolimus and its active metabolite sirolimus are cleared by hepatic CYP3A4 metabolism and biliary excretion, not renal elimination, so renal impairment does not mandate a dose change (efficacy/safety in severe renal impairment are not established; use caution). Hepatic impairment, not renal, drives dose reduction (and severe hepatic impairment is a contraindication). Standard RCC dosing is 25 mg IV weekly. | Yes Not meaningfully dialyzable. Sirolimus (the active moiety) has a large volume of distribution, extensive tissue and erythrocyte partitioning, and high protein/lipoprotein binding, so hemodialysis is not expected to remove clinically significant amounts; direct data are limited. |
| Teniposide LYTE Podophyllotoxin (topo II) | No standardized renal dose-reduction schema is well established given low renal clearance; use caution and consider individualized reduction in severe renal or hepatic impairment and with marked hypoalbuminemia. Follow local protocol. | Yes Not meaningfully dialyzable: extensive (>99%) plasma protein binding and a relatively small free fraction make removal by hemodialysis negligible. Do not rely on dialysis for clearance. |
| Tepotinib PSEUDO MET inhibitor | No starting-dose adjustment for mild-moderate renal impairment; severe impairment and dialysis are not well studied (use with caution). Modifications are driven by edema, ILD/pneumonitis, and hepatotoxicity. | — Highly protein-bound oral small molecule; not expected to be appreciably dialyzed. No validated ESKD dosing. |
| Thalidomide PRE Immunomodulatory drug (IMiD) | No specific renal dose adjustment is mandated (thalidomide is poorly renally cleared, eliminated largely by non-enzymatic hydrolysis); use cautiously and titrate to tolerance in advanced CKD. Dose on dialysis days after the session. | No Not significantly dialyzed in routine practice; no supplemental dosing required. Give after hemodialysis on dialysis days. |
| Thiotepa CYST Alkylator | Renal impairment increases thiotepa and TEPA exposure, so use caution and consider dose reduction in moderate-to-severe impairment; no rigidly validated CrCl band exists. Exposure is best managed by clinical PK awareness rather than a fixed formula. | — Small, lipophilic, rapidly cleared; specific HD-removal data are limited and dialysis is not used for drug clearance. In ESKD, exposure considerations argue for cautious dosing rather than reliance on dialysis. |
| Tislelizumab AIN PD-1 immune checkpoint inhibitor | No starting-dose adjustment for renal impairment is recommended; tislelizumab is given as a fixed 200 mg IV every 3 weeks. As a ~150 kDa monoclonal antibody it is cleared by reticuloendothelial proteolysis, not the kidney, so mild-to-moderate renal impairment does not alter exposure. Data in severe impairment/dialysis are limited. Dose modification is event-driven (hold/discontinue for immune-mediated nephritis), not pharmacokinetic. | No Not dialyzable. Large IgG4 monoclonal antibodies are not removed by hemodialysis or peritoneal dialysis; timing relative to dialysis is irrelevant. |
| Tisotumab vedotin PRE Antibody-drug conjugate (tissue factor/MMAE) | No renal dose adjustment is established; not studied in severe impairment/ESKD. Modify/hold for ocular, bleeding and other toxicities per label. | No The IgG–MMAE conjugate is not dialyzable; released MMAE is highly protein-bound and not meaningfully removed by dialysis. No ESKD dosing guidance exists. |
| Tivozanib HTN VEGFR TKI | No dose adjustment for mild-to-moderate renal impairment; tivozanib has not been studied in severe renal impairment, and it is primarily hepatically metabolized, so renal dosing rules are minimal. Monitor closely if used in advanced CKD. | Yes Highly protein-bound with a long half-life and hepatic clearance; not appreciably dialyzable and not adjusted for HD. Data in dialysis patients are sparse. |
| Topotecan PRE Topoisomerase I inhibitor | IV topotecan: no change for CrCl >=40 mL/min; reduce dose for CrCl 20-39 mL/min. Oral topotecan PK data support reduced doses in moderate-severe impairment. Insufficient data for CrCl <20 mL/min. | — Low molecular weight and renally cleared, so some removal by hemodialysis is plausible, but formal HD-timed dosing is not established; if used in dialysis patients, reduce dose and monitor counts closely. |
| Toripalimab AIN PD-1 immune checkpoint inhibitor | No starting dose adjustment for renal impairment is specified; toripalimab is a monoclonal antibody cleared by reticuloendothelial proteolysis, not renal excretion. Pharmacologic dose modification for kidney function is not required; instead, management is by holding/discontinuing for immune-related toxicity per severity grade. Mild-to-moderate renal impairment is not expected to alter exposure. | No Not dialyzable. As a ~150 kDa IgG4 monoclonal antibody it is not removed by hemodialysis or peritoneal dialysis; no supplemental dosing is needed in dialysis patients. |
| Tovorafenib PRE Type II pan-RAF (BRAF) inhibitor | No established renal dose adjustment; tovorafenib is hepatically metabolized with low renal elimination, so meaningful exposure change with reduced GFR is not expected. Pediatric dosing is body-surface-area based and unchanged for renal function in label-described populations. | — Not characterized; as a highly protein-bound small molecule with non-renal clearance it is unlikely to be appreciably dialyzed. No dialysis dosing data in this pediatric population. |
| Trabectedin ATN Marine alkylating agent | Standard 1.5 mg/m2 IV over 24 h every 3 weeks. Dose modification is gated by bilirubin/hepatic function, not CrCl; avoid in severe hepatic impairment. No established CrCl-based reduction; it has not been studied in CrCl <30 mL/min, so use caution. | No Not dialyzable — ~94-98% protein-bound with a large volume of distribution and predominantly biliary elimination (<10% urinary). Dialysis is used to support AKI, not to remove the drug. |
| Trametinib PRE MEK inhibitor | No renal dose adjustment is specified. Trametinib undergoes predominantly hepatic metabolism (deacetylation and oxidation) with mainly fecal excretion and only minor (roughly under 20%) urinary elimination, so kidney function has little effect on exposure; mild-to-moderate renal impairment does not require a change, and no formal recommendation exists for severe impairment or dialysis (not studied). Management of AKI is drug interruption plus supportive/immunosuppressive treatment as above, not a renal-clearance-based dose reduction. | Yes Not meaningfully dialyzable. Trametinib is highly plasma-protein bound (~97%) with a large volume of distribution and is cleared hepatically/fecally rather than renally, so hemodialysis is not expected to remove appreciable drug or serve as a route of elimination in overdose. There is no renal dosing benefit from dialysis, and no formal dialysis pharmacokinetic data exist. |
| Trastuzumab deruxtecan ATN Antibody-drug conjugate (HER2/DXd) | No starting-dose adjustment for mild (CLcr 60 to <90) or moderate (CLcr 30 to <60) renal impairment; however, a higher incidence of grade 1-2 ILD/pneumonitis has been observed in moderate impairment, so monitor those patients more frequently. The recommended dosage has not been established for severe impairment (CLcr <30). The cytotoxic DXd is hepatically metabolized (CYP3A4). | — Intact ADC and protein-bound DXd are not appreciably dialyzed. No supplemental dosing guidance established for HD/PD. |
| Trastuzumab emtansine (T-DM1) TMA Antibody-drug conjugate (HER2/DM1) | No starting-dose adjustment for mild-moderate renal impairment; data are lacking in severe impairment/ESKD. DM1 is hepatically metabolized; thrombocytopenia and hepatotoxicity (not renal clearance) drive most dose modifications. | — Not appreciably dialyzed (large ADC; non-cleavable linker, hepatically handled payload). |
| Tretinoin (ATRA) PRE Retinoid (differentiating agent) | No established renal dose adjustment; standard induction is 45 mg/m²/day. Dose interruptions are driven by differentiation syndrome, pseudotumor cerebri and hepatotoxicity rather than CrCl. | — Not characterized; ATRA is highly protein-bound and hepatically metabolized (and autoinduces its own metabolism), so it is not expected to be appreciably dialyzed. Dialysis, if needed, treats the AKI/fluid overload, not drug levels. |
| Trifluridine/tipiracil PRE Oral fluoropyrimidine + TP inhibitor | No starting-dose adjustment for mild (CrCl 60-89 mL/min) or moderate (CrCl 30-59) renal impairment — the full 35 mg/m2 twice daily is tolerated; for severe impairment (CrCl 15-29) reduce to 20 mg/m2 twice daily per the label and PK study. Not studied in ESKD/dialysis — avoid or use with extreme caution. | — Tipiracil is renally cleared and its dialyzability is not well characterized; no established dosing in dialysis-dependent patients. |
| Tucatinib PSEUDO HER2 TKI | No renal dose adjustment for mild-moderate impairment. The creatinine rise is NOT a reason to reduce tucatinib; but it can falsely lower estimated CrCl and inappropriately trigger capecitabine dose reduction — use cystatin C-based GFR or measured GFR for companion-drug dosing decisions. Limited data in severe impairment, and the label does not recommend the tucatinib + capecitabine + trastuzumab combination at CrCl <30 mL/min — a restriction it attributes to the capecitabine component. | — Not characterized; highly protein-bound, hepatically (CYP2C8/3A) cleared small molecule, unlikely to be appreciably dialyzed. No ESKD dosing data. |
| Vandetanib HTN VEGFR/EGFR/RET TKI | Reduce the starting dose to 200 mg for moderate impairment (CrCl 30-49 mL/min); use in severe impairment (CrCl <30 mL/min) is not recommended per label, because vandetanib is partly renally excreted and exposure rises with impairment; titrate with ECG and electrolyte monitoring. | Yes Long half-life (~19 days), large volume of distribution and high protein binding make it essentially non-dialyzable; HD does not provide meaningful removal and is not used for dosing. |
| VEGFR Tyrosine Kinase Inhibitors HTN VEGFR TKI | No renal-function-based dose adjustment is required for the oral VEGFR TKIs themselves — they undergo predominantly hepatic (CYP3A4) metabolism with minimal renal excretion, and labels for sunitinib, sorafenib, pazopanib, axitinib, cabozantinib, and lenvatinib state no starting-dose change for mild-to-severe CKD (cabozantinib and lenvatinib carry caution but no defined CrCl threshold). The clinically relevant "adjustment" is for the on-target toxicities: hold or dose-reduce for grade 3+ hypertension or nephrotic-range proteinuria and discontinue for TMA, rather than for measured GFR. | No Largely not dialyzable — these agents are small but highly protein-bound and have large volumes of distribution, so hemodialysis is not expected to remove meaningful drug, and no supplemental post-HD dosing is defined. Limited case-series data (chiefly sunitinib and sorafenib) suggest standard dosing can be used in HD patients without dialysis timing changes, though monitoring for amplified toxicity is advised. |
| Vemurafenib ATN BRAF inhibitor | No renal-based dose adjustment is specified for mild-to-moderate impairment. Because vemurafenib is hepatically metabolized (CYP3A4) and eliminated almost entirely in feces, with only ~1% renal excretion, exposure is not expected to change materially with reduced GFR, though data in severe impairment and ESKD are lacking. Dose modification is therefore driven by toxicity, not clearance: for drug-attributable AKI or intolerable toxicity, interrupt and, on recovery, resume at reduced dose (label steps 960 -> 720 -> 480 mg twice daily); permanently discontinue for recurrent severe events. Do not reduce below 480 mg twice daily. | Yes Not meaningfully dialyzable. Vemurafenib is >99% protein-bound, highly lipophilic, and eliminated predominantly in feces (~94%) with renal excretion near 1%; hemodialysis is not expected to remove appreciable drug and no post-dialysis supplemental dose is indicated. Dedicated dialysis pharmacokinetic data are lacking. |
| Venetoclax XTAL BCL-2 inhibitor | No dose adjustment for mild, moderate OR severe renal impairment (CrCl >=15 mL/min) — venetoclax is hepatically (CYP3A) cleared and does not accumulate renally, and the label makes that recommendation across all three bands rather than stopping at moderate. The renal number that changes management is a tumor-lysis threshold, not a clearance one: CrCl <80 mL/min calls for more intensive TLS prophylaxis and monitoring when starting treatment, because reduced clearance of urate and phosphate magnifies TLS risk. Below CrCl 15 and on dialysis the label makes no recommendation and data are limited. | — Not meaningfully dialyzed — highly protein-bound (>99%), hepatically (CYP3A) metabolized small molecule with negligible renal excretion. Dialysis is used to treat TLS metabolic complications, not to remove the drug. |
| Vepdegestrant PRE PROTAC estrogen-receptor degrader | No renal-impairment dose adjustment is established; vepdegestrant is an oral, metabolically cleared PROTAC and VERITAC-2 required adequate organ function. GFR is not the determinant of exposure, and dose modification is based on tolerability (hematologic, constitutional) rather than kidney function. | Yes Not characterized as dialyzable and not clinically relevant: as a large, protein-bound, metabolically cleared molecule, vepdegestrant is not expected to be removed by hemodialysis, and no renal-elimination or drug-removal scenario makes dialysis relevant for this agent. |
| Vimseltinib PSEUDO CSF1R tyrosine kinase inhibitor | No dedicated renal dose-adjustment requirement is established for clinically meaningful direct nephrotoxicity, as the drug is not a recognized nephrotoxin. Vimseltinib is given orally 30 mg twice weekly in 28-day cycles. Formal pharmacokinetic data in moderate-to-severe renal impairment and in dialysis patients are limited; prescribe with standard caution in advanced CKD and consult the current label for any renal/hepatic dosing language, since hepatic handling and CYP interactions are the more pertinent PK considerations for this agent. | Yes Not characterized. As a small-molecule kinase inhibitor that is highly protein-bound and predominantly hepatically metabolized, vimseltinib is unlikely to be meaningfully removed by hemodialysis, but no formal dialyzability data are available; do not assume dialysis clearance. |
| Vinblastine SIADH Vinca alkaloid | Hepatically metabolized (CYP3A) and biliary excreted - no renal dose adjustment; reduce for hepatic impairment/hyperbilirubinemia. Never give intrathecally. | No Large volume of distribution and extensive tissue binding; not dialyzable. Manage hyponatremia with fluid/sodium strategies. |
| Vincristine SIADH Vinca alkaloid | Hepatically (CYP3A) metabolized and biliary excreted - no renal dose adjustment. Reduce dose for hepatic dysfunction/hyperbilirubinemia. Note the absolute dose cap to limit neurotoxicity; never administer intrathecally (fatal). | No Highly tissue-bound with a very large volume of distribution; not dialyzable. Hyponatremia is managed with fluid/sodium strategies, not dialysis. |
| Vinflunine LYTE Vinca alkaloid | Per phase I PK data: 320 mg/m2 for CrCl >60 mL/min; 280 mg/m2 for CrCl 40-60 mL/min (inclusive of both bounds); 250 mg/m2 for CrCl 20 to <40 mL/min. These bands yield exposure comparable to patients with normal renal function. | No Not established as dialyzable in routine practice; vinflunine is largely hepatically metabolized (CYP3A4) with a large volume of distribution, making meaningful dialytic removal unlikely. Manage by dose banding, not dialysis timing. |
| Vinorelbine SIADH Vinca alkaloid | Hepatically metabolized (CYP3A) and biliary excreted - no renal dose adjustment; reduce for hepatic impairment/hyperbilirubinemia. Never give intrathecally. | No Extensive tissue binding and large volume of distribution; not dialyzable. Hyponatremia is managed by fluid/sodium strategies. |
| Vismodegib SIADH Hedgehog (SMO) inhibitor | No dose adjustment recommended for mild-moderate renal impairment; not formally studied in severe impairment/ESKD. Hepatic metabolism predominates and dosing is fixed (150 mg daily). | Yes Very highly protein-bound (>99%); not expected to be dialyzable and no ESKD dosing established. |
| Vorasidenib PSEUDO Mutant IDH1/2 inhibitor | No dedicated renal-impairment dose adjustment is established for mild-to-moderate impairment; vorasidenib is hepatically metabolized (CYP1A2/CYP3A) and dose modifications in the label are driven by hepatotoxicity, not renal function. Data at CrCl ≤40 mL/min and on dialysis are lacking; there the label directs monitoring for increased adverse reactions and modifying the dose accordingly. A creatinine-based eGFR fall from blocked tubular secretion should not by itself trigger renal dose reduction. | Yes Not characterized. Vorasidenib is a small molecule but is highly protein-bound and extensively hepatically cleared, so it is unlikely to be meaningfully removed by hemodialysis; no formal dialysis data exist. |
| Zanidatamab PRE HER2 bispecific antibody | No dedicated renal dose adjustment is specified; as a ~150 kDa monoclonal-type bispecific, clearance is not renal and exposure is not expected to change meaningfully with reduced GFR. No data in dialysis. Manage by holding/resuming for toxicity rather than CrCl-based reduction. | No Not dialyzable — large bispecific antibody cleared by reticuloendothelial proteolysis, not removed by hemodialysis or peritoneal dialysis. No ESKD-specific dosing guidance exists; standard dosing is reasonable with attention to volume status during infusion. |
| Zanubrutinib PRE BTK inhibitor | No dose adjustment for mild-to-moderate renal impairment; in severe renal impairment and on dialysis, exposure changes are modest and no dose adjustment is generally required, though data are limited. Hepatic impairment, not renal, drives reduction; minimal renal excretion of unchanged drug. | Yes Not meaningfully dialyzable — highly protein-bound, hepatically (CYP3A) cleared small molecule. No supplemental post-HD dose needed. |
| Zenocutuzumab PRE HER2×HER3 bispecific antibody | No pharmacokinetic renal dose adjustment is defined: zenocutuzumab is an IgG1 antibody cleared by reticuloendothelial catabolism rather than glomerular filtration, so creatinine clearance is not expected to change exposure, and dedicated data in severe renal impairment or dialysis are limited. Dose interruption is driven by infusion reactions and other toxicity rather than by GFR; pre-existing CKD mainly raises the stakes of diarrheal or infusion-related volume depletion and warrants closer supportive monitoring. | No Not dialyzable — a full-size IgG1 bispecific antibody vastly exceeds any dialysis-membrane cutoff and stays in the vascular/interstitial compartment, so hemodialysis does not remove the drug. Renal replacement therapy would only support an unrelated severe AKI, not clear the antibody. |
| Zidesamtinib PRE ROS1-selective TKI | No dosage modification is recommended for eGFR 30-90 mL/min; the label states the effect of severe renal impairment (eGFR <30 mL/min) or dialysis on zidesamtinib pharmacokinetics is unknown. Dose changes are driven by the drug's own toxicities (CPK elevation with myalgia, pancreatic enzyme elevation, QT), not by kidney function. | Yes Not characterized: the label explicitly lists the effect of dialysis on zidesamtinib pharmacokinetics as unknown. As an orally dosed, metabolically cleared kinase inhibitor it is unlikely to be meaningfully dialyzable, and no drug-removal scenario applies. |
| Ziftomenib PRE Menin inhibitor | No dedicated renal dose adjustment is established; ziftomenib is hepatically metabolized. Dose interruption is driven by differentiation syndrome, QTc and cytopenias rather than CrCl. Data in significant renal impairment/dialysis are absent. | — Not characterized; a protein-bound, hepatically cleared small molecule unlikely to be appreciably dialyzed. No ESKD dosing guidance. |
| Ziv-aflibercept HTN VEGF trap | No pharmacokinetic renal dose adjustment for a fusion-protein decoy; dose modification is driven by proteinuria thresholds and hypertension grade. Renal impairment does not alter clearance of the Fc-fusion molecule. | No Not dialyzable — a ~115 kDa Fc-fusion protein is not removed by hemodialysis or peritoneal dialysis; no dose change for dialysis patients. |
| Zolbetuximab PRE Anti-Claudin-18.2 monoclonal antibody | No dedicated renal dose adjustment is established; mild–moderate impairment does not require change and severe impairment/ESKD are not well studied. Management is antiemetic control and volume repletion rather than fixed renal dosing. | No The IgG1 antibody is not dialyzable and is cleared by proteolysis; no ESKD dose change is defined. Dialysis would support AKI management, not drug removal. |
| Zoledronic acid ATN Bisphosphonate | For multiple myeloma/bone metastases, the label gives a CrCl-banded reduction of the standard 4 mg dose: CrCl 50-60 mL/min → 3.5 mg, 40-49 → 3.3 mg, 30-39 → 3.0 mg; not recommended if CrCl <30 mL/min or in severe renal impairment. Always infuse over no less than 15 minutes (never bolus) and hydrate adequately. For hypercalcemia of malignancy, the risk-benefit must be weighed individually in severe renal impairment, with the 4 mg dose unmodified but careful hydration; withhold subsequent oncology doses until creatinine returns to within ~10% of baseline. | — Zoledronic acid is cleared almost entirely by the kidney with minimal hepatic metabolism, so accumulation is expected in advanced CKD/ESKD; pharmacokinetic data in dialysis are limited. It is poorly protein-bound and small, making it theoretically removable, but timing relative to hemodialysis is not well characterized and the drug is generally avoided rather than dose-timed around dialysis. The osteoporosis formulation (Reclast/Aclasta 5 mg) is contraindicated at CrCl <35 mL/min. |
| Zongertinib PSEUDO HER2 TKI | Not formally established; as a hepatically metabolized small molecule, meaningful renal-clearance dependence is not expected. A creatinine rise attributable to transporter inhibition should not by itself trigger dose reduction. Data in significant renal impairment/dialysis are absent. | — Not characterized; protein-bound, non-renally cleared — unlikely to be appreciably dialyzed. No ESKD dosing guidance. |
A teaching reference, not a dosing calculator — always confirm against the current prescribing information and your institutional protocol before adjusting therapy. Thresholds are summarized from each agent’s profile and its cited sources; the grouped rules are concise paraphrases verified against FDA labels. Medical-education content only — not medical advice.