The Injury Atlas See it on the nephron Does the kidney recover? Cross-drug outcomesRepresentative per-agent electrolyte disturbance incidence where a published figure is citable — open an agent's name for its profile and cited source, or hover its dot for the source inline. Agents without a citable figure are omitted; a tier without a number is not the same as a low number.
LYTE
Electrolyte Disturbance
Renal electrolyte derangement — magnesium/potassium/calcium wasting (cisplatin, anti-EGFR antibodies) or retention (FGFR-inhibitor hyperphosphatemia, tumor-lysis hyperkalemia/hyperphosphatemia).
148agents
Deep diveCisplatin ATN & hypomagnesemiaDeep diveEGFR-inhibitor hypomagnesemiaDeep diveIfosfamide FanconiDeep divePemetrexed tubulopathyDeep diveTumor lysisDeep diveBRAF/MEK tubularDeep diveBisphosphonate injuryDeep diveCAR-T AKI
Where it strikes
Distal Tubule / Collecting Duct
Fine-tuning of Na, K, Mg, acid & water
Agents’ overall severity
Each agent’s whole-drug severity grade, not the severity of this lesion specifically — an agent whose signature injury is elsewhere can still be graded severe here.
Severe· 6Moderate· 75Mild· 67
Agents’ overall reversibility
Often irreversible· 1Partially reversible· 18Variable· 19Reversible· 110
Agents’ onset window
How soon each agent’s kidney toxicity typically appears — a whole-drug tempo, not specific to this lesion.
Hyperacute (<24 h)· 2Acute (days)· 63Subacute (weeks)· 37Delayed (weeks–months)· 18Variable· 28
Real-world reporting for this lesion
FAERS across all lesions →Agents with a disproportionate FAERS reporting signal for electrolyte disturbance (reporting odds ratio with a 95% CI lower bound above 1) — a spontaneous-reporting signal, not incidence or proven causation. FAERS carries reporting and indication biases and has no denominator.
71Corroborated
Documented in the atlas profile and carrying a FAERS signal — the strongest claim the atlas makes.
42Documented, FAERS-silent
Documented in a profile with no reporting signal. Mostly expected: naming this lesion on a report can require a biopsy, and silence is not evidence against the literature.
33Not attributable
A real reporting signal that is not evidence for this drug-lesion pair: no MedDRA term names it, the naming subset asked alone came back flat, or the 2026-08 review attributed the reporting to the population, co-therapy, or class-level literature.
38Reported by name
The terms that name this lesion are disproportionate, but no profile documents it for that agent. Most are echoed by a sibling agent in the same class. Leads for review, never lesions the atlas claims.
5-FluorouracilAbemaciclibAbirateroneAcalabrutinibAdagrasibAfatinibAmivantamabArsenic trioxideAtezolizumabAxitinibAzacitidineBelantamab mafodotinBelzutifanBendamustineBevacizumabBicalutamideBinimetinibBleomycinBlinatumomabBortezomibBrentuximab vedotinCabazitaxelCabozantinibCapecitabineCapmatinibCarboplatinCarfilzomibCeritinibCetuximabCisplatinClofarabineCobimetinibCrizotinibCyclophosphamideCytarabineDabrafenibDacarbazineDasatinibDecitabineDenosumabDinutuximabDocetaxelDoxorubicinDurvalumabElotuzumabEncorafenibEnfortumab vedotinEpcoritamabErdafitinibEribulinErlotinibEtoposideEverolimusFludarabineFutibatinibGefitinibGemcitabineGemtuzumab ozogamicinGlasdegibGlofitamabHydroxyureaIbandronateIbritumomab tiuxetanIbrutinibIdarubicinIfosfamideImatinibImlunestrantInotuzumab ozogamicinInterleukin-2 (high-dose)IpilimumabIrinotecanIsatuximabIvosidenibIxazomibLanreotideLenvatinibLifileucelMelphalanMitotaneMitoxantroneNaxitamabNelarabineNeratinibNiraparibNirogacestatNivolumabObinutuzumabOctreotideOxaliplatinPaclitaxelPamidronatePanitumumabPazopanibPegaspargasePembrolizumabPemetrexedPemigatinibPenpulimabPentostatinPirtobrutinibPolatuzumab vedotinPralatrexatePralsetinibRadium-223 dichlorideRamucirumabRegorafenibRelacorilantRibociclibRituximabSacituzumab govitecanSelinexorSirolimusSonidegibSorafenibSotorasibSunitinibTalazoparibTalquetamabTamoxifenTemozolomideTemsirolimusThalidomideTislelizumabTisotumab vedotinTopotecanTovorafenibTrabectedinTrametinibTrastuzumab deruxtecanTrastuzumab emtansine (T-DM1)Trifluridine/tipiracilTucatinibVandetanibVemurafenibVenetoclaxVinblastineVincristineVinorelbineVismodegibZolbetuximabZoledronic acid
142 agents with a significant LYTE reporting signal.
At the bedside
EGFR hypomagnesemia deep dive →Anti-cancer magnesium wasting — anti-EGFR antibodies and platinums above all — is cumulative and often silent until severe. Grade a level to gauge urgency and route.
Magnesium grade & repletion
CTCAE v5.0Enter a serum magnesium level for its CTCAE grade and a directed-repletion frame. Drug-induced renal magnesium wasting (anti-EGFR antibodies, platinums) is cumulative — grade guides urgency and route.
Enter a level to see the CTCAE grade and repletion frame.
Educational aid only — not medical advice. Grades per NCI CTCAE v5.0, read directly from the column for the unit you enter. CTCAE defers to the reporting lab for the limits of normal; this tool assumes 1.7–2.6 mg/dL. Repletion route and dosing follow local protocol and clinical judgment.
Management approach
Full framework →Replace what is wasted; the drug usually continues.
Drug-level levers
- Therapy is typically continued with ongoing repletion.
- Dose-reduce or hold only for severe, symptomatic, or refractory derangements.
Pharmacologic toolkit
- Magnesium repletion — Oral and IV magnesium for anti-EGFR and cisplatin hypomagnesemia; losses are often substantial and recurrent.
- Potassium / calcium repletion — Correct coexisting hypokalemia and hypocalcemia (often magnesium-dependent).
When to biopsy
Not indicated — this is a functional tubular transport defect, not a structural lesion.
Monitoring
- · Serum magnesium, potassium, and calcium during and after therapy
Educational use only. Educational synthesis of the published literature — not a treatment protocol, dosing guide, or medical advice. Regimens and agents shown are illustrative of what the literature describes; verify against current guidelines (ASON / KDIGO / ASCO / NCCN) and individualize to the patient. Using this site creates no clinician–patient relationship.
What the guidelines say
All guidelines →Society and consensus recommendations that speak to electrolyte disturbance.
Each recommendation below is this atlas's faithful summary of the source, not a quotation from it — follow the PubMed link for the wording the society published. Summaries may be superseded; consult the current full text and individualize to the patient.
ADQIThe nephrotoxic effects of anti-cancer therapies: consensus report of the 34th Acute Disease Quality Initiative workgroupNat Rev Nephrol 2026 · PMID 41361704Provides expert-based statements (modified Delphi) on preventing and managing cisplatin/platinum-associated AKI, including isotonic IV hydration, attention to volume status and concomitant nephrotoxins, and incorporates evidence that IV magnesium supplementation may reduce cisplatin-associated AKI; emphasizes risk stratification and standardized AKI definitions.ADQIConventional cytotoxic chemotherapy-associated nephrotoxicity: consensus report of the 34th Acute Disease Quality Initiative (ADQI) WorkgroupKidney Int 2026 · PMID 41881107Cisplatin is identified as a leading cytotoxic nephrotoxin; the workgroup details preventive measures (adequate isotonic hydration, correction of volume depletion, avoidance of concurrent nephrotoxins, attention to electrolyte/magnesium wasting) and management of cisplatin-associated AKI, with a research agenda for knowledge gaps.KDIGOKDIGO Controversies Conference on onco-nephrology: understanding kidney impairment and solid-organ malignancies, and managing kidney cancerKidney Int 2020 · PMID 33126977Identifies platinum compounds (especially cisplatin) as leading cytotoxic causes of acute tubular injury, AKI, and electrolyte/magnesium wasting; calls for interdisciplinary onco-nephrology care, accurate GFR estimation, and individualized drug dosing in patients with reduced kidney function.KDIGOKDIGO Controversies Conference on onco-nephrology: kidney disease in hematological malignancies and the burden of cancer after kidney transplantationKidney Int 2020 · PMID 33276867Addresses chemotherapy-associated AKI/CKD in hematologic cancer, GFR estimation and chemotherapy dosing in patients with reduced kidney function, and management priorities and research gaps for onco-nephrology care.Expert ConsensusThe Prevention of Cisplatin-Induced Nephrotoxicity: A General Consensus Statement of a Group of Oncologist-Hematologists, Adult and Pediatric Nephrologists, Radiation Oncologists, Clinical Pathologists, Clinical Pharmacologists, and Renal Physiologists on Cisplatin Therapy in Cancer PatientsInt J Prev Med 2022 · PMID 35392316Consensus on modifiable factors for cisplatin nephrotoxicity prevention, addressing hydration methods, magnesium supplementation, dextrose, avoidance of NSAIDs and renin-angiotensin system inhibitors and contrast agents around cisplatin, GFR assessment, antioxidants, and patient factors (age, sex, female hormones).BCSHGuidelines for the management of tumour lysis syndrome in adults and children with haematological malignancies on behalf of the British Committee for Standards in HaematologyBr J Haematol 2015 · PMID 25876990Risk-adapted prophylaxis and management of TLS in haematological malignancy: hydration with allopurinol for lower-risk and rasburicase for high-risk patients, with monitoring of electrolytes and renal function to prevent and treat AKI.TLS Consensus PanelRecommendations for the evaluation of risk and prophylaxis of tumour lysis syndrome (TLS) in adults and children with malignant diseases: an expert TLS panel consensusBr J Haematol 2010 · PMID 20331465Stratify each patient as low/intermediate/high TLS risk using tumor type, bulk/stage, proliferation rate, baseline laboratory TLS, and renal impairment/involvement, then match prophylaxis intensity (monitoring vs allopurinol vs rasburicase) to the assigned risk level.TLS Expert PanelGuidelines for the management of pediatric and adult tumor lysis syndrome: an evidence-based reviewJ Clin Oncol 2008 · PMID 18509186Prevention is the best management: hydration plus prophylactic rasburicase for high-risk patients, hydration plus allopurinol or rasburicase for intermediate-risk, and monitoring for low-risk; for established TLS add aggressive hydration and diuresis plus allopurinol or rasburicase for hyperuricemia. Urinary alkalinization is NOT recommended.Cairo-BishopTumour lysis syndrome: new therapeutic strategies and classificationBr J Haematol 2004 · PMID 15384972Defines the Cairo-Bishop criteria distinguishing laboratory TLS (>=2 metabolic abnormalities: hyperuricemia, hyperkalemia, hyperphosphatemia, hypocalcemia within 3 days before to 7 days after therapy) from clinical TLS (laboratory TLS plus AKI, cardiac arrhythmia, or seizure), with a severity grading scheme adopted by subsequent guidelines.
Cited incidence across agents
Where the literature gives a representative electrolyte disturbance figure, the agents ranked highest first. Hover a dot for its cited note.
Offending agents
Signature offenders
28Agents for which electrolyte disturbance is the defining renal lesion.
NecitumumabDevelops cumulatively over weeks of repeated dosing and worsens with continued therapy; magnesium should be checked before each dose and for at least 8 weeks after completion because deficits can persist.Grade 3-4 hypomagnesemia occurred in about 9% of patients receiving necitumumab plus chemotherapy versus 1% with chemotherapy alone in the pivotal SQUIRE trial; any-grade hypomagnesemia is likely more frequent (as a class, anti-EGFR antibodies are associated with a gradual magnesium fall in many patients over time).ModerateErdafitinibEarly — typically within the first 1-2 cycles, used to guide pharmacodynamic up-titration.Hyperphosphatemia is the most common, on-target class adverse event — reported in ~73-78% of treated patients across studies and used as a pharmacodynamic marker for protocol-driven dose up-titration. Grade >=3 hyperphosphatemia is much less frequent (~2%).ModeratePemigatinibEarly — within the first cycles.Hyperphosphatemia is the most common adverse event in the pivotal FIGHT-202 trial, affecting roughly 60% of patients (any grade), with low rates of severe events; it is on-target and managed with monitoring, diet, and binders.ModerateFutibatinibEarly — within the first cycles.Hyperphosphatemia is the most common adverse event, reported in ~85% of patients (any grade, most low-grade) in the pivotal FOENIX-CCA2 trial; it is on-target, dose-related, and confirmed as a pharmacodynamic effect in first-in-human work.ModerateDenosumabWithin days to a few weeks of dosing (nadir often around 1-2 weeks); can be prolonged given the drug's months-long duration of effect and the absence of a reversal agent.Denosumab is not directly nephrotoxic and is not renally cleared, but the risk of severe hypocalcemia rises sharply as kidney function declines. In a population-based cohort, severe hypocalcemia occurred in 0.2% of all new users but in 14.9% of those with eGFR <15 mL/min/1.73 m2 or on dialysis (mild hypocalcemia 24.1% in that group). Reported rate: hypocalcemia in 17% — 850 patients with symptomatic newly diagnosed multiple myeloma and at least one lytic bone lesion who received at least… (Raje 2018, PMID 29429912).ModerateAbirateroneWithin the first weeks of therapy; recurs if glucocorticoid coverage is inadequate or interrupted.Mineralocorticoid-excess effects are common: in COU-AA-301 fluid retention, hypertension and hypokalemia were all more frequent than with placebo-prednisone. Severe (grade 3–4) hypokalemia, occasionally to 1.7–2.1 mEq/L, is reported even with concomitant prednisone. Meta-analysis confirms an increased relative risk of hypertension. A single-center retrospective cohort of 79 patients reported renal events in 63.3% of abiraterone-treated patients — AKI in 30.4%, half of whom progressed to chronic kidney disease (Pujol-Pujol 2025). Reported rate: grade >=3 hypokalemia in 12% — 597 men with newly diagnosed high-risk metastatic castration-sensitive prostate cancer randomized to abiraterone… (Fizazi 2019, PMID 30987939).ModerateAmivantamabElectrolyte changes during therapy and cumulative; AIN timing not well characterized (subacute, days–weeks after a triggering exposure by analogy to drug AIN).In CHRYSALIS, electrolyte disturbance — notably hypokalemia (grade 3–4 in ~5%) and hypomagnesemia/hypocalcemia — was among the laboratory adverse events, consistent with EGFR-pathway inhibition. Acute interstitial nephritis is an emerging, clinician-flagged signal that is not yet quantified in the published renal literature. Reported rate: grade >=3 hypokalemia in 5% — CHRYSALIS phase I safety population, n = 114 patients with EGFR exon 20 insertion-mutated NSCLC receiving amivantamab… (Park 2021, PMID 34339292).ModerateInfigratinibEarly (first cycle); reversible and dose-dependent, normalizing during the 7-day off-drug interval of the 21-on/7-off cycle.Hyperphosphatemia is the most common adverse event and the defining FGFR class effect — it occurred in 83 of 108 patients (~77%, any grade) in the pivotal trial. Infigratinib-specific nephrocalcinosis/calciphylaxis rates are not quantified (case reports/series only).ModerateDactinomycin (actinomycin D)TLS within hours to days of initiating effective chemotherapy; VOD typically within the first weeks of treatment.Direct nephrotoxicity is not an established feature of dactinomycin. The clinically relevant renal risk is tumor lysis syndrome (TLS) when used against bulky, chemosensitive pediatric tumors; precise incidence attributable to dactinomycin alone is not quantified, as it is given in multi-agent regimens.ModerateMechlorethamineTLS within hours to days of effective cytoreduction in bulky lymphoma.Direct nephrotoxicity is not a defining feature. The principal renal hazard is tumor lysis syndrome when treating bulky, rapidly proliferating lymphoma; incidence specifically attributable to mechlorethamine is not quantified because it is used within multi-agent regimens. The 0.016%/0.02% topical gel shows no detectable systemic absorption.ModerateAmsacrineTLS within hours to days of effective cytoreduction.Direct nephrotoxicity is not a prominent feature. The main renal hazard is tumor lysis syndrome during leukemia induction/salvage; incidence specific to amsacrine is not quantified. Pharmacokinetic studies show renal elimination plays only a minor role, with clearance dominated by hepatic metabolism and biliary excretion.ModerateMitotaneAdrenal insufficiency and its electrolyte/volume consequences develop over weeks of therapy as adrenolytic effect accrues; cisplatin-associated AKI in EDP-M is acute, within days of chemotherapy cycles.Intrinsic mitotane nephrotoxicity is not characteristically quantified. Clinically important renal events are indirect (adrenal insufficiency-related electrolyte/volume disturbance) or attributable to co-administered cisplatin in EDP-M; incidence not reliably enumerated for mitotane alone.ModerateStrontium-89 chlorideHematologic nadir typically develops over several weeks (e.g., weeks 4-8) given the long physical half-life; any renal/excretion-related concern relates to the early post-injection days when urinary excretion is highest.Intrinsic nephrotoxicity is not a defining or well-quantified effect; the prominent toxicity is transient myelosuppression (e.g., reversible hematologic toxicity reported in roughly half of treated patients in small series). Renal events are uncommon and not reliably enumerated.ModerateInavolisibHyperglycemia from PI3Kalpha inhibition is an on-target effect that can appear soon after dosing, sometimes with peak glucose elevations in the hours following ingestion, and typically reverses within days of holding the drug.Direct nephrotoxicity from inavolisib is not prominent and renal-specific data are limited; the headline metabolic toxicity is on-target hyperglycemia. In the INAVO120 phase 3 trial, grade 3 or 4 hyperglycemia occurred in 5.6 percent of the inavolisib group versus 0 percent with placebo, alongside higher rates of stomatitis and diarrhea (which can secondarily cause volume and electrolyte loss). A defined inavolisib-specific kidney lesion with an established electrolyte-event incidence rate is not characterized, so no headline signature rate is charted (the 5.6% grade 3/4 hyperglycemia figure is a metabolic, not electrolyte, signal).ModerateAvutometinibEarly. CPK elevation and diarrhea typically emerge within the first one to two cycles (first weeks) of therapy; in a BRAF/MEK-inhibitor cohort, treatment-associated AKI clustered within the first three months. Peripheral edema/fluid retention accrues over weeks to months. Rhabdomyolysis-associated AKI, when it occurs, parallels the peak CPK.No discrete acute-kidney-injury incidence has been reported for avutometinib. The best-quantified kidney-relevant signal is marked creatine phosphokinase (CPK) elevation: in the registrational RAMP 201 combination cohort (avutometinib + defactinib, n=115), grade >=3 CPK elevation occurred in 24% of patients — the single most common grade >=3 treatment-related adverse event — with grade >=3 diarrhea in 8% and anemia in 5%. A CPK rise of this magnitude is a recognized rhabdomyolysis-risk surrogate, not a measured AKI rate: most CPK elevations are asymptomatic skeletal-muscle elevations that do not injure the kidney, but sustained rhabdomyolysis-range values can precipitate pigment (myoglobin-cast) tubular injury, and high-grade diarrhea can drive prerenal azotemia and electrolyte loss. Across the MEK-inhibitor class the FAERS acute-kidney-injury signal is heterogeneous rather than uniformly low: reporting-odds-ratio approximately 1.3 for trametinib but approximately 4.4 for cobimetinib, the latter exceeding vemurafenib's approximately 3.3 in the same analysis (Sanagawa 2021) — though cobimetinib is given only with vemurafenib, so its pharmacovigilance signal cannot be read as a pure MEK effect. All figures derive from a small phase II dataset and are hedged accordingly.ModerateImatinibEdema early; tubular dysfunction and eGFR decline develop over months to years.Periorbital/peripheral edema and fluid retention are common. Clinically meaningful renal injury is uncommon: long-term front-line imatinib is associated with a modest, measurable decline in eGFR over years, while proximal tubular dysfunction (hypophosphatemia, aminoaciduria, rare Fanconi syndrome) and AKI (including rare urate nephropathy from disease cytoreduction) are described at the case level.MildNirogacestatDuring therapy; not well characterized.Hypophosphatemia occurred in 42% of nirogacestat-treated patients in the DeFi trial, alongside other electrolyte disturbances; the characteristic DeFi-trial toxicities were diarrhea, rash, nausea, fatigue and ovarian dysfunction. Beyond the phosphate signal, renal-specific incidence is not well quantified.MildSunvozertinibElectrolyte changes can appear within the first weeks to months of therapy; hypomagnesemia risk rises with treatment duration.No established AKI rate. As with the EGFR-inhibitor class, the renal-relevant signal is electrolyte disturbance — particularly hypomagnesemia (renal Mg wasting) and diarrhea-driven losses, with a hyponatremia/SIADH-like pattern possible — rather than structural nephron injury. WU-KONG6 reported diarrhea and skin/EGFR-pathway toxicities as dominant; renal-specific events are not quantified.MildVinflunineElectrolyte/prerenal effects can appear within days of a cycle; PK accumulation in renal impairment is immediate but mitigated by protocol dose reduction.No strong direct nephrotoxic signal. Vinflunine is given to renally impaired, cisplatin-unfit patients with a defined dose-reduction schema, and tolerability in renal impairment mirrors that of patients with normal renal function once dose-banded. SIADH/hyponatremia is a class-level vinca-alkaloid effect rather than a quantified vinflunine-specific rate. Reported rate: grade >=3 hyponatremia in 12% — 51 patients with relapse-sensitive or relapse-refractory small cell lung cancer treated with single-agent vinflunine… (Spigel 2010, PMID 20521355).MildTeniposideNo characteristic renal onset; pharmacokinetic exposure effects are immediate but clinically modest.Minimal direct nephrotoxicity. Teniposide is highly protein-bound with low renal clearance (only ~5-20% of a dose is recovered in urine versus a larger fraction for etoposide), so the kidney is a minor elimination route and direct renal injury is not a characteristic toxicity. Renal relevance is pharmacokinetic/exposure-related and not quantified as a discrete nephrotoxicity rate.MildOctreotideNot applicable for intrinsic injury; pharmacokinetic accumulation in renal failure is gradual.No characteristic intrinsic nephrotoxicity; octreotide is generally considered kidney-neutral. Renal events are rare, indirect, and not reliably quantified. Mild electrolyte disturbances are uncommon.MildLanreotideNot applicable for intrinsic injury; exposure rises gradually in renal impairment.No characteristic intrinsic nephrotoxicity; lanreotide is generally kidney-neutral. Renal adverse events are not a defining feature and are not reliably quantified; mild electrolyte effects are uncommon.MildDarolutamideNot applicable for intrinsic injury; exposure differences in renal impairment are present from initiation and steady state (reached in ~2 days).No characteristic intrinsic nephrotoxicity. In ARAMIS, rates of adverse events including hypertension were similar to placebo. Renal-relevant findings are pharmacokinetic (increased exposure in severe renal impairment); intrinsic renal injury incidence not meaningfully quantified.MildCetuximabDevelops insidiously over weeks to months of therapy and is cumulative — the nadir deepens the longer treatment continues, so the largest deficits typically appear after several months. Reversible: renal magnesium handling recovers over weeks (usually within about 4-8 weeks) after cetuximab is stopped.Hypomagnesemia is an on-target class effect. In the defining prospective cohort (Tejpar, Lancet Oncol 2007), 95/98 patients (97%) developed a declining serum magnesium slope on EGFR-antibody therapy. Cetuximab-specific pooled data give an any-grade incidence of ~36% (Cao, Chemotherapy 2010; 19 trials, 95% CI 22-54%), with grade 3-4 hypomagnesemia — a CTCAE serum-magnesium threshold, not a symptom rate — in roughly 5-6%; a pooled analysis of randomized anti-EGFR antibody trials (cetuximab and panitumumab together) reports an overall any-grade incidence of 17% across the class (Petrelli, Expert Opin Drug Saf 2011). Versus control, the relative risk is ~3.9 for cetuximab specifically and ~5.83 across anti-EGFR antibodies (Petrelli, Expert Opin Drug Saf 2011). Magnesium falls cumulatively, deepening with treatment duration.MildPanitumumabDevelops over weeks of therapy and is cumulative, deepening with treatment duration and repeated every-2-week dosing. Recovery after discontinuation is typically slow — over several weeks to a couple of months — as distal-tubule magnesium handling gradually normalizes; hypomagnesemia can persist or transiently worsen shortly after the last dose.Hypomagnesemia is the signature renal-tubular toxicity and one of panitumumab's most frequent adverse effects. Any-grade rates cluster around 30-40% across RAS/KRAS wild-type mCRC trials, with grade 3-4 hypomagnesemia in roughly 3-7%; it is dose- and duration-related and deepens with cumulative exposure (Van Cutsem, J Clin Oncol 2007, established it as a frequent toxicity of the registration monotherapy trial). Rates are consistently HIGHER than with cetuximab: a pooled analysis put the relative risk of hypomagnesemia at ~12.6 for panitumumab versus ~3.9 for cetuximab (Petrelli, Expert Opin Drug Saf 2011), and in the head-to-head ASPECCT trial grade 3-4 hypomagnesemia was 7% with panitumumab versus 3% with cetuximab (Price, Lancet Oncol 2014).MildFedratinibGI adverse events appear early — typically within the first one to two treatment cycles — and tend to diminish over time with supportive care and dose management; the associated electrolyte and creatinine changes track these early GI events. Reduced clearance in renal impairment is present from the first dose (higher exposure independent of time on drug).There is no established incidence of direct fedratinib-induced kidney injury; the renal story is pharmacokinetic and GI-driven rather than a discrete nephrotoxic lesion. In the pivotal placebo-controlled JAKARTA phase 3 trial, gastrointestinal symptoms were among the most common adverse events and "increased levels of serum creatinine" was reported as a common laboratory abnormality — but neither a rate of clinically significant AKI nor a discrete electrolyte-depletion incidence was separately quantified, so a headline nephrotoxicity percentage cannot be stated without overstating the evidence. The dedicated phase 1 renal-impairment study found systemic exposure (AUC) roughly 1.9-fold higher in severe renal impairment, which is the basis for a mandated dose reduction rather than an injury rate.MildRelacorilantElectrolyte shifts, if they develop, track cumulative cortisol/MR activation over the treatment course rather than a single dose, and are typically detected on routine chemistry monitoring during cycles rather than as an acute event.No discrete drug-specific incidence of relacorilant acute kidney injury is published; in the registrational phase 3 ROSELLA trial (Olawaiye, Lancet 2025; n=381) the adverse-event profile with relacorilant plus nab-paclitaxel was similar to nab-paclitaxel alone after adjusting for exposure, and no new safety signals were reported. The renal-relevant concern is electrolyte, specifically hypokalemia, inferred from the pharmacology of GR antagonism rather than from a large observed AKI signal. The precedent is mifepristone, a non-selective GR/PR antagonist, where blocking cortisol's own receptor allowed cortisol to activate the mineralocorticoid receptor and produce clinically significant, spironolactone-responsive hypokalemia (Chu, J Clin Endocrinol Metab 2001). Relacorilant is a selective GR antagonist designed to reduce this and other off-target effects, so the hypokalemia risk is expected to be milder — a monitoring point, not a dominant toxicity.MildGedatolisibHyperglycemia is an early, exposure-linked effect — fasting glucose moves within the first infusions and tracks the weekly dosing cycle; electrolyte drift appears on routine monitoring across early cycles rather than as an acute event.No discrete drug-specific incidence of gedatolisib acute kidney injury is published; the renal-relevant signal is laboratory-level. In the VIKTORIA-1 triplet arm the FDA label's laboratory table reports increased creatinine in 14% (grade 3-4 0.8%) versus 8% (0.8%) on fulvestrant alone, decreased sodium in 21% (grade 3-4 1.6%), decreased potassium in 19% (1.6%) and decreased magnesium in 19% (0%) — all-grade drift, with severe events rare. The dominant metabolic effect is on-target hyperglycemia: increased fasting glucose in 46% of triplet-arm and 57% of doublet-arm patients on the label's laboratory table, while grade >=3 treatment-related hyperglycemia in the VIKTORIA-1 publication was 2.3% in both gedatolisib arms (Hurvitz, J Clin Oncol 2026) — markedly gentler than daily oral PI3K-alpha inhibition. In a phase II HER2-positive combination, any-grade hyperglycemia was 25.0% with grade 3 in 2.3% (Kim, ESMO Open 2026).Mild
Also associated
120Agents that cause electrolyte disturbance as a secondary pattern alongside a different signature lesion.
CisplatinAcute — creatinine peaks ~day 4–7; magnesium wasting can persist for months.AKI in ~20–35% per cycle (classic teaching: ~1 in 3). Hypomagnesemia in 40–100%.SevereIfosfamideAcute tubulopathy during therapy; chronic Fanconi/CKD can emerge months–years later.Subclinical tubular dysfunction is common while overt Fanconi is not, and the gap is the point. In 183 children investigated prospectively at least 5 years out — none of whom received any platinum, so the toxicity is attributable — the tubular threshold for phosphate was reduced in 24% and glycosuria detected in 37%, yet glycosuria exceeded 0.5 g/24 h in only 5%, bicarbonate and calcium were normal in every patient, and 89.5% had normal tubular function overall at a median 10 years. GFR was abnormal in 21.5%. Ifosfamide dose and time since therapy both predicted tubulopathy. Rates elsewhere span 0% to 84% depending on the definition and cohort used, so a single figure is only meaningful with its threshold attached.SevereStreptozocinWithin weeks of therapy; worsens with cumulative dose; abrupt AKI possible on re-challenge.Nephrotoxicity is the major dose-limiting toxicity; transient proteinuria, tubular dysfunction and azotemia are common and a sizable minority develop clinically significant renal impairment, though precise rates are not uniformly quantified. Reported rate: decrease in estimated glomerular filtration rate of at least 25% during treatment in 30% — 111 patients (27 prospective + 84 retrospective) with locally advanced or metastatic well-differentiated digestive… (Legoux 2021, PMID 33751987).SevereVenetoclaxAcute — typically within hours to days of each dose-escalation step during the ramp-up.Tumor lysis syndrome is the defining renal risk, concentrated during the weekly dose ramp-up. Early-development unmitigated dosing caused fatal TLS; with the mandated 5-week ramp-up and risk-stratified prophylaxis, grade 3/4 laboratory TLS fell to 3.1% (MURANO), with clinical TLS rarer still, and structured protocols can drive it near zero.SevereTegafur-uracil (UFT)Variable; TMA/HUS typically emerges after weeks to months of cumulative exposure.Direct renal injury from UFT is rare and largely class-level. Fluoropyrimidine-associated thrombotic microangiopathy / hemolytic-uremic syndrome is a rare, mostly case-report-level event, frequently in combination regimens (e.g., with mitomycin C). No reliable drug-specific incidence rate is established.SevereSonrotoclaxEarly and dose-timed. Tumor lysis clusters around the initial ramp-up doses and the first full target dose — the window of maximal, synchronous cytoreduction — typically developing within about 12–72 hours of an effective dose. Kidney injury therefore concentrates in the first days of treatment and at each dose escalation, with risk falling once the bulk of disease has been debulked and full dosing is tolerated. This front-loaded timing is the entire rationale for the stepwise ramp-up.No clean, drug-specific published incidence of sonrotoclax acute kidney injury exists as a discrete endpoint; the renal risk is inferred from the tumor-lysis physiology that defines potent BCL-2 inhibition. The precedent is venetoclax, where laboratory and clinical tumor lysis syndrome were frequent enough — including early fatal cases — that a mandatory ramp-up schedule, risk-stratified prophylaxis, and inpatient monitoring became standard of care (Tambaro & Wierda, Lancet Haematol 2020). Because sonrotoclax is more potent than venetoclax and induces apoptosis faster, its tumor-lysis potential is at least as high, which is precisely why its development and label built in a stepwise dose ramp-up from the outset. Reported drug-specific AKI rates should not be overstated until mature peer-reviewed trial safety data are published. Reported rate: tumor lysis syndrome in 7% — 125 patients with BTK-inhibitor-pretreated relapsed/refractory mantle cell lymphoma enrolled in the global phase I/II… (Eyre 2026, PMID 42385124).SeverePemetrexedDelayed / cumulative; risk rises after ~10 cycles.Clinically relevant eGFR decline (≥25%) in ~21%; ~8% discontinue for nephrotoxicity. Cumulative-dose dependent.ModerateImmune Checkpoint InhibitorsDelayed — median ~14 weeks after starting therapy.ICI-associated AKI ~2–5% (higher with combination therapy); ~93% of biopsies show interstitial nephritis.ModerateInterleukin-2 (high-dose)Acute — during the treatment cycle.Oliguria / prerenal AKI is very common during therapy at high dose — but reversible.ModerateNedaplatinDays after dosing; cumulative with repeated cycles.Lower renal cortical platinum accumulation and less frequent nephrotoxicity than equimolar cisplatin; dose-related proximal tubular injury still occurs, but high-grade AKI is uncommon and not robustly quantified in the renal literature. Myelosuppression (notably thrombocytopenia), not nephrotoxicity, is the dose-limiting toxicity. Reported rate: serum creatinine elevation in 9.8% — Patients with gastrointestinal cancer (esophageal, stomach, colon) in a 16-institution Japanese phase II study of… (Taguchi 1992, PMID 1558398).ModerateBendamustineTLS within hours to days of the first cycle; TMA delayed and rare.Direct nephrotoxicity is uncommon; the principal renal risk is acute kidney injury from tumor lysis syndrome in high-burden disease, classically during the first cycle. TLS with renal failure is documented from the first reported case onward; TMA is rare and case-level.ModerateCytarabineHours to days after initiating therapy in high-burden disease.Intrinsic tubular nephrotoxicity is uncommon; the major renal risk is AKI from tumor lysis syndrome during leukemia/lymphoma cytoreduction, reported at case and series level including fatal TLS. Direct cytarabine-nephrotoxicity primary literature is genuinely sparse.ModerateFludarabineTLS within days of starting therapy; systemic toxicity accrues with impaired clearance.Direct nephrotoxicity is uncommon; the chief renal risks are tumor-lysis-syndrome AKI during cytoreduction and increased systemic toxicity when the renally cleared drug accumulates in renal impairment. About 60% of the active metabolite 2-F-ara-A is renally eliminated, so renal function directly drives exposure. Reported rate: tumor lysis syndrome in 0.33% — 6,137 patients with intermediate- or high-risk advanced chronic lymphocytic leukemia treated with fludarabine 20-40… (Cheson 1998, PMID 9667245).ModerateAzacitidineDuring treatment cycles (days to weeks).Proximal tubular dysfunction (proximal/type 2 renal tubular acidosis, polyuria, and glucose/amino-acid/electrolyte wasting) was described with higher-dose azacitidine; with current low-dose subcutaneous/IV regimens overt AKI is uncommon and renal incidence is not well quantified (case-level).ModeratePlicamycin (mithramycin)With repeated / cumulative dosing (days to weeks).Cumulative, dose-related nephrotoxicity is a recognized dose-limiting toxicity; when used for hypercalcemia, its antiresorptive potency can overshoot to symptomatic hypocalcemia. Precise modern incidence is not well quantified because the drug is now essentially obsolete. The comparative hypercalcemia-tolerability review cited here pooled trials of at least 10 patients and reported serum creatinine elevation in 5% of plicamycin-treated patients, alongside hepatotoxicity in 26% and nausea/vomiting in 23%. The creatinine figures it gives for etidronate (8%), clodronate (5%) and pamidronate (2%) are bisphosphonate rates from the same review and are not plicamycin's.ModerateVandetanibWithin the first weeks of therapy.In the pivotal phase III ZETA trial, any-grade hypertension occurred in about 32% of vandetanib-treated patients versus 5% with placebo; proteinuria occurs as an antiangiogenic class effect.ModerateMosunetuzumabEarly — during cycle 1 step-up dosing, coincident with CRS (first days to ~2 weeks).No direct tubular nephrotoxic signal. AKI is a downstream/case-level consequence of cytokine release syndrome (CRS, ~44% any-grade, almost all grade 1-2 and concentrated in cycle 1) and tumor lysis syndrome; renal-specific incidence is not quantified. Reported rate: tumor lysis syndrome in 0.9% — 218 patients with relapsed/refractory non-Hodgkin lymphoma, including 90 with relapsed/refractory follicular lymphoma,… (Matasar 2024, PMID 38195322).ModerateEpcoritamabEarly — during cycle 1 step-up dosing with CRS.No direct tubular signal. AKI is case-level and downstream of CRS (~50% any-grade, predominantly grade 1-2 with subcutaneous step-up dosing) and tumor lysis; renal incidence is not separately quantified — emerging data. Reported rate: clinical tumor lysis syndrome in 5% — 42 patients with Richter transformation (Kater 2026, PMID 41380698).ModerateGlofitamabEarly — concentrated around cycle 1 step-up dosing and the first full dose.No direct tubular signal. AKI is case-level, downstream of CRS (~63% any-grade, grade >=3 in ~4% after obinutuzumab pretreatment and step-up dosing) and tumor lysis; renal incidence not separately quantified — emerging data.ModerateEnfortumab vedotinVariable; tubular/prerenal AKI tracks with intercurrent GI toxicity, and hyperglycemic-AKI events are often reported after the second or third dose.Renal injury is not a prominent or well-quantified trial signal, and EV is usable across the spectrum of renal function (including eGFR <30). When AKI occurs it spans prerenal (GI-toxicity dehydration), hyperglycemia/DKA-associated, and case-level tubular (ATN) patterns. In EV-201 cohort 2, three of 89 patients had treatment-related deaths within 30 days (one each from AKI, metabolic acidosis and multi-organ dysfunction), underscoring a real but uncommon acute renal-metabolic risk.ModerateTrastuzumab deruxtecanVariable; reported during ongoing therapy, sometimes resolving over months after discontinuation.Renal data are emerging and under-published. AKI/proteinuria are reported at case level; a reversible proximal-tubule Fanconi syndrome (glucosuria, phosphate/potassium wasting, non-anion-gap acidosis) has been described and attributed to the deruxtecan payload. Renal-specific incidence is not quantified.ModerateGemtuzumab ozogamicinEarly — tumor lysis with induction; VOD typically within weeks, notably around hematopoietic stem-cell transplant.Direct nephrotoxicity is not a prominent signal. AKI is chiefly secondary to tumor lysis syndrome and to hepatic sinusoidal obstruction syndrome/veno-occlusive disease (VOD), the latter a recognized, sometimes fatal complication that produces hepatorenal-type AKI. Renal-specific incidence is not quantified.ModerateInotuzumab ozogamicinEarly — tumor lysis during initial therapy; VOD typically peri-transplant.Direct nephrotoxicity is not a prominent signal. AKI is chiefly secondary to tumor lysis and to hepatic sinusoidal obstruction syndrome/veno-occlusive disease (VOD) — a notable, sometimes fatal complication, particularly around subsequent allogeneic stem-cell transplant. Renal-specific incidence is not quantified.ModerateIvosidenibDifferentiation syndrome typically days to weeks after starting therapy (median ~30 days); tumor lysis early during cytoreduction.Differentiation (IDH) syndrome is a recognized, potentially fatal complication — reported in roughly 10-19% of AML patients across IDH-inhibitor experience (e.g. ~10.4-11.7% with the IDH2 inhibitor enasidenib in pooled/phase 1-2 analyses) — and can drive AKI through capillary leak, fluid overload, hypotension, and inflammation; tumor lysis can also occur with cytoreduction.ModerateEnasidenibDifferentiation syndrome typically days to weeks after starting (median onset ~30 days; reported range days to ~4–5 months).IDH-inhibitor differentiation syndrome (the main route to AKI) occurs in roughly 10% of enasidenib-treated AML patients (10.4% any-grade in a pooled trial analysis; ~7% grade ≥3 in the first-in-human study). Tumor lysis is a secondary risk. Direct tubular nephrotoxicity is not well quantified.ModerateArsenic trioxideDifferentiation syndrome within the first weeks of induction; QT/electrolyte effects throughout treatment.Differentiation syndrome (the main route to AKI) occurs in a substantial minority of APL patients; grade 3–4 renal toxicity in ATO-based regimens is uncommon in randomized data. Direct nephrotoxicity is not well quantified, but QT prolongation and electrolyte disturbances are frequent and clinically important.ModerateRituximabAcute — typically within hours to a few days of the first infusion.Clinical tumor lysis with the first cycle is uncommon with modern prophylaxis (~1% clinical TLS in a real-world fractionated-rituximab aggressive-B-NHL series), but risk rises sharply with bulky disease, high LDH and Burkitt histology.ModerateObinutuzumabAcute — within hours to days of the first (split) dose.Carries a high tumor-lysis risk in CLL — among the highest of the anti-CD20 agents — particularly with the first (split) infusion in high-burden disease (the CLL11 trial enrolled patients with CrCl 30–69 mL/min and saw higher infusion reactions/TLS). Direct nephrotoxicity is case-level.ModerateRevumenibDuring early treatment as leukemic differentiation and lysis occur (first days–weeks).Differentiation syndrome and tumor lysis syndrome are on-target risks identified during development (differentiation syndrome carries a boxed warning). Resulting AKI is hemodynamic (capillary leak, fluid shifts) and/or crystal/metabolic (TLS); renal-specific incidence is not separately well quantified. QTc prolongation is an additional class effect.ModerateCapivasertibEarly in therapy, tracking diarrhea/hyperglycemia (first cycles).Diarrhea and hyperglycemia are the characteristic on-target toxicities (diarrhea very common; hyperglycemia frequent, occasionally severe). AKI, when it occurs, is largely a downstream pre-renal consequence of diarrhea-related volume loss and osmotic/metabolic disturbance; direct renal incidence is not well quantified. Rash is common but not nephrotoxic.ModerateLifileucelAcute — within hours to days of high-dose IL-2 administration during the conditioning/expansion phase.AKI is common in the overall regimen but is driven by the high-dose IL-2 component (and lymphodepletion), not the TILs themselves. In the pooled C-144-01 experience renal/AKI events fell within the expected high-dose IL-2 toxicity spectrum; a clean drug-specific AKI rate for the TIL product alone is not established. By analogy to other adoptive cell therapies, AKI in the broader CAR-T literature runs 5-33%.ModerateZiftomenibDifferentiation syndrome typically within the first weeks of therapy as blasts differentiate; QTc prolongation is also seen.Renal-specific data are not established. The class-defining serious toxicity is differentiation syndrome — reported in 12/83 (15%) of patients in the KOMET-001 phase 1 trial (with higher severity in KMT2A-rearranged patients, halting that cohort's enrollment) — which can cause capillary leak, fluid overload and AKI. Tumor-lysis risk accompanies rapid blast clearance. No drug-specific renal incidence is published.ModerateLutetium-177 PSMA-617 (vipivotide)Renal changes are delayed/gradual; xerostomia can appear early during treatment.Clinically significant nephrotoxicity is uncommon in trial populations and is not well quantified; in VISION renal adverse events were infrequent. Dosimetry consistently shows the kidney is the highest-dose internal organ, but the dose-limiting clinical toxicities are usually xerostomia (salivary/lacrimal uptake) and myelosuppression rather than renal failure. Reported rate: grade >=3 ctcae nephrotoxicity worsening to grade 3 in 9.4% — 32 consecutive heavily pre-treated mCRPC patients selected by 68Ga-PSMA-11 PET/CT and given 177Lu-PSMA-617 monotherapy… (Maffey-Steffan 2020, PMID 31776632).ModerateTrabectedinRhabdomyolysis often around the 4th cycle; hepatotoxicity/myelosuppression nadir ~days 5-15.The drug is not directly nephrotoxic and shows no cumulative renal toxicity; clinically important AKI is rare and driven by rhabdomyolysis. The per-cycle rhabdomyolysis rate is not quantified (case-level). The dominant organ toxicity is hepatic — grade 3-4 transaminitis fell from ~34% to ~2% with dexamethasone premedication. Reported rate: rhabdomyolysis in 0.7% — 10,841 trabectedin-treated patients pooled from the Yondelis pharmacovigilance and clinical-trials databases, April… (Grosso 2012, PMID 22484722).ModerateSelinexorEarly — within the first cycle/few weeks; front-loaded.Hyponatremia is common and dose-limiting. All-grade hyponatremia affected 39% of the selinexor-dexamethasone patients tabulated in the FDA label's STORM adverse-reaction table, reaching grade 3-4 in 22% — making it the leading grade >=3 non-hematologic toxicity, and one of the six grade 3-4 laboratory abnormalities the label lists at >=10%. Both rates come from the trial's safety tables rather than its abstract, which does not mention hyponatremia; a separate phase 1 dose-escalation cohort reported grade >=3 hyponatremia at a concordant 23%. Combination regimens run lower: in BOSTON grade 3-4 hyponatremia was ~8-9%, and in SADAL ~8%.ModeratePentostatinDuring or after dosing cycles; generally reversible with dose reduction or discontinuation.At modern low doses clinically significant nephrotoxicity is uncommon and a precise contemporary incidence is not quantified; serious dose-related AKI was historically tied to higher-dose regimens. Tumor lysis can add a secondary AKI mechanism in bulky disease.ModerateIdecabtagene vicleucelWithin the first 1-2 weeks (the CRS window).Published CAR-T AKI incidence runs roughly 5-30% across cohorts and is mostly mild (KDIGO stage 1); in one cohort any-grade AKI reached ~30% by day 100 with rapid recovery. Most AKI parallels cytokine-release syndrome (CRS) and reverses within ~30 days.ModerateCiltacabtagene autoleucelAKI in the first 1-2 weeks; the movement disorder is delayed (weeks).CRS-associated AKI mirrors the BCMA CAR-T class (roughly 5-30% across cohorts, mostly mild) and generally reverses with supportive care. A distinct, non-renal signature toxicity is a delayed movement-and-neurocognitive (parkinsonism-like) syndrome, named MNTs by NCCN: about 3% of ciltacabtagene recipients across CARTITUDE-1 and CARTITUDE-4 showed parkinsonism consistent with it, grade 3 or worse in 2%.ModerateAlpelisibHyperglycemia typically within the first 1-2 weeks; prerenal AKI follows volume depletion or a hyperglycemic crisis.Hyperglycemia is essentially on-target and very common: any-grade hyperglycemia ~64% and grade 3/4 hyperglycemia ~36.6% in SOLAR-1, with diabetic ketoacidosis reported rarely in pharmacovigilance. The renal injury is secondary (osmotic diuresis/volume depletion or DKA) rather than a direct lesion; a discrete AKI incidence is not well quantified.ModerateGilteritinibDifferentiation syndrome from a few days up to ~3 months (often within the first month); TLS early; PRES variable.Differentiation syndrome (boxed warning) occurs in roughly 3% of treated patients and can cause capillary leak, fluid overload and renal dysfunction; tumor lysis and PRES are labeled risks. Discrete AKI incidence is not separately quantified and is largely a consequence of these syndromes.ModerateNeratinibDiarrhea characteristically within the first days-to-weeks; prerenal AKI follows uncontrolled fluid loss.Diarrhea is near-universal without prophylaxis: in ExteNET, grade 3 diarrhea occurred in ~40% without antidiarrheal prophylaxis, falling substantially with loperamide and dose-escalation strategies (CONTROL). The resulting volume-depletion prerenal AKI is not separately quantified.ModerateOlutasidenibDifferentiation syndrome within days to a few months (often early); tumor lysis early in treatment.Differentiation syndrome (boxed warning) occurred in ~14% of patients (grade >=3 ~9%, with rare fatality) in the pivotal cohort; tumor lysis is a labeled risk. Discrete AKI incidence is not separately quantified and is largely consequent on these syndromes.ModerateLoncastuximab tesirineEdema/effusions accumulate over cycles; prerenal changes track the fluid shifts.Edema and effusions (pleural, pericardial, peritoneal) are characteristic PBD-payload toxicities and were common in LOTIS-2; the resulting fluid shifts and AKI are not separately quantified. Tumor lysis is an additional consideration in responding lymphoma.ModerateMelphalan flufenamide (melflufen)Cytopenias within the first cycles; any renal change is typically subacute and multifactorial.Direct nephrotoxicity is not a prominent trial signal; the renal relevance is pharmacokinetic and disease-context. A dedicated phase II study (BRIDGE) in myeloma patients with moderate or severe renal impairment characterized melphalan exposure across renal function and supported a reduced 30 mg dose for moderate impairment, with no new safety signals but substantial treatment-emergent toxicity (including deaths in a heavily pretreated population). As a melphalan-delivery system, its renal liabilities mirror the alkylator class (myelosuppression, and the alkylator-associated risk of tubular injury at high exposure).ModerateCatumaxomabCytokine-release symptoms within hours of each intraperitoneal infusion; any prerenal AKI follows the inflammatory/volume insult.No characteristic intrinsic nephrotoxicity. The dominant treatment-related toxicity is cytokine-release-related (pyrexia, nausea, vomiting, chills, fatigue) plus intraperitoneal-administration effects (abdominal pain); transient transaminase rises and lymphopenia are common but usually clinically minor. Cytokine release with fever, GI losses, and large-volume ascites/paracentesis creates a setting for prerenal/hemodynamic AKI rather than a direct renal lesion. Drug-specific renal incidence is not quantified.ModerateFotemustineDelayed — weeks to months, and cumulative with repeated cycles; chronic interstitial injury may appear after prolonged exposure.Renal toxicity is generally reported as mild within fotemustine regimens, but, consistent with the nitrosourea class, delayed tubulointerstitial injury/ATN can occur; in one combination study renal toxicity was mild yet possibly contributed to two deaths. Drug-specific incidence is not well quantified and is often confounded by co-administered cisplatin.ModerateNimustine (ACNU)Delayed and cumulative — typically over months of repeated cycles, mirroring the nitrosourea class.Drug-specific human renal-toxicity data for nimustine are thin; renal risk is asserted largely at the class level. Like other nitrosoureas, cumulative dosing is associated with delayed tubulointerstitial injury and CKD, but a reliable nimustine-specific incidence is not established. Dose-limiting toxicity is hematologic (delayed myelosuppression).ModerateDoxifluridineVariable; class-level TMA typically after prolonged cumulative exposure.No drug-specific nephrotoxicity incidence is established. Renal risk is inferred at the fluoropyrimidine-class level (rare TMA/HUS); direct doxifluridine renal injury reports are sparse.ModerateCarmofur (HCFU)Variable; class-level TMA after cumulative exposure.No established drug-specific renal incidence. Renal risk is class-level (rare fluoropyrimidine TMA/HUS). Carmofur's characteristic serious toxicity is leukoencephalopathy, not nephrotoxicity.ModerateToripalimabDelayed; PD-1-related AIN characteristically appears 3-10 months after initiation (later than CTLA-4 agents), though it can occur at any point during or after treatment.Drug-specific renal data are limited; reasoning from the PD-1 class is required. Across PD-1/PD-L1 agents, clinically significant immune-related AKI (predominantly AIN) occurs in roughly 1-5% of patients, with attributable PD-L1-related AKI under 1% in one large cohort but pooled estimates as high as ~3-5% with platinum co-therapy. In the JUPITER-02 registrational trial, immune-related adverse events were more frequent with toripalimab (54.1% vs 21.7%) and grade ≥3 irAEs occurred in 9.6%, but kidney-specific irAEs were not individually quantified.ModerateRetifanlimabUsually delayed — weeks to several months after initiation (median ~3 months for ICI-AIN), but can occur at any point including after discontinuation.Renal immune-related adverse events are uncommon with PD-1 monotherapy. Across the checkpoint-inhibitor class, checkpoint-attributed AKI occurs in roughly 2-5% of treated patients (a 2023 meta-analysis of 24,048 patients pooled it at 5.7%) and biopsy-confirmed immune-related AIN in approximately 1-3%, with higher rates when combined with CTLA-4 blockade or nephritogenic co-medications (PPIs, NSAIDs). Any-cause AKI in real-world ICI cohorts runs far higher (~16-17%) but is mostly prerenal or non-immune rather than true ICI-nephritis. Retifanlimab's registrational program did not flag nephritis as a prominent signal; in the phase III POD1UM-303 anal-cancer trial the dominant grade ≥3 events were chemotherapy-driven cytopenias (neutropenia 35%, anemia 20%), not renal events.ModerateCosibelimabDelayed and variable — typically weeks to months after initiation. Pooled ICI data place median time to AKI at roughly 3-4 months (~108 days), though onset ranges from a few weeks to after treatment discontinuation.Drug-specific renal data are limited. In the pivotal phase 1 metastatic CSCC cohort (n=78), immune-related adverse events occurred in 23.1% of patients (grade 3 in 2.6%; no grade 4/5), with no nephritis-specific signal reported and a favorable overall safety profile. By class, immune-mediated nephritis/AKI with checkpoint inhibitors is uncommon: a 2023 systematic review and meta-analysis of 27 studies (24,048 patients) found a pooled all-cause AKI incidence of ~5.7%, with clinically significant immune-mediated nephritis substantially lower (roughly 1-3%), and anti-PD-L1 agents tending toward the lower end of that range versus CTLA-4 or combination regimens.ModeratePenpulimabVariable and often delayed: ICI-associated AIN commonly emerges weeks to several months after initiation (median around 3-4 months), and can appear after multiple cycles or even after discontinuation. Chemotherapy-related ATN in the combination regimen tends to occur earlier, peri-infusion.Penpulimab-specific renal data are limited. In the pivotal first-line phase 3 trial (penpulimab plus chemotherapy), grade >=3 immune-related adverse events occurred in only 4.1% of patients, and renal events were not separately prominent; the most common toxicities were hematologic. By class, immune checkpoint inhibitor-associated AKI (predominantly acute tubulointerstitial nephritis) occurs in roughly 2-5% of patients on PD-1 monotherapy, with higher rates when combined with nephrotoxic chemotherapy. Platinum (cisplatin) and gemcitabine in the registrational backbone independently contribute ATN and (rarely) thrombotic microangiopathy risk, so observed kidney injury in this regimen is often multifactorial.ModerateSugemalimabDelayed — typically weeks to months after initiation; in the multicenter ICI-AKI cohort median time from checkpoint-inhibitor start to AKI was about 14 weeks (IQR 6-37), later than most other drug-induced AIN.No sugemalimab-specific renal-injury incidence has been published; the GEMSTONE registrational trials reported no nephritis among the most common grade 3-4 treatment-related adverse events (which were dominated by myelosuppression and immune-mediated pneumonitis). By extrapolation from the PD-1/PD-L1 checkpoint-inhibitor class, immune-related AKI occurs in roughly 2-5% of treated patients (higher with combination checkpoint blockade), with clinically significant/biopsy-confirmed acute interstitial nephritis being the dominant lesion. A separate real-world cohort of 1,037 ICI-treated patients supplies the drug-attributable denominator this class otherwise lacks: 18.2% developed AKI of any cause, but only 3.6% (37 patients) had AKI attributed to the checkpoint inhibitor itself — a class figure, not a sugemalimab-specific one.ModerateTelisotuzumab vedotin (Teliso-V)Onset is not well characterized for this agent; with cytotoxic ADC payloads, tubular injury would typically evolve over days to a few weeks of cumulative exposure.Drug-specific renal toxicity data for telisotuzumab vedotin are sparse. In the pivotal LUMINOSITY trial the dominant toxicities were peripheral neuropathy, peripheral edema, hypoalbuminemia, fatigue, and nausea; clinically significant nephrotoxicity was not highlighted as a frequent or signature event. Any renal risk is therefore largely class-extrapolated from MMAE-bearing ADCs rather than measured for this agent. A precise renal incidence rate cannot be stated from existing literature.ModerateAfamitresgene autoleucel (Afami-cel)AKI typically emerges during the acute CRS window in the first days to roughly two weeks after infusion, coinciding with peak cytokine activity.Drug-specific renal injury rates for afami-cel are not well defined; the SPEARHEAD-1 trial reported cytokine release syndrome (CRS) in most treated patients, predominantly low grade, as the dominant systemic toxicity. Acute kidney injury is best understood as a downstream, CRS-associated hemodynamic event rather than a measured signature toxicity. By analogy to CAR-T cellular therapy, AKI incidence in the broader engineered-T-cell setting spans roughly 5 to 33 percent depending on population and CRS severity. A precise afami-cel-specific incidence cannot be stated from current literature.ModerateObecabtagene autoleucel (Obe-cel)Onset clusters with peak CRS in the first one to two weeks after infusion; tumor lysis tends to occur early as leukemic burden is cleared.Obe-cel-specific renal injury rates are not separately well characterized; in the FELIX trial, CRS and immune effector cell-associated neurotoxicity were mostly low grade, with notably low high-grade rates. Across CD19 CAR-T programs, AKI is reported in roughly 5 to 33 percent of patients, driven mainly by CRS-related hemodynamics and tumor lysis, and is usually reversible. In one CAR-T AKI cohort, 18 percent developed AKI, most often from volume depletion or CRS, with renal recovery in the large majority. The lower high-grade CRS rate of obe-cel would be expected to translate into a comparatively lower burden of severe CRS-associated AKI, though direct data are limited.ModeratePembrolizumabDelayed and highly variable, typically weeks to months after initiation; multicenter cohorts reported median onsets around 14-16 weeks. Can occur after a single dose or after many months, and may recur on rechallenge.In real-world cohorts of patients receiving immune checkpoint inhibitors, any AKI is common (roughly 16-18%), but AKI attributable to the checkpoint inhibitor itself (ICPi-AKI) is less frequent. A single-center cohort reported AKI in 16.5% of ICI-treated patients with checkpoint-attributable nephrotoxicity in a minority, while a larger real-world study found ICPi-AKI in about 3.6%. Acute interstitial nephritis is the dominant biopsy lesion (>80% in the largest multicenter series). These figures are pooled across PD-1/PD-L1/CTLA-4 agents rather than pembrolizumab-specific.ModerateVemurafenibEarly — most cases arise within the first weeks to three months of therapy (all AKI events in the Teuma cohort occurred in the first trimester of treatment); later onset is uncommon.Clinically meaningful AKI is a recognized but variably quantified effect, and vemurafenib is the strongest renal offender of the BRAF/MEK class. Small serum-creatinine rises are common and usually low-grade; overt AKI produced the first case series of 8 patients with significant-to-severe renal insufficiency (Launay-Vacher, Cancer 2014) and 132 vemurafenib AKI reports to FDA FAERS over 3 years, far exceeding dabrafenib's 13 (Jhaveri, JAMA Oncol 2015). The monotherapy denominator comes from a retrospective single-center cohort of 74 patients with BRAF-V600-mutant metastatic melanoma, with creatinine measured before treatment, monthly on treatment and 3 months after stopping: 44 of 74 (59.5%) met the KDIGO threshold of a 1.5-fold creatinine rise, and 40 of those 44 (91%) were stage 1. Read that figure with its definition attached — it is creatinine-based, and BRAF/MEK inhibitors also blunt tubular creatinine secretion, so a share of any such cohort is pseudo-AKI rather than tubular injury; the authors biopsied two stage-1 patients to demonstrate real tissue damage. Men were over-represented among the AKI-positive patients (75% versus 40%). Adding a MEK inhibitor lowers it substantially: in the companion cobimetinib cohort 9 of 38 (24%) developed AKI, all within three months and mostly stage 1-2, about a 60% reduction versus monotherapy.ModerateEverolimusSubacute — proteinuria typically emerges over the first weeks to months of therapy; thrombotic microangiopathy usually appears within weeks to months, often in the setting of concurrent calcineurin-inhibitor or anti-VEGF exposure.Proteinuria is a class effect of mTOR inhibitors, and with systematic monitoring it is close to universal. A retrospective review of 129 first-line metastatic renal-cell patients found any-grade proteinuria in 81% overall and in 96% of the everolimus arm (44 patients) — the highest of the three regimens compared, against 80% on pazopanib and 64% on bevacizumab. Almost all of it was minor: the study's grade 3-4 proteinuria (24%, 6 patients) occurred entirely in the bevacizumab group, none in the everolimus arm, and 35 of the everolimus patients (80%) simply continued at the same dose under monitoring. So the striking number is detection, not injury — heavy proteinuria and overt podocytopathy remain uncommon, and most nephrotic-range and biopsy-proven FSGS data are still extrapolated from the sirolimus/transplant literature. A phase II trial combining everolimus with bevacizumab reported grade 3-4 proteinuria of 25%, which reflects the added anti-VEGF effect and overstates everolimus alone. Thrombotic microangiopathy is rare and drawn mainly from case reports, typically with concomitant calcineurin-inhibitor or anti-VEGF exposure.ModerateSorafenibHypertension typically emerges within the first few weeks of treatment; proteinuria develops over weeks to months of continued exposure. Nephrotic syndrome and thrombotic microangiopathy are variable, generally appearing after weeks to months but occasionally sooner.Hypertension is the dominant renal-vascular signal: a systematic review/meta-analysis of 9 trials (4,599 patients) reported an all-grade incidence of 23.4% (95% CI 16.0-32.9%) and high-grade (grade 3-4) incidence of 5.7% (Wu 2008), and a larger meta-analysis of 93 trials (20,494 patients) gave concordant figures of 21.3% all-grade and 5.9% high-grade, with higher rates in renal-cell and thyroid cancer and rising incidence with longer treatment duration (Yang 2017). Proteinuria is a VEGF-pathway class effect: across VEGF-signaling inhibitors mild/asymptomatic proteinuria is reported in roughly 21-63% and heavy (nephrotic-range) proteinuria in up to about 6.5% of renal-cell carcinoma patients (Izzedine 2009); drug-specific quantitative proteinuria data for sorafenib alone are more limited. Nephrotic-range proteinuria and renal-limited thrombotic microangiopathy are documented but uncommon.ModeratePacritinibDiarrhea is an early effect, typically emerging within the first days-to-weeks of therapy and most pronounced over roughly the first 8 weeks; it tends to be self-limited and to improve with continued treatment, antidiarrheals, and dose management. Any prerenal azotemia and electrolyte disturbance tracks the diarrhea temporally and is therefore early and episodic rather than cumulative or delayed.Pacritinib has no established intrinsic nephrotoxicity; its renal risk is a downstream consequence of its dominant gastrointestinal toxicity. Diarrhea is the signature adverse effect — in the phase 2 study grade 1/2 diarrhea occurred in ~69% of patients and nausea in ~49% (Komrokji 2015), and in the PERSIST-1 phase 3 trial grade 3-4 diarrhea occurred in ~5%. In real-world FAERS pharmacovigilance, gastrointestinal disorders were the top disproportionality system-organ-class and diarrhea the most-reported preferred term (Zhang 2025). High-volume diarrhea (often with nausea/vomiting) can precipitate volume depletion, hypokalemia/hypomagnesemia, and prerenal azotemia, but a specific incidence of pacritinib-attributable acute kidney injury has not been separately quantified — so no headline AKI rate is quoted here.ModerateOdronextamabEarly and dose-timed. Both CRS and TLS cluster around cycle 1 — the step-up doses and the first full target dose — which is precisely why a graded step-up schedule and admission/monitoring windows are built into administration. CRS usually begins within hours to 1-2 days of a dose; TLS classically develops within about 12-72 hours of initiating effective cytoreduction. Kidney injury therefore concentrates in the first days to first couple of weeks of treatment, with risk falling once the initial tumor burden has been debulked and full dosing is tolerated.There is no clean, drug-specific published incidence of odronextamab acute kidney injury as a discrete endpoint; the renal risk is inferred from its cytokine-release and tumor-lysis complications, which the ELM trials do quantify. In the phase 1 ELM-1 trial (Bannerji, Lancet Haematol 2022; n=145 heavily pretreated relapsed/refractory B-NHL), grade >=3 hypophosphatemia occurred in 27/145 (19%), cytokine release syndrome was the single most common serious adverse event (41/145, 28%), and one of four treatment-related deaths was due to tumor-lysis syndrome. With the optimized 0.7/4/20 mg step-up in the phase 2 ELM-2 cohorts, any-grade CRS was 53.3% (grade >=3 1.7%) in DLBCL (Kim WS, Nat Cancer 2025) and 56% (grade >=3 1.7%) in follicular lymphoma (Kim TM, Ann Oncol 2024) — CRS remained the dominant treatment-emergent adverse event even after mitigation. Kidney injury in this setting rides on these events (CRS hemodynamics, TLS crystal nephropathy, sepsis) rather than on any intrinsic tubular toxicity, so exact AKI rates are not well established and should not be overstated. Reported rate: grade >=3 hypophosphatemia in 19% — 145 heavily pretreated patients with CD20-positive relapsed or refractory B-cell non-Hodgkin lymphoma receiving… (Bannerji 2022, PMID 35366963).ModerateLisocabtagene maraleucelEarly — within the first days to about two weeks after the single infusion, tracking the CRS window. In a 155-patient cohort the median time to peak creatinine was 9.5 days (range 3-30); pediatric CD19 CAR-T AKI all occurred within 14 days; TLS-associated injury clusters around days 3-9.No liso-cel-specific AKI rate is established — the renal literature pools across CD19 and BCMA CAR-T products. In a meta-analysis of 15 studies (694 patients), 22% developed AKI, most KDIGO stage 1 and reversible (Yang, Clin Immunol 2024). Single-center CAR-T cohorts report roughly 18-34% (Sharp, Br J Haematol 2025 — 18%; Gupta, Am J Kidney Dis 2020 — 19%; Ahmed, Clin Lymphoma Myeloma Leuk 2022 — 29%; Vincendeau/Zafrani ICU cohort, Clin Kidney J 2024 — 34%), with focused reviews quoting ~30% (Khan, Clin Hematol Int 2023). Because liso-cel carries the lowest grade ≥3 CRS of the CD19 CAR-Ts (2% in TRANSCEND NHL 001) and CRS severity is the dominant AKI driver, its CRS-related renal burden is expected to track at the lower end — but this is inference, not a measured liso-cel figure.ModerateGallium nitrateDuring or within a few days of the 5-day continuous infusion — usually within the first week of a cycle. Creatinine generally trends back toward baseline once the drug is stopped and hydration is maintained.Nephrotoxicity is the dose-limiting toxicity. At the approved antihypercalcemic dose (200 mg/m2/day by continuous IV infusion x 5 days) a rise in serum creatinine is reported in roughly 10% of patients; at higher antineoplastic doses it is far more frequent — e.g., dose-limiting azotemia in 4 of the first 10 patients (40%) at 700 mg/m2 in the SWOG advanced-bladder-cancer trial, which forced a longer inter-cycle interval. Precise incidence is uncertain because the supporting trials are small and heterogeneous, so the headline figure should be read with caution.ModeratePivekimab sunirineEarly and treatment-cycle-timed. Tumor lysis clusters in the first days after an effective dose, particularly the first cycle when disease burden is highest, developing within roughly 12–72 hours of cytoreduction. Capillary-leak physiology, by analogy to other CD123 agents, tends to appear during the early treatment cycles and around infusions. Kidney injury therefore concentrates in the first cycle or two, with risk falling as disease is debulked and the highest-risk early doses are passed.There is no published pivekimab-specific incidence of acute kidney injury as a discrete endpoint, and the drug's own renal signal is thin; the risk is best understood as indirect and inherited from its target and disease setting. In the first-in-human phase 1/2 study in relapsed/refractory acute myeloid leukemia (Daver, Lancet Oncol 2024; n=91), the dose-limiting toxicities were reversible hepatic veno-occlusive disease and neutropenia, and the most common grade ≥3 events at the recommended phase 2 dose were febrile neutropenia, infusion-related reactions, and anemia — not a discrete renal lesion. The renal-risk framing therefore rests on two things: (1) tumor lysis syndrome, an on-target hazard whenever a large CD123-positive leukemic or BPDCN mass is lysed rapidly, and (2) capillary-leak syndrome, the class concern of CD123-directed therapy documented most clearly with the other approved BPDCN agent, tagraxofusp (capillary-leak syndrome in ~19–21%, with hypoalbuminemia and edema and occasional deaths; Pemmaraju, NEJM 2019 and JCO 2022). Pivekimab-specific capillary-leak/AKI rates are not established and should not be overstated.ModerateCarboplatinAcute when it occurs (high-dose regimens).Clinically significant nephrotoxicity uncommon at standard doses; emerges mainly at high/myeloablative doses.MildBRAF / MEK InhibitorsAcute–subacute during therapy.Pharmacovigilance shows vemurafenib > dabrafenib. Mild creatinine elevation common, serious AKI uncommon. Reported rate: acute kidney injury in 21% — 199 patients who received dabrafenib/trametinib in a single large US healthcare system between 2010 and 2019… (Seethapathy 2022, PMID 33355659).MildMelphalanDays after high-dose administration.High-dose intravenous melphalan can cause hyponatremia/SIADH; in a small high-dose series most patients showed declining sodium, but this is reported at case/series level rather than as a large quantified rate. Melphalan PK is not adversely affected by renal failure, so transplant in renal impairment is feasible.MildTemozolomideDuring cycles of therapy; variable.Generally renally well tolerated; renal clearance of the parent drug is a minor elimination pathway and dedicated PubMed searches for temozolomide nephrotoxicity/SIADH return essentially no indexed series. Hyponatremia/SIADH is an occasional, case/toxicity-table-level event, and rare acute interstitial nephritis has been reported in combination contexts.MildDecitabineEarly after a treatment cycle (days) for tumor lysis; TMA over weeks.Tumor lysis syndrome with AKI is a recognized but uncommon complication when bulky/proliferative disease responds; renal incidence specific to decitabine is not well quantified (case-level). Rare biopsy-proven renal thrombotic microangiopathy has been reported.MildHydroxyureaVery early (within 12-24 hours of high-dose treatment).Acute tumor lysis syndrome from hydroxyurea is rare and reported at case level, almost exclusively with high-dose cytoreduction of leukemias carrying a high blast burden. Standard-dose hydroxyurea is not characteristically nephrotoxic.MildNelarabineEarly after treatment initiation (days).Tumor lysis syndrome with attendant AKI is a labeled risk when bulky T-ALL responds rapidly; drug-specific renal incidence is not well quantified (case-level). The dose-limiting and most feared toxicity is neurologic, not renal.MildOsimertinibReported within roughly the first weeks to a few months of therapy (around two months in several published cases).Syndrome of inappropriate antidiuretic hormone (SIADH)-type hyponatremia is described at the case level; occasional acute kidney injury and rare proteinuria are reported. True structural kidney injury is not quantified as a discrete endpoint in randomized data, where overall renal adverse events are uncommon. The common osimertinib renal finding is instead a pseudo-decrease in creatinine-based eGFR from inhibited tubular creatinine secretion, quantified for osimertinib specifically by Ilyas et al. (Kidney Med 2026) and, at the cohort level, in the AMBORA real-world analysis: among 238 patients on 38 oral antitumor agents likely to cause pseudo-worsening, mean eGFR fell 6.8 mL/min within 30 days and by >=20 mL/min in 17.2% — a whole-group figure, not an osimertinib-specific rate.MildAfatinibDays to weeks after starting therapy, tracking with the onset and severity of diarrhea (often within the first cycles).Diarrhea is very common with afatinib (the dominant class toxicity, all-grade in the large majority and grade >=3 in roughly 10-15% in LUX-Lung trials), and the consequent dehydration can precipitate prerenal AKI. Pharmacovigilance data identify afatinib as carrying the strongest renal-failure/AKI signal among EGFR agents, frequently co-reported with diarrhea; trial-based renal incidence is not separately quantified.MildBrentuximab vedotinEarly — tumor lysis in the first cycle(s) of bulky disease.Direct nephrotoxicity is minimal. Tumor lysis syndrome occurs at low rates (<=5% in anaplastic large-cell lymphoma experience) and is the principal pathway to AKI/electrolyte disturbance; renal-specific incidence is not quantified.MildPolatuzumab vedotinEarly — tumor lysis during initial cycles of bulky disease.Renal data are limited; direct nephrotoxicity is not a prominent trial signal. AKI is case-level and chiefly tumor-lysis- or volume-mediated. Renal-specific incidence is not quantified.MildPomalidomideTumor lysis typically within days of starting therapy in high-burden disease.Pomalidomide pharmacokinetics are not substantially altered by renal impairment - it is extensively metabolized hepatically, with <5% renal excretion of unchanged drug - and pooled trial data show a similar safety profile and dosing through moderate renal impairment (CrCl 30 to <60). Dialysis patients are the exception - the label reports about 38% higher AUC and 64% more serious adverse events there, with a reduced starting dose given after the session. The principal renal hazard is tumor lysis syndrome (TLS), which is uncommon and case-level in myeloma.MildThalidomideTumor lysis within days of initiation in high-burden disease; bradycardia over weeks of dosing.Thalidomide is not a direct nephrotoxin; the principal renal hazard is tumor lysis syndrome, which is uncommon in myeloma and reported at the case level. Sinus bradycardia is a recognized dose-related non-renal effect that, with the drug’s sedative/hypotensive properties, can compound prerenal physiology. Venous thromboembolism is the other dominant class toxicity.MildCrizotinibCreatinine rise often within weeks and reverses on discontinuation; cysts develop and grow over months.Crizotinib commonly causes a reversible rise in serum creatinine and is distinctively associated with renal cysts: in the Halpenny series, new or enlarging cysts in 16% (9 of 57 serially imaged patients) and frankly complex cysts in 4% (2 of 57) — the 16% headline is the any-cyst rate, not a complex-cyst or AKI rate. Peripheral edema and electrolyte disturbances (including hypophosphatemia and hypokalemia) are reported. In real-world ALK-inhibitor cohorts, creatinine-based AKI/CKD events are frequent but mostly mild and reversible; frank kidney failure is uncommon.MildSelumetinibVariable; adverse events can appear after prolonged dosing.Long-term pediatric trial data (SPRINT, up to ~5 years) show a manageable safety profile with no new safety signals; significant nephrotoxicity is not prominent, with creatinine changes generally modest. CK elevation is a recognized MEK-class laboratory effect.MildZanubrutinibTumor lysis early (first cycle); otherwise renal function typically stable.Direct nephrotoxicity is not a prominent signal. Cardiovascular toxicity (atrial fibrillation, hypertension) is lower than ibrutinib in pooled and head-to-head (ASPEN, ALPINE) analyses. Tumor lysis can occur with rapid cytoreduction of bulky CLL/lymphoma; renal events are case-level and not well quantified.MildDaratumumabTumor lysis (if any) early; renal benefit accrues over treatment as paraprotein/free light chains fall.Direct nephrotoxicity is uncommon; tumor lysis can occur with high tumor burden. Crucially, daratumumab-based regimens IMPROVE outcomes (PFS, and OS in relapsed disease) in myeloma patients with renal insufficiency, including dialysis-dependent patients, and can drive renal recovery.MildIsatuximabTumor lysis (if any) early; renal benefit over the treatment course.Direct nephrotoxicity is uncommon; tumor lysis can occur with high tumor burden. In the ICARIA-MM and IKEMA renal-impairment subgroups, isatuximab regimens remained effective and produced renal responses; real-world data show inferior PFS with eGFR <60 but persistent benefit.MildPalbociclibOften within the first 1-2 cycles (median onset roughly 30-35 days); creatinine plateaus and reverses after dose hold or discontinuation.A reversible rise in serum creatinine is common, but true structural kidney injury is uncommon. CDK4/6 inhibitors block the proximal-tubule transporters that secrete creatinine, producing a 'pseudo-AKI' picture. In a single-center palbociclib cohort 16% (8 of 50) met creatinine-based AKI criteria (Ly, PMID 39648753); the 17.5% often quoted is the whole mixed CDK4/6-inhibitor cohort of 234 patients, not the palbociclib arm. Where cystatin C was available, 73% of those events proved to be pseudo-AKI rather than a true GFR decline.MildRibociclibFirst cycles (median onset roughly 6 weeks for the creatinine signal); reversible on hold or discontinuation. QTc effects are dose- and concentration-dependent and seen early.Like other CDK4/6 inhibitors, ribociclib produces a frequent, reversible creatinine rise via inhibition of tubular creatinine secretion (pseudo-AKI ~14% in a class-effect analysis); clinically meaningful structural AKI is uncommon. A retrospective cohort of palbociclib/ribociclib patients found a >=20% creatinine-clearance decline in about 23%.MildEtoposideTLS typically within hours to a few days of starting cytotoxic therapy in sensitive tumors; exposure-related myelosuppression accrues over cycles.Etoposide is renally cleared (~30-40% as unchanged drug, so dose-adjust in renal impairment) and is a frequent component of regimens for bulky, rapidly proliferating tumors that can trigger tumor lysis syndrome (TLS). Direct etoposide nephrotoxicity is not a recognized signal; TLS-related AKI risk depends on tumor burden and tumor type rather than a per-drug rate.MildVincristineDays after dosing, often within the first 1-2 cycles; resolves after the drug is withheld.Vincristine-associated SIADH with hyponatremia is a recognized but uncommon, largely case-level adverse effect; a global pharmacovigilance analysis estimated a reporting rate of about 1.3 per 100,000 treated patients, with a possible over-representation in Asian patients. FAERS disproportionality analysis also flags inappropriate ADH secretion as a vinca-class signal.MildVinblastineDays after administration, generally within the first cycles.Vinblastine can cause SIADH with hyponatremia; this is a recognized class effect reported at case level rather than as a quantified rate. Rare Raynaud phenomenon and other vascular events (especially in germ-cell regimens) are also described.MildVinorelbineDays after dosing, sometimes after several cycles (one report after three cycles).SIADH with hyponatremia is reported with vinorelbine at case level; FAERS pharmacovigilance analysis of vinca alkaloids flags inappropriate ADH secretion as a shared signal. Quantitative incidence is not established.MildIbandronateAcute when it occurs (days), related to dose and infusion rate; antiresorptive electrolyte effects within the first days.Lower renal risk than zoledronate or pamidronate. In a 2-year phase III breast-cancer trial, adverse renal events with IV ibandronate were ~4% versus ~4.5% with placebo — essentially at background. Bisphosphonates as a class can cause toxic ATN (zoledronate) or collapsing FSGS (pamidronate), but ibandronate is the renal-safety outlier within the class. Reported rate: serum creatinine increase >=44.2 micromol/l in 2% — Women with breast cancer and bone metastases receiving intravenous ibandronate 6 mg every 3-4 weeks for up to 6 months,… (von 2008, PMID 18334511).MildEnzalutamideHypertension emerges over weeks to months of therapy.Hypertension is the dominant renovascular signal. A 2024 JAMA Oncology meta-analysis of androgen-receptor signaling inhibitors found a markedly increased risk of grade ≥3 hypertension (relative risk ~2.25); an earlier meta-analysis showed the same for enzalutamide specifically. Direct intrinsic kidney injury is uncommon; rare hyponatremia appears mainly in combination regimens. Reported rate: hypertension in 11.9% — Pooled analysis of 7 randomized clinical trials of enzalutamide in prostate cancer, 7347 patients (Zhu 2019, PMID 31557062).MildTamoxifenFlare hypercalcemia within the first days to weeks; hyponatremia case-level and variable.Direct nephrotoxicity is not a feature. Tumor-flare hypercalcemia occurs early in patients with osteolytic bone metastases (about 13% — 12 of 93 — in one hypercalcemic breast-cancer series). Euvolemic hyponatremia (SIADH-type) is reported only at the case level.MildPirtobrutinibEarly after initiation in high-burden disease (first cycle); TLS is usually a single early event.Direct nephrotoxicity is not characteristic. Tumor lysis syndrome is an identified risk when rapidly debulking high-burden lymphoid malignancy; renal-specific incidence is low and not well quantified. BTK inhibitors as a class are also associated with hypertension and bleeding/atrial fibrillation (non-renal).MildLazertinibDuring therapy; case-level and variable.Hyponatremia is a recognized signal of third-generation EGFR TKIs (an osimertinib-class effect); for lazertinib specifically the renal/sodium data are limited and not well quantified. EGFR blockade also causes electrolyte wasting (hypomagnesemia, hypokalemia), and combination with amivantamab adds to these effects.MildZanidatamabVariable; tied to GI/volume events during treatment cycles rather than a fixed latency.No drug-specific nephrotoxicity rate is established. In HERIZON-BTC-01 the dominant toxicities were diarrhea and infusion reactions; any AKI is expected to be largely prerenal/volume-mediated (diarrhea, reduced intake) or related to the underlying biliary obstruction, rather than a direct tubular effect.MildImetelstatAny tumor-lysis-type risk would be early after initiation; otherwise no defined renal onset.No established direct nephrotoxicity. In IMerge the dominant toxicities were cytopenias (thrombocytopenia, neutropenia); renal injury was not a defining adverse event. Tumor-lysis-type metabolic risk is theoretical and most relevant with high disease burden, not a quantified rate in lower-risk MDS.MildMirdametinibNot well defined; edema and any creatinine changes evolve during ongoing therapy.No established intrinsic nephrotoxicity. Across MEK-inhibitor experience (including the NF106 mirdametinib trial) the characteristic toxicities are rash, edema, diarrhea and CK elevation; renal events are not a defining signal and any creatinine change is qualitative rather than a quantified AKI rate.MildRuxolitinibAny tumor-lysis risk is early (first cycles); withdrawal syndrome occurs within days of stopping; otherwise no defined renal onset.No established intrinsic nephrotoxicity. Over a decade of safety data show cytopenias and infections (including opportunistic) as the dominant toxicities. Renal concerns are indirect: rare tumor-lysis at treatment initiation in bulky myelofibrosis, the need for dose reduction in renal impairment, and a recognized ruxolitinib-withdrawal syndrome on abrupt cessation — rather than direct tubular injury.MildQuizartinibHighest around induction (tumor lysis, neutropenic sepsis); ongoing electrolyte monitoring through therapy.No established intrinsic nephrotoxicity. In QuANTUM-First the dominant grade 3-4 events were febrile neutropenia, hypokalemia and pneumonia; QT prolongation is a hallmark. Renal injury is indirect — tumor-lysis at induction, sepsis/cytopenia-related prerenal/ischemic AKI, and electrolyte derangements. AKI is common in AML induction generally (KDIGO-defined rates are high in cohort studies), but a quizartinib-attributable rate is not defined. Reported rate: grade >=3 hypokalemia in 12% — Adults with relapsed or refractory FLT3-ITD-positive acute myeloid leukemia treated with single-agent quizartinib (60… (Cortes 2019, PMID 31175001).MildIbritumomab tiuxetanTLS is early (hours to days); cytopenias are delayed (weeks).Direct renal radiation toxicity is essentially negligible — yttrium-90 is a pure beta-emitter and the kidney is not a critical organ on dosimetry; the dose-limiting toxicity is delayed myelosuppression. The renal hazard is indirect tumor lysis syndrome (TLS) in bulky/high-burden disease; a drug-specific TLS rate is not well quantified and is rare.MildLurbinectedinVariable across cycles (not tightly defined) — monitor with each dose.Not directly tubulotoxic; clinically significant AKI is rare and arises from rhabdomyolysis or tumor lysis. Rhabdomyolysis was formally recognized post-approval (FDA FAERS) and as an isolated phase 1 dose-limiting toxicity; the trial rate is not quantified. The dominant toxicity is hematologic (grade >=3 neutropenia ~41%) with frequent transaminase elevations.MildCladribineTumor-lysis AKI is acute (24-72 h); high-dose sensorimotor neuropathy is delayed (weeks).At standard hairy-cell-leukemia doses cladribine is renally quiet; clinically significant nephrotoxicity is uncommon and dose-related, worst at historical high investigational doses. The dominant renal hazard is tumor lysis syndrome in bulky/leukocytotic disease, reported at the case level rather than as a population incidence.MildMobocertinibDiarrhea early (within the first week); AKI follows. Prerenal AKI is typically reversible with early volume repletion and diarrhea control.Diarrhea is near-universal: any-grade ~83% (up to ~93% pooled), grade >=3 ~20-21%, with median onset ~5 days. AKI is predominantly prerenal; a real-world cohort reported grade >=3 renal failure in ~6%. Precise drug-attributable AKI and QT rates are not robustly quantified beyond class warnings. Reported rate: grade >=3 renal failure in 6% — 16 patients with EGFR exon 20 insertion-mutated NSCLC receiving mobocertinib 160 mg once daily as monotherapy under… (Kian 2022, PMID 36203432).MildMitoxantroneTumor lysis hours to days post-infusion.Direct nephrotoxicity is low and not quantified; the principal renal risk is tumor lysis syndrome when used in bulky/rapidly proliferating hematologic malignancies. Benign blue-green discoloration of urine/sclera is expected (the anthracenedione chromophore), not injury.MildIdarubicinHours to days after starting induction.Minimal intrinsic nephrotoxicity; the dominant renal threat is tumor lysis syndrome in acute leukemia. In 114 consecutive adult AML patients receiving induction, fulminant tumor lysis with acute renal failure occurred in 6.1% (95% CI 2.5-12.2), most of whom required hemodialysis; five of those seven patients had inv(16), so risk in that subgroup is substantially higher than the cohort-wide rate. That cohort used cytarabine-daunorubicin induction, so the figure reflects anthracycline-based induction generally — an idarubicin-specific AKI rate is not quantified.MildVismodegibMuscle spasms within the first weeks-to-months; hyponatremia is sporadic and variable in timing.Muscle spasms are near-universal (~64-71%), with dysgeusia and alopecia close behind; hyponatremia is reported but uncommon and not precisely quantified for an SIADH mechanism. Direct kidney injury is rare.MildGlasdegibMuscle spasms and QT changes within early cycles; prerenal/electrolyte issues track intercurrent illness and intake.Muscle spasms, QT prolongation, cytopenias, edema, nausea and mucositis are the labeled toxicities; the FDA notes a use limitation in severe renal impairment (a renal-impairment trial was a post-marketing requirement). Direct nephrotoxicity is not a defined signal, and AKI is largely secondary (dehydration, sepsis, tumor lysis).MildMidostaurinTumor lysis early in induction; prerenal/electrolyte issues track intercurrent illness; edema across treatment.Given with intensive chemotherapy, the dominant toxicities are cytopenias, nausea/vomiting, mucositis, edema and QT changes; tumor lysis is a treatment-related (largely chemotherapy-driven) hazard. No characteristic or established midostaurin-specific direct nephrotoxicity is recognized apart from a single anecdotal case report of pauci-immune necrotizing glomerulonephritis, and AKI is multifactorial (volume loss, sepsis, TLS).MildAvapritinibEdema and cognitive effects across treatment; GI-related prerenal changes track intercurrent toxicity.Edema (periorbital/peripheral) is very common, and intracranial hemorrhage and cognitive/CNS effects are labeled toxicities; nausea/diarrhea contribute to volume shifts. Direct nephrotoxicity is not a defined signal and AKI, when it occurs, is secondary (fluid shifts, GI losses, mastocytosis mediator release).MildTazemetostatTumor lysis, if it occurs, is early after response; prerenal effects track intercurrent GI toxicity.Tazemetostat is generally well tolerated with low direct organ toxicity; the noted boxed risk is secondary T-cell lymphoma/myeloid malignancy. Tumor lysis is an uncommon, treatment-related concern in responding lymphoma. A discrete AKI rate is not quantified and direct nephrotoxicity is low. Reported rate: grade >=3 hyponatremia in 7% — 74 patients with relapsed or refractory malignant pleural mesothelioma (99% BAP1-inactivated) receiving single-agent… (Zauderer 2022, PMID 35588752).MildTafasitamabInfusion reactions early (first cycle); tumor lysis early in responders.Infusion-related reactions occur early (largely first cycle) and cytopenias are common; tumor lysis is an uncommon, treatment-related concern in responding lymphoma. Direct nephrotoxicity is not a recognized signal and AKI is secondary.MildMogamulizumabInfusion reactions early; rash over weeks; tumor lysis early in responders.Drug rash and infusion reactions are characteristic; tumor lysis occurred in roughly 2-3% in some series. AKI is rare and largely secondary to tumor lysis or volume shifts; a discrete AKI incidence is not well quantified. Reported rate: tumor lysis syndrome in 2.5% — 484 patients (safety analysis population) with CCR4-positive relapsed or refractory adult T-cell leukemia-lymphoma in a… (Ishitsuka 2017, PMID 28597329).MildChlorambucilHyponatremia, when reported, has occurred during ongoing dosing, including with low doses; timing is variable.Chlorambucil has minimal direct nephrotoxicity. Drug-associated SIADH with hyponatremia is reported only rarely, in isolated case reports; tumor lysis is uncommon given its indolent-disease indications and gradual cytoreduction. No reliable incidence figure exists.MildLinvoseltamabDays — coincident with step-up dosing and CRS in the first 1-2 weeks; CRS in LINKER-MM1 occurred predominantly during step-up dosing.No drug-specific renal toxicity signal was reported in the LINKER-MM1 registrational program; AKI is not a labeled or characteristic adverse event. Any kidney injury is expected to be indirect and infrequent, mediated chiefly by cytokine release syndrome (CRS), infection/sepsis, and (early) tumor lysis. By class analogy to CAR-T and other immune-effector therapies, AKI occurs in roughly 5-21% of T-cell-redirection recipients, is usually mild (KDIGO stage 1) and transient with recovery in ~79% within a month, and tracks with higher-grade CRS. No linvoseltamab-specific incidence is published.MildEnsartinibA benign creatinine rise tends to appear early and stabilize; cyst development in the ALK-TKI class is generally a later, cumulative imaging finding over months of therapy.Renal-specific incidence for ensartinib is not separately quantified; in the eXalt3 phase 3 trial serious adverse events, dose reductions, and discontinuations were similar to crizotinib with no new safety signals, and edema and a creatinine rise are described for ensartinib. The renal signature is therefore class-extrapolated from the ALK TKIs, where crizotinib is the index agent for both a benign reduced-tubular-secretion creatinine rise and the development/progression of renal cysts. No defined ensartinib-attributable kidney lesion or incidence rate is established. Reported rate: creatinine elevation in 35.4% — 48 patients with advanced ALK- or ROS1-positive NSCLC enrolled at 2 centers in China and treated with single-agent oral… (Ma 2022, PMID 36647478).MildDabrafenibVariable and biphasic. Pyrexia-associated AKI clusters early, in the first weeks to months of therapy and coincides with febrile episodes. Biopsy-proven granulomatous/acute interstitial nephritis has appeared anywhere from a few weeks to as late as ~5 years into treatment.AKI is relatively common on dabrafenib-based therapy but usually mild and reversible. In the largest cohort, 42/199 (21%) of patients on dabrafenib/trametinib developed AKI within 12 months, and roughly 24% of those episodes occurred during the drug-induced febrile (pyrexia) syndrome (Seethapathy 2022). Pharmacovigilance places dabrafenib well below vemurafenib: FAERS acute-kidney-injury reporting-odds-ratio approximately 1.35 (95% CI 1.15–1.60) for dabrafenib versus approximately 3.28 for vemurafenib (Sanagawa 2021). Biopsy-proven granulomatous/acute interstitial nephritis and clinically significant electrolyte disorders (hyponatremia, hypokalemia, hypophosphatemia) are each individually rare — documented mainly in case reports and small FAERS counts. Registrational trials did not flag renal toxicity; the signal emerged post-marketing.MildTemsirolimusSubacute — typically weeks to months into weekly dosing; not firmly characterized for temsirolimus.Not firmly quantified for temsirolimus specifically. Proteinuria is the recognized mTOR-inhibitor glomerular signal, but for temsirolimus it is documented mostly at the class/case level rather than in drug-specific renal endpoints (everolimus proteinuria runs high yet is usually grade 1-2 — e.g., 96% all-grade in one first-line mRCC cohort). In the pivotal temsirolimus ARCC trial, metabolic lab abnormalities (hyperglycemia, hyperlipidemia, hypophosphatemia) dominated and frank nephrotoxicity was uncommon; drug-specific AKI and nephrotic syndrome appear only in case reports. Reported rate: grade >=3 hypophosphatemia in 5% — 82 East Asian (Sun 2012, PMID 22844126).MildSevabertinibDiarrhea and its prerenal consequences are typically early and recur with dosing across the first cycles; hypomagnesemia accrues over weeks of continued therapy (duration-related) and reverses over several weeks after interruption or discontinuation.No discrete published incidence of sevabertinib acute kidney injury exists as a standalone endpoint; the renal risk is inferred from its dominant on-target toxicity. In the registrational phase 1-2 SOHO-01 study (Le, N Engl J Med 2025; n=209), diarrhea was the single most common adverse event, occurring in 84-91% of patients depending on cohort, with grade 3 or higher diarrhea in 5-23%; grade 3+ drug-related adverse events overall were 31%, and only 3% discontinued for toxicity. Diarrhea of this frequency and severity is a well-recognized driver of prerenal, volume-depletion acute kidney injury and of electrolyte loss. Separately, HER/EGFR-pathway inhibition causes renal magnesium wasting through the tubular EGFR-TRPM6 axis (Costa, Target Oncol 2011); this is most pronounced with anti-EGFR monoclonal antibodies and is expected to be milder with a HER2-directed TKI, but hypomagnesemia remains a monitoring point.MildZenocutuzumabNo drug-specific direct renal onset. Infusion-related effects are hyperacute (during/around the infusion); diarrhea-related prerenal physiology, if it occurs, follows the diarrheal episodes across treatment.Zenocutuzumab carries no meaningful direct renal signal and no discrete published incidence of drug-related acute kidney injury. In the registrational phase 2 eNRGy study (Schram, N Engl J Med 2025; n=204) adverse events were primarily grade 1 or 2, the most common treatment-related events were diarrhea (18%), fatigue (12%), and nausea (11%), infusion-related reactions occurred in 14%, and only one patient discontinued for a treatment-related event. The only renal-relevant route is indirect: diarrhea and, less often, infusion reactions can produce volume depletion and prerenal physiology if significant. Unlike T-cell-engaging bispecifics, this HER2xHER3 antibody does not carry a cytokine-release or tumor-lysis mechanism, so it lacks that class's renal hazards.Mild