The Injury Atlas See it on the nephron Does the kidney recover? Cross-drug outcomesRepresentative per-agent acute tubular necrosis 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.
ATN
Acute Tubular Necrosis
Direct death of tubular epithelial cells — the dose-limiting lesion of the platinums and zoledronate.
75agents
Deep diveCisplatin ATN & hypomagnesemiaDeep diveIfosfamide FanconiDeep divePemetrexed tubulopathyDeep diveICI nephritisDeep diveHD-MTX nephropathyDeep diveBRAF/MEK tubularDeep diveBisphosphonate injuryDeep diveCAR-T AKI
Where it strikes
Proximal Tubule
Bulk reabsorption + drug uptake (OCT2, OATs)
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· 5Moderate· 52Mild· 18
Agents’ overall reversibility
Often irreversible· 1Partially reversible· 22Variable· 13Reversible· 39
Agents’ onset window
How soon each agent’s kidney toxicity typically appears — a whole-drug tempo, not specific to this lesion.
Acute (days)· 30Subacute (weeks)· 23Delayed (weeks–months)· 9Variable· 13
Real-world reporting for this lesion
FAERS across all lesions →Agents with a disproportionate FAERS reporting signal for acute tubular necrosis (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.
14Corroborated
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.
0Not 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.
30Reported 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.
ATN is systematically undercounted in FAERS — most true cases are filed under the generic “acute kidney injury” term rather than a distinct acute tubular necrosis code, so the literature-only column is expected to run large here.
5-FluorouracilAbemaciclibAmivantamabBendamustineBleomycinBortezomibBusulfanCarboplatinCarmustine (BCNU)CetuximabCisplatinClofarabineCobimetinibCyclophosphamideCytarabineDasatinibDecitabineDostarlimabDoxorubicinEtoposideEverolimusFludarabineGemcitabineHydroxyureaIfosfamideImatinibIpilimumabMelphalanMethotrexate (high-dose)NivolumabOxaliplatinPaclitaxelPamidronatePembrolizumabPemetrexedRituximabSirolimusTemsirolimusTisotumab vedotinTopotecanTrabectedinVinblastineZoledronic acidZongertinib
44 agents with a significant ATN reporting signal.
Management approach
Full framework →Prevention is the mainstay; once established, supportive care while the tubule recovers.
Drug-level levers
- Hold the agent for a significant creatinine rise; resume only after recovery.
- Dose-reduce or extend the dosing interval for lower-grade or recurrent injury.
- Switch within class to a less nephrotoxic platinum (carboplatin or nedaplatin) when a platinum must continue.
- Switch out of class to a non-nephrotoxic regimen if re-exposure risk is unacceptable.
Pharmacologic toolkit
- Volume expansion — Isotonic saline before and after dosing is the best-evidenced preventive measure for cisplatin ATN.
- Magnesium repletion — Replace urinary magnesium and potassium losses; magnesium supplementation may be renoprotective.
- Avoid co-nephrotoxins — Hold NSAIDs, aminoglycosides, and iodinated contrast where possible.
When to biopsy
Rarely needed — the diagnosis is usually clinical (timing, muddy-brown granular casts). Reserve biopsy for atypical features or when an alternative lesion (AIN, TMA) is suspected.
Monitoring
- · Creatinine / eGFR before each cycle
- · Serum magnesium and potassium
- · Urine output and sediment
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 acute tubular necrosis.
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.ASONDiagnosis and management of immune checkpoint inhibitor-associated nephrotoxicity: a position statement from the American Society of Onco-nephrologyKidney Int 2025 · PMID 39455026ICI-AKI most commonly presents as acute interstitial nephritis; nephrology consultation and kidney biopsy should be considered for stage 2 or higher AKI or suspected glomerular disease, but where biopsy is not feasible, prompt empiric corticosteroids (prednisone ~1 mg/kg/day) should be started for clinically suspected ICI-AKI since early steroids improve renal recovery, with cautious individualized consideration of ICI rechallenge after recovery.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.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).SIRMSIRM-SIN-AIOM: appropriateness criteria for evaluation and prevention of renal damage in the patient undergoing contrast medium examinations-consensus statements from Italian College of Radiology (SIRM), Italian College of Nephrology (SIN) and Italian Association of Medical Oncology (AIOM)Radiol Med 2022 · PMID 35303246Recommends eGFR-based renal risk assessment and pre/post-contrast isotonic saline or sodium bicarbonate hydration; advises maintaining a 5-7 day interval between iodinated contrast administration and cisplatin in cancer patients to reduce additive nephrotoxicity.PUMCH Expert PanelClinical recommendations on diagnosis and treatment of immune checkpoint inhibitor-induced renal immune-related adverse eventsThorac Cancer 2020 · PMID 32232975Screen and monitor with serum creatinine, urinalysis/sediment, and 24-hour urine protein; strongly recommend kidney biopsy to confirm ICI-related ATIN and exclude other AKI causes, withdraw nephrotoxins (PPIs, NSAIDs), and initiate corticosteroids when a grade 2 or higher renal irAE is highly suspected, with multidisciplinary decisions on ICI withdrawal and rechallenge.ASCO / CCORole of Bone-Modifying Agents in Metastatic Breast Cancer: An American Society of Clinical Oncology-Cancer Care Ontario Focused Guideline UpdateJ Clin Oncol 2017 · PMID 29035643Endorses denosumab 120 mg SC q4w, pamidronate 90 mg IV q3-4w, or zoledronic acid 4 mg IV q12w or q3-4w; nitrogen bisphosphonates require renal function monitoring and dose/interval adjustment for impaired clearance, whereas denosumab needs no renal dose adjustment (with hypocalcemia risk in CKD).
Cited incidence across agents
Where the literature gives a representative acute tubular necrosis figure, the agents ranked highest first. Hover a dot for its cited note.
Offending agents
Signature offenders
26Agents for which acute tubular necrosis is the defining renal 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%.SevereZoledronic acidAcute — days to weeks after infusion(s).Nephrotoxicity is the dose-limiting toxicity but largely avoidable; no precise population rate. Reported rate: renal toxicity in 17% — 852 patients with symptomatic newly diagnosed multiple myeloma and at least one lytic bone lesion who received at least… (Raje 2018, PMID 29429912).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).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.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.ModerateLenalidomideVariable; azotemia reported from weeks to several months after initiation.AKI/azotemia is uncommon but recognized, described mainly in case series of plasma-cell dyscrasias with underlying renal insufficiency; not reliably quantified as an incidence. Rare Fanconi syndrome and TMA are reported. Because ~80% of lenalidomide is renally cleared as unchanged drug, accumulation in renal impairment is the dominant driver of toxicity, including myelosuppression.ModerateDatopotamab deruxtecan (Dato-DXd)Not well characterized (recent approval); by class analogy a subacute tubular pattern during cumulative dosing.Renal signal is theoretical and not yet quantified, extrapolated from the ADC class. In TROPION-PanTumor01 and the phase III TROPION-Breast01 the dominant toxicities were mucosal (stomatitis ~50%) and ocular events, nausea, and interstitial lung disease; grade ≥3 treatment-related adverse events were lower than chemotherapy (~21%), and kidney-specific events were not prominent.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).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.ModerateRaltitrexedWithin the first one to two cycles, often heralded by exaggerated systemic toxicity in patients with reduced GFR.Not well quantified as a discrete renal endpoint. Raltitrexed is substantially renally eliminated: in a PK study, mild-to-moderate renal impairment roughly doubled drug exposure (AUC ratio ~2.0) and nearly doubled terminal half-life, with severe/grade 3-4 toxicity and adverse-event hospitalizations more frequent in the impaired group. The class precedent CB3717, raltitrexed's quinazoline antifolate forerunner, was withdrawn from development for crystal-related nephrotoxicity.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).ModerateProcarbazineVariable; tumor-lysis-related AKI within days of starting in bulky disease, hypersensitivity-type injury after re-exposure.Not well quantified at the drug-specific level. Procarbazine appears in classic onconephrology reviews of the renal complications of cytotoxic therapy as an agent with recognized renal/urological complications, and it is part of multi-agent lymphoma regimens in which acute renal failure (often multifactorial — tumor lysis, volume depletion, combined nephrotoxins) is described. Discrete procarbazine-attributable nephrotoxicity is largely case-/review-level rather than quantified.ModerateSamarium-153 lexidronamMyelosuppression nadirs within weeks; recovery typically over the following weeks.Clinically meaningful nephrotoxicity is uncommon; the dominant and dose-limiting toxicity is reversible myelosuppression. No reliable drug-specific AKI incidence is established. Renal caution stems from renal/urinary excretion of the unbound radiopharmaceutical.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.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.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.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).MildEncorafenibWeeks into therapy when it occurs.Renal injury with BRAF/MEK therapy is uncommon and largely case-level (tubular injury and acute interstitial nephritis reported); usually mild and reversible with drug interruption. In COLUMBUS, grade 3-4 creatine-phosphokinase elevation (7%) and hypertension (6%) were the renally relevant events with encorafenib plus binimetinib.MildCobimetinibWeeks into therapy.AKI with BRAF/MEK therapy is uncommon and mostly mild; a pharmacovigilance analysis found adding a MEK inhibitor to vemurafenib was associated with a ~60% reduction in acute kidney injury versus vemurafenib alone.MildBinimetinibWeeks into therapy.Clinically significant intrinsic nephrotoxicity is uncommon; modest creatinine elevations occur and CK elevation is a recognized MEK-class effect. In COLUMBUS, grade 3-4 blood-CK increase occurred in ~7% with encorafenib plus binimetinib; rare rhabdomyolysis can secondarily threaten the kidney.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).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.MildSonidegibCK elevations during the first weeks-to-months of therapy; rhabdomyolysis-driven AKI would follow a significant muscle-injury event.Asymptomatic creatine-kinase elevation is more common with sonidegib than vismodegib (a class-distinguishing signal), and rhabdomyolysis is a labeled but rare event. Clinically significant pigment nephropathy/ATN is uncommon but is the feared renal consequence.MildIobenguane I-131Biphasic — modest, often transient creatinine changes within weeks of a therapeutic dose; the characteristic radiation nephropathy is delayed, typically appearing 6-12 months or later after cumulative renal irradiation, sometimes years out.Reported renal toxicity is uncommon and usually low-grade. In a dosimetry-guided high-activity 131I-MIBG cohort, 3 of 14 patients (21%) had transient grade 1 renal toxicity (Maric 2023, small single-center series using conventional 131I-MIBG). In the registrational high-specific-activity trial (Azedra, n=68 dosed), renal failure was not among the most common treatment-emergent events — nausea, myelosuppression and fatigue dominated — and clinically significant (grade >=3) nephrotoxicity was rare. The kidney concern is driven less by acute events than by the delayed, cumulative absorbed radiation dose, so headline incidence figures come from small cohorts and should be read as low-grade signal rather than a robust rate.Mild
Also associated
49Agents that cause acute tubular necrosis as a secondary pattern alongside a different signature lesion.
IfosfamideAcute 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).SevereCarfilzomibVariable — frequently early (first cycles), but TMA can also appear later, sometimes after a treatment break and re-escalation.Renal complications are common and a recognized class concern: in a 114-patient real-world cohort, ~17% had carfilzomib-attributable renal events (TMA ~5%, albuminuria >1 g/day ~6%, otherwise-unexplained grade >=3 AKI ~5%), occurring mostly early and unpredictably. On the prospective CARDAMON trial 8 patients experienced TMA (6 of 8 hypertensive at presentation, 7 of 8 with AKI); after a protocol amendment adding aggressive hypertension management, carfilzomib step-up dosing at the start of maintenance and dexamethasone premedication, the rate fell from 4.2 to 1.6 events per 1,000 patient-cycles with no further maintenance events. Pharmacovigilance (FAERS) shows carfilzomib carries by far the strongest TMA signal among proteasome inhibitors.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.SevereMethotrexate (high-dose)Acute — within hours to days of infusion.AKI in ~2–12% of patients and 2–39% of high-dose courses, with severe (AKIN grade ≥2) nephrotoxicity in ~2% of courses.ModeratePemetrexedDelayed / cumulative; risk rises after ~10 cycles.Clinically relevant eGFR decline (≥25%) in ~21%; ~8% discontinue for nephrotoxicity. Cumulative-dose dependent.ModerateCAR-T Cell TherapyAcute — within the CRS window (first days–weeks).AKI ~5–33% across cohorts (commonly ~10–30%), mostly mild and reversible.ModeratePralatrexateDuring treatment cycles; exposure-dependent.Drug-specific renal-injury rates are not well quantified; renal handling resembles methotrexate, and severe renal impairment substantially increases pralatrexate exposure and toxicity (more cytopenias/mucositis). Antifolate crystal-related tubular injury is therefore a class-based, conservative concern rather than a measured rate.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).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).ModerateSirolimusVariable—weeks to months after initiation or dose escalation; proteinuria characteristically emerges or worsens within months after calcineurin-inhibitor withdrawal/conversion.New or worsening proteinuria occurs in a substantial minority of treated patients in transplant cohorts (more pronounced after conversion from a calcineurin inhibitor than with de novo use), but oncology-specific renal incidence is not well quantified and is described largely at the case and small-series level. Acute renal dysfunction (e.g., delayed graft recovery) is recognized but variable. Reported rate: proteinuria in 23.1% — 18 of 78 kidney, pancreas and islet transplant recipients given sirolimus de novo or after conversion, 5 of the 18 (27.8%) reaching nephrotic range; a transplant-immunosuppression figure, not an oncology one (Franco 2007, PMID 17362756).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.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).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.ModerateIbrutinibHypertension develops over weeks–months (can be early); tumor lysis is early (first cycle); glomerular/interstitial lesions are case-level over weeks to months.New or worsened hypertension is common (~26% in a real-world CLL cohort comparing it with acalabrutinib; higher with longer follow-up). AKI at CLL presentation and with tumor lysis is well described. Drug-attributable AKI from interstitial nephritis or glomerular endotheliosis is case-level.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.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.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.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%.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.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).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.ModerateNivolumabCharacteristically delayed compared with other drug-induced AIN: median time from ICI initiation to AKI was about 14 weeks (IQR 6-37) in a 138-patient multicenter cohort, and 91 days in the original series; onset ranges from weeks to many months and can follow drug discontinuation.Clinically significant ICI-attributed AKI is uncommon but not rare. A 2023 systematic review/meta-analysis of real-world data (18 studies, ~12,000 ICI-treated patients) found a pooled incidence of all-cause AKI during ICI therapy of about 16%, but AKI specifically attributed to the ICI of roughly 3.5%. Risk is higher with combination ICI regimens (e.g., nivolumab-ipilimumab) than with PD-1 monotherapy. Among biopsied ICI-AKI, acute tubulointerstitial nephritis is the dominant lesion (>90%); glomerular lesions and thrombotic microangiopathy are reported 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.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.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.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.ModerateOxaliplatinAcute if immune-mediated (often on re-challenge).Lowest nephrotoxic potential of the platinums; AKI is rare and case-level, in some cases immune-mediated.MildmTOR InhibitorsWeeks–months.Everolimus commonly causes all-grade proteinuria, with high-grade uncommon; mTOR-inhibitor proteinuria/FSGS is well described. Temsirolimus case-level only.MildErlotinibWeeks to months after starting therapy; proteinuria/creatinine typically improve over weeks after discontinuation in reported cases.Glomerular disease (including minimal-change-type nephrotic syndrome) and acute kidney injury are reported rarely, at the case level; pharmacovigilance data show measurable disproportionality signals for AKI/renal failure (and rare TMA) but no robust trial-based incidence. Reported rate: proteinuria in 3% — Erlotinib-MONOTHERAPY comparator arm of 4 randomized controlled trials in EGFR-mutation-positive advanced NSCLC (Deng 2022, PMID 35985780).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.MildImatinibEdema 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.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.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).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.Mild