The Injury Atlas See it on the nephron Does the kidney recover? Cross-drug outcomesRepresentative per-agent prerenal / hemodynamic aki 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.
PRE
Prerenal / Hemodynamic AKI
Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.
101signature agents
Where it strikes
No single structural nephron site — this is a functional / pre-renal process driven by reduced perfusion upstream of the nephron, so the parenchyma is intact.
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.
Moderate· 44Mild· 57
Agents’ overall reversibility
Partially reversible· 2Variable· 11Reversible· 88
Agents’ onset window
How soon each agent’s kidney toxicity typically appears — a whole-drug tempo, not specific to this lesion.
Hyperacute (<24 h)· 3Acute (days)· 51Subacute (weeks)· 15Delayed (weeks–months)· 4Variable· 24
Management approach
Full framework →Restore perfusion and treat the driver (cytokine release); the kidney itself is usually structurally intact.
Drug-level levers
- Supportive — the agent is not directly nephrotoxic; AKI tracks the systemic syndrome (cytokine release, capillary leak, volume loss).
- Hold the agent for severe systemic toxicity per cytokine-release-syndrome grading.
Pharmacologic toolkit
- Volume resuscitation — Judicious fluids for hypoperfusion, balanced against capillary-leak edema.
- Tocilizumab / CRS-directed therapy — For CAR-T or bispecific cytokine release syndrome, IL-6 blockade (tocilizumab) ± corticosteroids treats the driver of prerenal AKI.
- Tumor-lysis prophylaxis — Where a high tumor burden coexists.
When to biopsy
Not indicated — prerenal / hemodynamic AKI is established by context; reserve biopsy for AKI that fails to recover after resuscitation.
Monitoring
- · Creatinine, urine output, volume status
- · Cytokine-release-syndrome grade
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 prerenal / hemodynamic aki.
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.KDIGODiagnosis, evaluation, and management of acute kidney injury: a KDIGO summary (Part 1)Crit Care 2013 · PMID 23394211Defines/stages AKI by serum creatinine and urine output; emphasizes avoiding nephrotoxins, maintaining euvolemia/perfusion, dose-adjusting drugs to kidney function, and monitoring high-risk patients — the framework applied to nephrotoxic anti-cancer agents.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).
Cited incidence across agents
Where the literature gives a representative prerenal / hemodynamic aki figure, the agents ranked highest first. Hover a dot for its cited note.
Offending agents
Signature offenders
101Agents for which prerenal / hemodynamic aki is the defining renal lesion.
CAR-T Cell TherapyAcute — within the CRS window (first days–weeks).AKI ~5–33% across cohorts (commonly ~10–30%), mostly mild and reversible.ModerateInterleukin-2 (high-dose)Acute — during the treatment cycle.Oliguria / prerenal AKI is very common during therapy at high dose — but reversible.ModerateClofarabineEarly, typically within the first treatment cycle (days).A systemic inflammatory response syndrome (SIRS) / capillary-leak syndrome with associated AKI was reported in roughly 4% of treated children in the registration program; hypotension was among the most common grade 3 or greater adverse events in the pivotal phase II trial. Precise renal incidence is not well quantified and most AKI data are case-level. Reported rate: renal insufficiency in 6% — Adults with relapsed and/or refractory non-Hodgkin lymphoma receiving SINGLE-AGENT clofarabine (1-h IV daily x5, q28d)… (Nabhan 2011, PMID 21425150).ModerateBlinatumomabEarly, typically during the first days of an infusion cycle (CRS) or with rapid tumor cytoreduction (TLS), concentrated around initiation and dose step-up.Acute kidney injury is predominantly secondary to cytokine release syndrome (CRS) and tumor lysis syndrome (TLS) rather than a direct drug effect; renal injury is described mainly at the case/series level and is not robustly quantified as a primary endpoint. By analogy to immune-effector-cell therapies, AKI is generally low-grade and rapidly reversible when the syndrome is controlled.ModerateTeclistamabEarly, concentrated around step-up (priming) dosing and the first full doses when CRS risk is highest (first days to weeks).Cytokine release syndrome is very common with teclistamab (about 72% of patients in the pivotal MajesTEC-1 trial, predominantly grade 1-2); CRS-associated acute kidney injury is an emerging, case-level signal superimposed on frequent baseline myeloma-related kidney disease, and is not separately well quantified. Reported rate: acute kidney injury in 29% — 10 of 34 patients with relapsed/refractory multiple myeloma treated with teclistamab, all of whom had received at least four prior lines of chemotherapy, versus 13% (4 of 30) after CAR-T in the same retrospective comparison; the difference was not statistically significant (HR 3.38, 95% CI 0.93-12.31, P = .065), and the authors leave open whether the excess is attributable to teclistamab or to disease progression (Charkviani 2025, PMID 39805729).ModerateTalquetamabEarly, around step-up (priming) dosing and the initial full doses when CRS risk peaks.Cytokine release syndrome is common with talquetamab (about three-quarters of patients in MonumenTAL-1, predominantly grade 1-2); CRS-associated acute kidney injury is an emerging, case-level signal that is not separately well quantified, superimposed on frequent baseline myeloma kidney disease.ModerateElranatamabEarly, concentrated around the two-step priming doses and the first full doses.Cytokine release syndrome is common with elranatamab (about 58% in the pivotal MagnetisMM-3 trial, largely grade 1-2 with the two-step priming regimen); CRS-associated acute kidney injury, and occasionally tumor-lysis-related injury, are emerging case-level signals that are not separately well quantified, superimposed on frequent myeloma kidney disease.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.ModerateSacituzumab govitecanVariable; prerenal AKI tracks with GI toxicity during treatment cycles.AKI is mainly prerenal, driven by the severe diarrhea/nausea and neutropenia that dominate the ASCENT safety profile; renal-specific incidence is not well quantified. A biopsy-proven severe acute tubulointerstitial nephritis requiring hemodialysis has also been reported (case-level).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.ModerateTretinoin (ATRA)Usually within the first 1–3 weeks of induction (bimodal: first week and third week).Differentiation (retinoic acid) syndrome — the main route to AKI — occurs in roughly 2–37% of APL patients depending on criteria and prophylaxis (commonly cited around 25%); acute renal failure is part of its defining end-organ spectrum.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.ModerateTagraxofuspTypically during the first treatment cycle, often within days of the first doses; recurrence in later cycles is uncommon with proactive monitoring.Capillary leak syndrome (CLS) is a boxed-warning toxicity occurring in ~19-21% of treated patients in the registrational trial (mostly grade 2; grade >=3 in ~4% — 2% grade 3 plus 2% grade 4 — with two deaths); the resulting hypotension, hypoalbuminemia, and fluid shifts can precipitate prerenal AKI and, with prolonged hypoperfusion, ischemic ATN. Renal-specific AKI incidence is not separately quantified.ModerateTarlatamabCRS typically within the first cycle, often after the first full (post-priming) doses; AKI tracks the CRS course.Cytokine release syndrome is the dominant on-target toxicity — common (majority of patients in early studies), mostly low-grade, and mitigated by step-up/priming dosing and inpatient monitoring of initial doses. AKI is principally a downstream consequence of CRS (hypotension, fever, capillary leak, volume shifts) rather than a direct tubular toxin; renal-specific incidence is not separately well quantified.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.ModerateDenileukin diftitoxAcute, peri-infusion (first 1-2 cycles); generally not cumulative.Capillary-leak syndrome (CLS) occurred in ~20.3% (grade >=3 ~5.8%) in the 2024 denileukin diftitox-cxdl trial. With the original formulation hypoalbuminemia was very common (~79%, ~15% grade 3/4) and a vascular-leak syndrome occurred in roughly a quarter of patients. AKI here is prerenal/hemodynamic rather than a quantified direct renal injury rate.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.ModerateDinutuximabInfusion-associated and acute — pain, capillary leak and blood-pressure swings occur during/around each infusion.Severe neuropathic pain is near-universal, and capillary-leak syndrome and hypertension are common, sometimes severe, infusion-associated toxicities (driven partly by concurrent IL-2). The resulting fluid shifts and prerenal AKI are managed proactively but not separately quantified.ModerateTebentafuspEarly — first 1–3 weekly doses, coinciding with peak CRS.Cytokine release syndrome is very common early in treatment and, with the associated hypotension, is the principal mechanism of acute kidney injury; severe sepsis-like CRS with hypotension has been reported. The pivotal phase 3 trial established CRS, hypotension and rash as defining toxicities, mitigated by weekly step-up dosing. A dedicated tebentafusp renal/AKI study does not exist; renal injury is inferred from the CRS literature.ModerateZolbetuximabAround infusions, especially the first cycles, tracking the nausea/vomiting peak.Direct nephrotoxicity is not a recognized feature. The defining, dose-limiting toxicity in the pivotal SPOTLIGHT and GLOW trials is severe nausea and vomiting (an on-target effect on gastric mucosa), which can cause volume depletion and prerenal acute kidney injury. A quantified renal-injury rate is not reported; the renal risk is mechanistic/indirect.ModerateTrifluridine/tipiracilWithin the first one to two cycles, especially early severe neutropenia in patients with reduced creatinine clearance.Direct intrinsic nephrotoxicity is not a prominent feature; the renal relevance is pharmacokinetic. The tipiracil component is mainly renally excreted, so its exposure rises with declining GFR: a phase I study found tipiracil AUC increased significantly with renal-impairment severity and required a dose reduction (to 20 mg/m2 twice daily) in severe impairment, while grade >= 3 adverse events — chiefly hematologic (anemia, neutropenia) — were more frequent across the impaired cohorts. Real-world data confirm more early severe neutropenia in patients with reduced creatinine clearance.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.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.ModerateTrametinibVariable. Pyrexia-associated AKI tends to appear early, tracking the febrile syndrome that often begins within the first weeks to few months of dabrafenib/trametinib. The rare biopsy-proven interstitial nephritis and glomerulonephritis cases have presented later — generally around 2 to 6 months into therapy.The renal signal from trametinib itself is modest. In an FDA Adverse Event Reporting System (FAERS) disproportionality analysis, trametinib carried a statistically significant but low acute-kidney-injury reporting odds ratio of 1.32 (95% CI 1.11-1.56) — well below vemurafenib's — and at mean steady-state plasma concentrations trametinib produced no measurable cytotoxicity in cultured proximal-tubular, glomerular endothelial or glomerular epithelial cells (Sanagawa, Anticancer Drugs 2021). Most of the quantified AKI burden comes from combination use: in a single-center retrospective cohort of 199 patients receiving dabrafenib/trametinib, 42 (21%) met an AKI definition (1.5x creatinine rise) within 12 months, and roughly a quarter of those episodes (about 5% of the whole cohort) occurred during a treatment-induced pyrexia syndrome (Seethapathy, Nephrol Dial Transplant 2022). Biopsy-proven interstitial nephritis and glomerular lesions are rare and reported only as individual cases; kidney impairment was rarely reported in the pivotal monotherapy trial.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.ModerateNaxitamabAcute and infusion-locked — hypotension, hypertension, and the rest of the infusion-reaction complex begin within minutes to a few hours of starting the infusion and are most pronounced during the early cycles; significant infusion-related events become rare after the first few treatment cycles.Frank acute kidney injury is not a systematically reported endpoint for naxitamab and no validated AKI incidence figure exists; the renal-relevant risk is hemodynamic rather than a direct nephrotoxic lesion. The closest quantitative anchor comes from the pivotal single-arm phase 2 Trial 201 (NCT03363373), where naxitamab-related grade 3 adverse events were dominated by hypotension in 58% and pain in 54% of patients — the infusion-reaction physiology that can transiently compromise renal perfusion. Pharmacovigilance corroborates the signal: in an FDA Adverse Event Reporting System analysis of anti-GD2 antibodies, hypotension, hypertension, urticaria, and capillary-leakage syndrome were among the most frequent and strongest naxitamab-associated signals. Because these figures describe hemodynamic events (not measured creatinine-defined AKI), the numeric AKI rate is left unquantified.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.ModerateTasonerminRapid and procedure-linked. If systemic leakage occurs, hypotension and SIRS physiology appear during or within hours of the perfusion (peak systemic TNF-alpha and the cytokine surge fall in the first 3-12 h), with any azotemia manifesting over the first 24-48 h. Rhabdomyolysis/compartment-syndrome-related injury also emerges within the first 24 h.No robust drug-specific renal AKI incidence exists. In the large multicenter TNF-alpha + melphalan limb-perfusion series, systemic toxicity was 'minimal to moderate,' readily managed, with no toxic deaths, and clinically significant renal injury was uncommon when systemic leakage was controlled (Eggermont, Ann Surg 1996). Renal insufficiency clusters in the minority with high systemic TNF-alpha leakage: transient renal insufficiency was seen in leak-affected patients during early TNF-alone perfusions (Posner 1995), whereas a series that tolerated even 12-65% leakage found hypotension the dominant toxicity and observed no renal toxicity (Stam 2000). Reported risk is therefore leakage-dependent rather than a fixed rate, so no single incidence figure is quoted.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.ModerateDacarbazineVariable; hepatic VOD typically days to weeks after exposure.Direct nephrotoxicity is minimal and not well quantified; the notable vascular toxicity is hepatic veno-occlusive disease / sinusoidal obstruction (now recognized as not rare), with renal effects largely secondary to severe systemic illness, hepatic injury or volume loss.MildCapecitabineAcute, during cycles with GI toxicity; TMA delayed and rare.Intrinsic nephrotoxicity is uncommon; the main renal issue is prerenal AKI from drug-induced diarrhea and volume depletion. Renal impairment increases toxicity - in the PK study, all patients with severe impairment (CrCl <30) had grade 3-4 adverse events - so labeling mandates dose adjustment by creatinine clearance and, below CrCl 30, establishes no dose (avoid unless no alternative).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.MildMirvetuximab soravtansineVariable; tracks with GI toxicity during treatment cycles.Direct nephrotoxicity is not a prominent trial signal; ocular (keratopathy/blurred vision, ~50% any-grade across pooled trials) and GI/fatigue toxicities dominate. AKI is case-level and chiefly volume-mediated (GI toxicity). 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.MildNilotinibVascular events accrue over months to years of therapy.Nilotinib carries a recognized risk of arterial occlusive events and metabolic effects (dysglycemia, hyperlipidemia), but direct renal toxicity is limited; in comparative CML cohorts nilotinib generally did not cause significant eGFR decline relative to imatinib. Any kidney impact is largely mediated through vascular disease and perfusion rather than intrinsic nephrotoxicity.MildCeritinibPrerenal AKI can occur whenever GI toxicity causes significant fluid loss, often early in therapy.Ceritinib causes frequent gastrointestinal toxicity (nausea, vomiting, diarrhea in the majority of patients), which can lead to volume depletion and prerenal AKI; as an ALK inhibitor it can also produce generally mild, reversible creatinine elevations. The prerenal AKI risk is largely a downstream effect of GI losses and is not precisely quantified.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.MildSotorasibWhen AKI occurs, it is acute during the first weeks–months of therapy, typically tracking GI toxicity.Clinically significant nephrotoxicity is uncommon and case-level in humans (the dominant on-target/off-tumor toxicity is hepatotoxicity). Proximal tubular toxicity is prominent in rats via a reactive mercapturate-pathway metabolite. Human renal incidence is not well quantified.MildAdagrasibEarly — within the first weeks of therapy.Renal effects are usually mild: a creatinine rise (partly from inhibited tubular creatinine secretion) plus prerenal AKI from GI losses. The KRYSTAL-1 registrational program reported renal-related lab changes; a dedicated PubMed-indexed pseudo-AKI/albuminuria study for adagrasib does not yet exist, so the precise incidence is unquantified.MildBelzutifanAnemia and hypoxia develop over the first weeks of therapy.Anemia is the most common on-target adverse event (the leading grade 3 event in pivotal trials) and hypoxia is frequent. Direct nephrotoxicity is not a prominent or well-quantified signal; renal function changes mostly reflect underlying RCC/nephrectomy status.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.MildIrinotecanAcute cholinergic diarrhea within hours of infusion; delayed diarrhea after ~24 hours and over subsequent days, with AKI following cumulative volume loss.Direct nephrotoxicity is not a recognized feature; the principal renal risk is prerenal AKI from severe early (cholinergic) and delayed diarrhea with volume depletion. Severe (grade 3-4) irinotecan toxicity, mostly diarrhea/neutropenia, occurs in roughly a quarter to a third of patients and is enriched in UGT1A1 poor metabolizers. AKI incidence specifically attributable to irinotecan is not well quantified.MildTopotecanExposure-related hematologic toxicity manifests across treatment cycles; prerenal AKI follows intercurrent volume loss.Topotecan is substantially renally cleared, so impaired kidney function increases drug exposure and myelosuppression risk; pharmacokinetic studies show topotecan AUC rises ~109% (moderate) and ~174% (severe impairment), supporting dose reduction. Direct topotecan-induced nephrotoxicity is not a recognized signal, and drug-attributable AKI incidence is not well quantified.MildPaclitaxelInfusion reactions occur during or shortly after administration (typically first/second exposure); any prerenal AKI follows the hemodynamic instability.Paclitaxel has low direct nephrotoxicity. Hypersensitivity/infusion reactions - historically attributed to the Cremophor EL (polyoxyethylated castor oil) vehicle via complement activation, with newer evidence for IgE-mediated reactions - and associated fluid shifts can transiently compromise renal perfusion, but structural kidney injury is uncommon and not well quantified.MildDocetaxelFluid retention develops cumulatively (often after several cycles / cumulative dose); hypersensitivity reactions occur during infusion.Docetaxel has low direct renal toxicity. Its characteristic fluid-retention syndrome (peripheral edema, effusions, weight gain) reflects increased capillary permeability rather than tubular injury; AKI directly attributable to docetaxel is uncommon and not well quantified, and the drug has been used successfully even in kidney-transplant recipients.MildCabazitaxelAKI follows intercurrent gastrointestinal or infectious complications during treatment cycles.Cabazitaxel has low direct nephrotoxicity; AKI is uncommon and usually mediated by gastrointestinal losses (diarrhea, occurring in a substantial minority), neutropenic sepsis, or hemodynamic instability rather than direct tubular toxicity. In real-world safety data, grade >=3 diarrhea and febrile neutropenia each occur in roughly 5% of patients. A drug-specific renal AKI rate is not well established.MildEribulinExposure-related toxicity accrues across cycles; prerenal AKI follows volume loss.Eribulin is not a recognized direct nephrotoxin. Pharmacokinetic study shows reduced clearance and ~1.5-fold higher exposure with moderate-to-severe renal impairment, supporting dose adjustment; any AKI is generally prerenal and not well quantified.MildAsparaginaseLinked to intercurrent complications during induction/intensification therapy.Direct asparaginase nephrotoxicity is uncommon; classic toxicities are hypersensitivity (up to ~30% with E. coli-derived enzyme), pancreatitis, hepatic dysfunction, hyperammonemia, and coagulopathy/thrombosis. When AKI occurs it is typically secondary to pancreatitis, hemodynamic instability, or thrombotic complications rather than a direct tubular toxin, and is not well quantified.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.MildTovorafenibNot well defined; any change emerges during ongoing therapy rather than at a fixed onset.No established intrinsic nephrotoxicity. In FIREFLY-1 the prominent toxicities were hair-color change, rash, anemia and fatigue; renal events were not a defining signal, and any creatinine elevation is described qualitatively rather than as a quantified AKI rate.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).MildCasdatifanNot established; class anemia/hypoxia effects emerge during ongoing therapy.Renal-specific data are not established. By analogy to the first-in-class HIF-2α inhibitor belzutifan, expected on-target effects include anemia (belzutifan: ~27-90% across trials) and hypoxia, plus possible fluid retention/edema; these are class effects rather than direct nephron injury. No casdatifan-specific renal incidence is published.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.MildRadium-223 dichlorideGI effects early; hematologic nadir over weeks. No characteristic renal onset.Direct renal toxicity is minimal and not a recognized feature; renal labs are typically unaffected. The dominant toxicities are gastrointestinal (diarrhea, nausea) and myelosuppression. Any AKI is essentially always attributable to other causes (obstruction, dehydration, concomitant nephrotoxins).MildPegaspargaseToxicities cluster during induction/first doses; AKI is usually reversible with treatment of the underlying thrombosis or pancreatitis.Direct nephrotoxicity is not recognized; AKI is indirect and uncommon. Symptomatic thrombosis occurs in ~1.5-5% of children and is higher (~5-10%+) in adults/adolescents-and-young-adults, and clinical pancreatitis in ~5-10%. A drug-specific AKI incidence is not quantified (it is a downstream complication, not a tracked endpoint).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).MildEstramustineEdema/VTE within weeks to the first 2 months.Renal injury is hemodynamic/prerenal rather than a quantified direct rate. The dominant safety liability is venous (and arterial/cardiovascular) thromboembolism with fluid retention/edema; in randomized data the majority of cardiovascular complications occurred within the first year.MildIdelalisibDiarrhea/colitis often delayed — a median of several months into therapy; transaminitis is typically earlier (first weeks).Severe immune-mediated diarrhea/colitis occurs in roughly 14-20% (grade 3+) and transaminitis is common; secondary prerenal AKI from volume loss is not separately quantified. Direct renal lesions are rare.MildDuvelisibDiarrhea/colitis often after several months; rash and transaminitis can appear earlier.Diarrhea/colitis is common (any-grade ~50%, grade 3+ roughly 15-20% in DUO); the resulting volume-depletion prerenal AKI is not separately tabulated. Direct nephrotoxicity is uncommon.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).MildPexidartinibHepatotoxicity can occur early (often within the first 1-2 months) or later; secondary renal effects track the severity of the systemic/hepatic illness.The defining toxicity is serious, sometimes cholestatic, hepatotoxicity (boxed warning, REMS program); hair-color change, fatigue and GI effects are common. Direct nephrotoxicity is not a recognized signal, and renal effects are secondary (dehydration during illness, hepatorenal physiology in severe liver injury).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).MildTisotumab vedotinNot characterized for renal events; any prerenal AKI would track volume depletion (days).Direct nephrotoxicity is not a recognized signal. In the pivotal innovaTV 301 and innovaTV 204 trials the defining toxicities were ocular (conjunctivitis, dry eye, keratitis), bleeding/epistaxis and peripheral neuropathy; a quantified renal-injury rate was not reported. Renal involvement, if any, is indirect/case-level.MildElacestrantNot characterized for renal events; any prerenal AKI would track GI toxicity.Direct nephrotoxicity is not a recognized feature. In the pivotal phase 3 EMERALD trial the dominant toxicities were nausea, fatigue, vomiting and decreased appetite; a discrete renal-injury rate was not reported. Any renal involvement is best understood as indirect/case-level (e.g., volume depletion from GI toxicity).MildElotuzumabNot applicable for direct renal injury; infusion reactions occur during/shortly after the first infusions.Elotuzumab itself has no characteristic direct nephrotoxicity. A dedicated phase Ib study in myeloma patients with normal renal function, severe renal impairment (CrCl < 30 mL/min, not on dialysis), and end-stage renal disease on dialysis found comparable elotuzumab pharmacokinetics across all groups, with grade 3-4 adverse events of similar frequency and no need for dose adjustment. The relevant renal context is the underlying myeloma kidney disease the regimen treats, plus the partner-drug toxicities (lenalidomide is renally cleared).MildBleomycinPharmacokinetic accumulation is immediate in renal impairment; clinical (pulmonary) toxicity is cumulative over weeks to months.Bleomycin is not a classic direct nephrotoxin; the actionable renal issue is exposure-driven. Roughly two-thirds of a dose is cleared renally, and terminal half-life rises exponentially once creatinine clearance falls below ~25-35 mL/min, magnifying systemic (especially pulmonary) toxicity. Direct kidney injury is not well quantified and is largely confounded by co-administered cisplatin.MildAltretamine (hexamethylmelamine)Any mild creatinine change tends to occur during cycles and to reverse after dosing; timing is not well defined.Altretamine is not regarded as substantially nephrotoxic. Mild, generally reversible elevations in serum creatinine have been noted in trials, but the dose-limiting toxicities are gastrointestinal (nausea/vomiting), neurologic (peripheral and central neurotoxicity) and hematologic. No reliable renal incidence figure is established, and reported renal changes are confounded by frequent combination with cisplatin.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.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.MildVepdegestrantNo drug-specific renal onset. Any prerenal creatinine change would follow an intercurrent volume-depleting event rather than the drug's own timeline.Vepdegestrant carries no meaningful renal signal and no discrete published incidence of drug-related acute kidney injury. In the phase 3 VERITAC-2 trial (Campone, N Engl J Med 2025; n=624) grade 3 or higher adverse events occurred in 23.4% of patients — modestly above fulvestrant (17.6%) — and only 2.9% discontinued for adverse events, with a profile dominated by hematologic and constitutional effects rather than a nephrotoxic one. Any renal contribution would be indirect (for example, prerenal physiology if a patient became volume-depleted from an intercurrent illness), not an intrinsic kidney toxicity of the drug.MildDordaviproneNo drug-specific renal onset. QT effects are the on-treatment finding to monitor; any prerenal creatinine change would follow an intercurrent volume-depleting event.Dordaviprone carries no meaningful renal signal and no discrete published incidence of drug-related acute kidney injury. Its clinically important safety consideration is cardiac — QT-interval prolongation — rather than renal, and the intermittent oral schedule is generally well tolerated. Across its glioma program (Arrillaga-Romany, Neuro Oncol 2024, describes the phase 3 ACTION design and prior recurrent-disease efficacy), the toxicity profile is dominated by fatigue and QT effects, not nephrotoxicity. Any renal contribution would be indirect (prerenal physiology from intercurrent illness) rather than an intrinsic tubular or glomerular toxicity.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.MildZidesamtinibNo drug-specific renal onset. Edema accrues over early months of therapy as with other ROS1 TKIs; any renal event would follow its own precipitant rather than the drug's timeline.No drug-specific renal adverse-event incidence is published, and — notably for this class — creatinine increase does not appear in the FDA label's laboratory-abnormality table — which tabulates only abnormalities that worsened in >=20% of patients — nor in its >=2% grade 3-4 summary, so the absence establishes a rate below those cutoffs, not zero. The most common adverse reactions on the label's pooled safety population are edema (38%), peripheral neuropathy (25%), constipation (17%), fatigue (16%) and dyspnea (15%); the tabulated laboratory abnormalities are led by increased cholesterol and triglycerides (47% each) and increased CPK (37%), with decreased hemoglobin (30%), increased amylase (23%) and increased alkaline phosphatase (21%) further down the table. This absence of a creatinine signal is consistent with the drug's selective design but rests on early registrational data — it is an observation about what the label reports, not proof of renal inertness.MildIberdomideNo drug-specific renal onset window exists, because no renal lesion is attributed to the drug. Its own time-course risks are hematologic and thrombotic and accrue over the first cycles; a creatinine change follows its own precipitant - disease progression, intercurrent illness, a co-administered nephrotoxin - on that cause's timeline rather than the drug's.No renal lesion is attributed to iberdomide, and the randomized comparison is the reason that can be said plainly rather than assumed. In the FDA label's EXCALIBER-RRMM safety population, renal impairment - a composite adverse-reaction term - occurred in 11% of patients on iberdomide with daratumumab/hyaluronidase and dexamethasone (N=204) and in 8% on the daratumumab/hyaluronidase, bortezomib and dexamethasone comparator arm (N=204), with grade 3-4 rates of 3.4% and 3.9% respectively - numerically lower on the iberdomide arm. In relapsed or refractory myeloma the kidney is a target organ of the disease itself (cast nephropathy, hypercalcemia, volume depletion), so a single-arm rate of 11% would have read as drug toxicity; the comparator shows most of it belongs to the population. The label carries no renal warning, and the boxed warning is embryo-fetal toxicity and serious venous and arterial thromboembolism. Phase 3 results are not yet published, so these figures come from the label rather than from a peer-reviewed report.Mild