ATN

Acute Tubular Necrosis

Direct death of tubular epithelial cells — the dose-limiting lesion of the platinums and zoledronate.

65agents

Where it strikes

Proximal Tubule

Bulk reabsorption + drug uptake (OCT2, OATs)

Distal Tubule / Collecting Duct

Fine-tuning of Na, K, Mg, acid & water

See it on the nephron

Severity mix

Severe· 5Moderate· 41Mild· 19

Reversibility

Often irreversible· 1Partially reversible· 18Variable· 9Reversible· 37

Signature offenders

Agents 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%.Severe PemetrexedDelayed / cumulative; risk rises after ~10 cycles.Clinically relevant eGFR decline (≥25%) in ~21%; ~8% discontinue for nephrotoxicity. Cumulative-dose dependent.Moderate Zoledronic acidAcute — days to weeks after infusion(s).Nephrotoxicity is the dose-limiting toxicity but largely avoidable; no precise population rate.Moderate NedaplatinDays 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.Moderate AzacitidineDuring 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).Moderate Plicamycin (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.Moderate Enfortumab 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 notably 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.Moderate Trastuzumab 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.Moderate LenalidomideVariable; 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.Moderate Datopotamab 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 actually lower than chemotherapy (~21%), and kidney-specific events were not prominent.Moderate TrabectedinRhabdomyolysis 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). For context, the dominant organ toxicity is hepatic — grade 3-4 transaminitis fell from ~34% to ~2% with dexamethasone premedication.Moderate PentostatinDuring 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.Moderate RaltitrexedWithin 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 dedicated pharmacokinetic 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 specifically because of crystal-related nephrotoxicity.Moderate Melphalan 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).Moderate ProcarbazineVariable; 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.Moderate Samarium-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.Moderate CarboplatinAcute when it occurs (high-dose regimens).Clinically significant nephrotoxicity uncommon at standard doses; emerges mainly at high/myeloablative doses.Mild OxaliplatinAcute if immune-mediated (often on re-challenge).Lowest nephrotoxic potential of the platinums; AKI is rare and case-level, often immune-mediated.Mild BRAF / MEK InhibitorsAcute–subacute during therapy.No denominator-based rate; pharmacovigilance shows vemurafenib > dabrafenib. Mild creatinine elevation common, serious AKI uncommon.Mild EncorafenibWeeks 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 grade 3-4 events with encorafenib plus binimetinib.Mild CobimetinibWeeks into therapy.AKI with BRAF/MEK therapy is uncommon and mostly mild; notably, a pharmacovigilance analysis found that adding a MEK inhibitor to vemurafenib was associated with a ~60% reduction in acute kidney injury versus vemurafenib alone.Mild IbandronateAcute 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.Mild LurbinectedinVariable 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.Mild SonidegibCK elevations during the first weeks-to-months of therapy; rhabdomyolysis-driven AKI would follow a significant muscle-injury event.Asymptomatic creatine-kinase elevation is notably more common with sonidegib than vismodegib (a class-distinguishing signal; increased CK is among its characteristic labs), and rhabdomyolysis is a labeled but rare event. Clinically significant pigment nephropathy/ATN is uncommon but is the feared renal consequence.Mild BleomycinPharmacokinetic 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.Mild Altretamine (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.Mild

Also associated

Agents 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 proximal tubulopathy is near-universal; overt Fanconi ~5% (range 1.4–30%), higher in young children.Severe StreptozocinWithin 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. A single re-challenge after a stable course can still precipitate acute renal failure.Severe CarfilzomibVariable — 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, TMA occurred at ~1.6-4.2 events per 1,000 patient-cycles, with most patients hypertensive and almost all developing AKI. Pharmacovigilance (FAERS) shows carfilzomib carries by far the strongest TMA signal among proteasome inhibitors.Severe VenetoclaxAcute — 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, clinical TLS fell to ~3% (e.g., grade 3/4 laboratory TLS 3.1% in MURANO), and structured protocols can drive it near zero.Severe Methotrexate (high-dose)Acute — within hours to days of infusion.AKI in ~2–12% of high-dose courses.Moderate CAR-T Cell TherapyAcute — within the CRS window (first days–weeks).AKI ~5–33% across cohorts (commonly ~10–30%), mostly mild and reversible.Moderate PralatrexateDuring 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.Moderate ClofarabineEarly, 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.Moderate SirolimusVariable—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.Moderate BlinatumomabEarly, 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.Moderate TeclistamabEarly, 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.Moderate TalquetamabEarly, 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.Moderate ElranatamabEarly, 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.Moderate Sacituzumab 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).Moderate EnasidenibDifferentiation 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.Moderate IbrutinibHypertension 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.Moderate Tretinoin (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.Moderate Arsenic 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.Moderate RituximabAcute — 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.Moderate ObinutuzumabAcute — within hours to days of the first (split) dose.Carries a notably 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.Moderate TagraxofuspTypically 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 (grade >=3 in ~7%, with rare deaths) in the pivotal trial; 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.Moderate TarlatamabCRS 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.Moderate LifileucelAcute — 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%.Moderate Idecabtagene 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.Moderate Ciltacabtagene 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.Moderate FotemustineDelayed — 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.Moderate Nimustine (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 in practice is hematologic (delayed myelosuppression).Moderate MechlorethamineTLS within hours to days of effective cytoreduction in bulky lymphoma.Direct nephrotoxicity is not a defining feature. The principal renal hazard is tumor lysis syndrome when treating bulky, rapidly proliferating lymphoma; incidence specifically attributable to mechlorethamine is not quantified because it is used within multi-agent regimens. The 0.016%/0.02% topical gel shows no detectable systemic absorption.Moderate AmsacrineTLS within hours to days of effective cytoreduction.Direct nephrotoxicity is not a prominent feature. The main renal hazard is tumor lysis syndrome during leukemia induction/salvage; incidence specific to amsacrine is not quantified. Pharmacokinetic studies show renal elimination plays only a minor role, with clearance dominated by hepatic metabolism and biliary excretion.Moderate Strontium-89 chlorideHematologic nadir typically develops over several weeks (e.g., weeks 4-8) given the long physical half-life; any renal/excretion-related concern relates to the early post-injection days when urinary excretion is highest.Intrinsic nephrotoxicity is not a defining or well-quantified effect; the prominent toxicity is transient myelosuppression (e.g., reversible hematologic toxicity reported in roughly half of treated patients in small series). Renal events are uncommon and not reliably enumerated.Moderate mTOR InhibitorsWeeks–months.Everolimus all-grade proteinuria ~10–14%, high-grade ~1–2%. Temsirolimus case-level only.Mild ErlotinibWeeks 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.Mild AfatinibDays 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.Mild ImatinibEdema 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.Mild BinimetinibWeeks 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.Mild SotorasibWhen 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.Mild AdagrasibEarly — 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.Mild PegaspargaseToxicities 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. For context, 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).Mild MobocertinibDiarrhea 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.Mild

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