The Injury Atlas See it on the nephron
LYTE
Electrolyte Wasting
Renal loss of magnesium, potassium or calcium — cisplatin and the anti-EGFR antibodies.
129agents
Where it strikes
Distal Tubule / Collecting Duct
Fine-tuning of Na, K, Mg, acid & water
Severity mix
Severe· 5Moderate· 56Mild· 68
Reversibility
Often irreversible· 1Partially reversible· 11Variable· 14Reversible· 103
Signature offenders
22Agents for which electrolyte wasting is the defining renal lesion.
NecitumumabDevelops cumulatively over weeks of repeated dosing and worsens with continued therapy; magnesium should be checked before each dose and for at least 8 weeks after completion because deficits persist.Grade 3-4 hypomagnesemia occurred in about 9% of patients receiving necitumumab plus chemotherapy versus 1% with chemotherapy alone in the pivotal SQUIRE trial; any-grade hypomagnesemia is substantially more frequent (a majority of patients on EGFR-antibody therapy develop some magnesium fall over time).ModerateErdafitinibEarly — typically within the first 1-2 cycles, used to guide pharmacodynamic up-titration.Hyperphosphatemia is the most common, on-target class adverse event — reported in the large majority of treated patients (~73-78% across studies) and used as a pharmacodynamic marker for protocol-driven dose up-titration. Grade >=3 hyperphosphatemia is much less frequent (~2%).ModeratePemigatinibEarly — within the first cycles.Hyperphosphatemia is the most common adverse event in the pivotal FIGHT-202 trial, affecting roughly 60% of patients (any grade), with low rates of severe events; it is on-target and managed with monitoring, diet, and binders.ModerateFutibatinibEarly — within the first cycles.Hyperphosphatemia is the most common adverse event, reported in the large majority of patients in the pivotal FOENIX-CCA2 trial (~85% any grade, most low-grade); it is on-target, dose-related, and confirmed as a pharmacodynamic effect in first-in-human work.ModerateDenosumabWithin days to a few weeks of dosing (nadir often around 1-2 weeks); can be prolonged given the drug's months-long duration of effect and the absence of a reversal agent.Denosumab is not directly nephrotoxic and is not renally cleared, but the risk of severe hypocalcemia rises sharply as kidney function declines. In a population-based cohort, severe hypocalcemia occurred in 0.2% of all new users but in 14.9% of those with eGFR <15 mL/min/1.73 m2 or on dialysis (mild hypocalcemia 24.1% in that group).ModerateAbirateroneWithin the first weeks of therapy; recurs if glucocorticoid coverage is inadequate or interrupted.Mineralocorticoid-excess effects are common: in COU-AA-301 fluid retention, hypertension and hypokalemia were all more frequent than with placebo-prednisone. Severe (grade 3–4) hypokalemia, occasionally to 1.7–2.1 mEq/L, is reported even with concomitant prednisone. Meta-analysis confirms an increased relative risk of hypertension.ModerateInfigratinibEarly (first cycle); reversible and dose-dependent, normalizing during the 7-day off-drug interval of the 21-on/7-off cycle.Hyperphosphatemia is the most common adverse event and the defining FGFR class effect — it occurred in 83 of 108 patients (~77%, any grade) in the pivotal trial. Infigratinib-specific nephrocalcinosis/calciphylaxis rates are not quantified (case reports/series only).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.ModerateDactinomycin (actinomycin D)TLS within hours to days of initiating effective chemotherapy; VOD typically within the first weeks of treatment.Direct nephrotoxicity is not an established feature of dactinomycin. The clinically relevant renal risk is tumor lysis syndrome (TLS) when used against bulky, chemosensitive pediatric tumors; precise incidence attributable to dactinomycin alone is not quantified, as it is given in multi-agent regimens.ModerateMechlorethamineTLS within hours to days of effective cytoreduction in bulky lymphoma.Direct nephrotoxicity is not a defining feature. The principal renal hazard is tumor lysis syndrome when treating bulky, rapidly proliferating lymphoma; incidence specifically attributable to mechlorethamine is not quantified because it is used within multi-agent regimens. The 0.016%/0.02% topical gel shows no detectable systemic absorption.ModerateAmsacrineTLS within hours to days of effective cytoreduction.Direct nephrotoxicity is not a prominent feature. The main renal hazard is tumor lysis syndrome during leukemia induction/salvage; incidence specific to amsacrine is not quantified. Pharmacokinetic studies show renal elimination plays only a minor role, with clearance dominated by hepatic metabolism and biliary excretion.ModerateMitotaneAdrenal insufficiency and its electrolyte/volume consequences develop over weeks of therapy as adrenolytic effect accrues; cisplatin-associated AKI in EDP-M is acute, within days of chemotherapy cycles.Intrinsic mitotane nephrotoxicity is not characteristically quantified. Clinically important renal events are indirect (adrenal insufficiency-related electrolyte/volume disturbance) or attributable to co-administered cisplatin in EDP-M; incidence not reliably enumerated for mitotane alone.ModerateStrontium-89 chlorideHematologic nadir typically develops over several weeks (e.g., weeks 4-8) given the long physical half-life; any renal/excretion-related concern relates to the early post-injection days when urinary excretion is highest.Intrinsic nephrotoxicity is not a defining or well-quantified effect; the prominent toxicity is transient myelosuppression (e.g., reversible hematologic toxicity reported in roughly half of treated patients in small series). Renal events are uncommon and not reliably enumerated.ModerateCetuximab & PanitumumabDevelops over weeks of therapy; worsens with duration.Any-grade hypomagnesemia ~17% overall (RR 5.83); higher with panitumumab. Prolonged therapy >30%.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.MildNirogacestatDuring therapy; not well characterized.Electrolyte and phosphate disturbances (including hypophosphatemia) are reported among adverse events; the characteristic DeFi-trial toxicities were diarrhea, rash, nausea, fatigue and ovarian dysfunction. Renal-specific incidence is not well quantified.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).MildVinflunineElectrolyte/prerenal effects can appear within days of a cycle; PK accumulation in renal impairment is immediate but mitigated by protocol dose reduction.No strong direct nephrotoxic signal. Vinflunine is given to renally impaired, cisplatin-unfit patients with a defined dose-reduction schema, and tolerability in renal impairment mirrors that of patients with normal renal function once dose-banded. SIADH/hyponatremia is a class-level vinca-alkaloid effect rather than a quantified vinflunine-specific rate.MildTeniposideNo characteristic renal onset; pharmacokinetic exposure effects are immediate but clinically modest.Minimal direct nephrotoxicity. Teniposide is highly protein-bound with low renal clearance (only ~10-25% of a dose is recovered in urine versus a larger fraction for etoposide), so the kidney is a minor elimination route and direct renal injury is not a characteristic toxicity. Renal relevance is pharmacokinetic/exposure-related and not quantified as a discrete nephrotoxicity rate.MildOctreotideNot applicable for intrinsic injury; pharmacokinetic accumulation in renal failure is gradual.No characteristic intrinsic nephrotoxicity; octreotide is generally considered kidney-neutral. Renal events are rare, indirect, and not reliably quantified. Mild electrolyte disturbances are uncommon and not well enumerated.MildLanreotideNot applicable for intrinsic injury; exposure rises gradually in renal impairment.No characteristic intrinsic nephrotoxicity; lanreotide is generally kidney-neutral. Renal adverse events are not a defining feature and are not reliably quantified; mild electrolyte effects are uncommon.MildDarolutamideNot applicable for intrinsic injury; exposure differences in renal impairment are present from initiation and steady state (reached in ~2 days).No characteristic intrinsic nephrotoxicity. In ARAMIS, rates of adverse events including hypertension were similar to placebo. Renal-relevant findings are pharmacokinetic (increased exposure in severe renal impairment); intrinsic renal injury incidence not meaningfully quantified.Mild
Also associated
107Agents that cause electrolyte wasting as a secondary pattern alongside a different signature lesion.
CisplatinAcute — creatinine peaks ~day 4–7; magnesium wasting can persist for months.AKI in ~20–35% per cycle (classic teaching: ~1 in 3). Hypomagnesemia in 40–100%.SevereIfosfamideAcute tubulopathy during therapy; chronic Fanconi/CKD can emerge months–years later.Subclinical proximal tubulopathy is near-universal; overt Fanconi ~5% (range 1.4–30%), higher in young children.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. A single re-challenge after a stable course can still precipitate acute renal failure.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, clinical TLS fell to ~3% (e.g., grade 3/4 laboratory TLS 3.1% in MURANO), and structured protocols can drive it near zero.SevereTegafur-uracil (UFT)Variable; TMA/HUS typically emerges after weeks to months of cumulative exposure.Direct renal injury from UFT is rare and largely class-level. Fluoropyrimidine-associated thrombotic microangiopathy / hemolytic-uremic syndrome is a rare, mostly case-report-level event, frequently in combination regimens (e.g., with mitomycin C). No reliable drug-specific incidence rate is established.SeverePemetrexedDelayed / cumulative; risk rises after ~10 cycles.Clinically relevant eGFR decline (≥25%) in ~21%; ~8% discontinue for nephrotoxicity. Cumulative-dose dependent.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.ModerateBendamustineTLS within hours to days of the first cycle; TMA delayed and rare.Direct nephrotoxicity is uncommon; the principal renal risk is acute kidney injury from tumor lysis syndrome in high-burden disease, classically during the first cycle. TLS with renal failure is documented from the first reported case onward; TMA is rare and case-level.ModerateCytarabineHours to days after initiating therapy in high-burden disease.Intrinsic tubular nephrotoxicity is uncommon; the major renal risk is AKI from tumor lysis syndrome during leukemia/lymphoma cytoreduction, reported at case and series level including fatal TLS. Direct cytarabine-nephrotoxicity primary literature is genuinely sparse.ModerateFludarabineTLS within days of starting therapy; systemic toxicity accrues with impaired clearance.Direct nephrotoxicity is uncommon; the chief renal risks are tumor-lysis-syndrome AKI during cytoreduction and increased systemic toxicity when the renally cleared drug accumulates in renal impairment. About 60% of the active metabolite 2-F-ara-A is renally eliminated, so renal function directly drives exposure.ModerateAzacitidineDuring treatment cycles (days to weeks).Proximal tubular dysfunction (proximal/type 2 renal tubular acidosis, polyuria, and glucose/amino-acid/electrolyte wasting) was described with higher-dose azacitidine; with current low-dose subcutaneous/IV regimens overt AKI is uncommon and renal incidence is not well quantified (case-level).ModeratePlicamycin (mithramycin)With repeated / cumulative dosing (days to weeks).Cumulative, dose-related nephrotoxicity is a recognized dose-limiting toxicity; when used for hypercalcemia, its antiresorptive potency can overshoot to symptomatic hypocalcemia. Precise modern incidence is not well quantified because the drug is now essentially obsolete.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.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.ModerateGlofitamabEarly — concentrated around cycle 1 step-up dosing and the first full dose.No direct tubular signal. AKI is case-level, downstream of CRS (~63% any-grade, grade >=3 in ~4% after obinutuzumab pretreatment and step-up dosing) and tumor lysis; renal incidence not separately quantified — emerging data.ModerateEnfortumab vedotinVariable; tubular/prerenal AKI tracks with intercurrent GI toxicity, and hyperglycemic-AKI events are often reported after the second or third dose.Renal injury is not a prominent or well-quantified trial signal, and EV is 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.ModerateTrastuzumab deruxtecanVariable; reported during ongoing therapy, sometimes resolving over months after discontinuation.Renal data are emerging and under-published. AKI/proteinuria are reported at case level; a reversible proximal-tubule Fanconi syndrome (glucosuria, phosphate/potassium wasting, non-anion-gap acidosis) has been described and attributed to the deruxtecan payload. Renal-specific incidence is not quantified.ModerateGemtuzumab ozogamicinEarly — tumor lysis with induction; VOD typically within weeks, notably around hematopoietic stem-cell transplant.Direct nephrotoxicity is not a prominent signal. AKI is chiefly secondary to tumor lysis syndrome and to hepatic sinusoidal obstruction syndrome/veno-occlusive disease (VOD), the latter a recognized, sometimes fatal complication that produces hepatorenal-type AKI. Renal-specific incidence is not quantified.ModerateInotuzumab ozogamicinEarly — tumor lysis during initial therapy; VOD typically peri-transplant.Direct nephrotoxicity is not a prominent signal. AKI is chiefly secondary to tumor lysis and to hepatic sinusoidal obstruction syndrome/veno-occlusive disease (VOD) — a notable, sometimes fatal complication, particularly around subsequent allogeneic stem-cell transplant. Renal-specific incidence is not quantified.ModerateIvosidenibDifferentiation syndrome typically days to weeks after starting therapy (median ~30 days); tumor lysis early during cytoreduction.Differentiation (IDH) syndrome is a recognized, potentially fatal complication — reported in roughly 10-19% of AML patients across IDH-inhibitor experience (e.g. ~10.4-11.7% with the IDH2 inhibitor enasidenib in pooled/phase 1-2 analyses) — and can drive AKI through capillary leak, fluid overload, hypotension, and inflammation; tumor lysis can also occur with cytoreduction.ModerateEnasidenibDifferentiation syndrome typically days to weeks after starting (median onset ~30 days; reported range days to ~4–5 months).IDH-inhibitor differentiation syndrome (the main route to AKI) occurs in roughly 10% of enasidenib-treated AML patients (10.4% any-grade in a pooled trial analysis; ~7% grade ≥3 in the first-in-human study). Tumor lysis is a secondary risk. Direct tubular nephrotoxicity is not well quantified.ModerateArsenic trioxideDifferentiation syndrome within the first weeks of induction; QT/electrolyte effects throughout treatment.Differentiation syndrome (the main route to AKI) occurs in a substantial minority of APL patients; grade 3–4 renal toxicity in ATO-based regimens is uncommon in randomized data. Direct nephrotoxicity is not well quantified, but QT prolongation and electrolyte disturbances are frequent and clinically important.ModerateRituximabAcute — typically within hours to a few days of the first infusion.Clinical tumor lysis with the first cycle is uncommon with modern prophylaxis (~1% clinical TLS in a real-world fractionated-rituximab aggressive-B-NHL series), but risk rises sharply with bulky disease, high LDH and Burkitt histology.ModerateObinutuzumabAcute — within hours to days of the first (split) dose.Carries a 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.ModerateAmivantamabElectrolyte changes during therapy and cumulative; AIN timing not well characterized (subacute, days–weeks after a triggering exposure by analogy to drug AIN).In CHRYSALIS, electrolyte disturbance — notably hypokalemia (grade 3–4 in ~5%) and hypomagnesemia/hypocalcemia — was among the notable laboratory adverse events, consistent with EGFR-pathway inhibition. Acute interstitial nephritis is an emerging, clinician-flagged signal that is not yet quantified in the published renal literature.ModerateRevumenibDuring early treatment as leukemic differentiation and lysis occur (first days–weeks).Differentiation syndrome and tumor lysis syndrome are recognized 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 enrolment) — which can cause capillary leak, fluid overload and AKI. Tumor-lysis risk accompanies rapid blast clearance. No drug-specific renal incidence is published.ModerateLutetium-177 PSMA-617 (vipivotide)Renal changes are delayed/gradual; xerostomia can appear early during treatment.Clinically significant nephrotoxicity is uncommon in trial populations and is not well quantified; in VISION renal adverse events were infrequent. Dosimetry consistently shows the kidney is the highest-dose internal organ, but the dose-limiting clinical toxicities are usually xerostomia (salivary/lacrimal uptake) and myelosuppression rather than renal failure.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). For context, the dominant organ toxicity is hepatic — grade 3-4 transaminitis fell from ~34% to ~2% with dexamethasone premedication.ModerateSelinexorEarly — within the first cycle/few weeks; front-loaded.Hyponatremia is common and dose-limiting. In STORM it occurred in ~22% of patients and was predominantly grade >=3 — the most common grade >=3 non-hematologic toxicity. In BOSTON any-grade hyponatremia affected roughly a third of the selinexor arm (grade 3-4 ~8-9%); in SADAL grade 3-4 hyponatremia occurred in ~8%.ModeratePentostatinDuring or after dosing cycles; generally reversible with dose reduction or discontinuation.At modern low doses clinically significant nephrotoxicity is uncommon and a precise contemporary incidence is not quantified; serious dose-related AKI was historically tied to higher-dose regimens. Tumor lysis can add a secondary AKI mechanism in bulky disease.ModerateIdecabtagene vicleucelWithin the first 1-2 weeks (the CRS window).Published CAR-T AKI incidence runs roughly 5-30% across cohorts and is mostly mild (KDIGO stage 1); in one cohort any-grade AKI reached ~30% by day 100 with rapid recovery. Most AKI parallels cytokine-release syndrome (CRS) and reverses within ~30 days.ModerateCiltacabtagene autoleucelAKI in the first 1-2 weeks; the movement disorder is delayed (weeks).CRS-associated AKI mirrors the BCMA CAR-T class (roughly 5-30% across cohorts, mostly mild) and generally reverses with supportive care. A distinct, non-renal signature toxicity is a delayed movement-and-neurocognitive (parkinsonism-like) syndrome.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.ModerateCopanlisibAcute and infusion-bound — within hours of each dose, resolving within ~24 h.On-infusion-day hyperglycemia occurs in ~50-56% (grade 3+ ~40%) and transient hypertension in ~30-40% (grade 3 ~25-30%), both peaking within hours of the infusion and largely resolving by the next day. Sustained renal injury is uncommon.ModerateGilteritinibDifferentiation syndrome from a few days up to ~3 months (often within the first month); TLS early; PRES variable.Differentiation syndrome (boxed warning) occurs in roughly 3% of treated patients and can cause capillary leak, fluid overload and renal dysfunction; tumor lysis and PRES are labeled risks. Discrete AKI incidence is not separately quantified and is largely a consequence of these syndromes.ModerateNeratinibDiarrhea characteristically within the first days-to-weeks; prerenal AKI follows uncontrolled fluid loss.Diarrhea is near-universal without prophylaxis: in ExteNET, grade 3 diarrhea occurred in ~40% without antidiarrheal prophylaxis, falling substantially with loperamide and dose-escalation strategies (CONTROL). The resulting volume-depletion prerenal AKI is not separately quantified.ModerateOlutasidenibDifferentiation syndrome within days to a few months (often early); tumor lysis early in treatment.Differentiation syndrome (boxed warning) occurred in ~14% of patients (grade >=3 ~9%, with rare fatality) in the pivotal cohort; tumor lysis is a labeled risk. Discrete AKI incidence is not separately quantified and is largely consequent on these syndromes.ModerateLoncastuximab tesirineEdema/effusions accumulate over cycles; prerenal changes track the fluid shifts.Edema and effusions (pleural, pericardial, peritoneal) are characteristic PBD-payload toxicities and were common in LOTIS-2; the resulting fluid shifts and AKI are not separately quantified. Tumor lysis is an additional consideration in responding lymphoma.ModerateMelphalan flufenamide (melflufen)Cytopenias within the first cycles; any renal change is typically subacute and multifactorial.Direct nephrotoxicity is not a prominent trial signal; the renal relevance is pharmacokinetic and disease-context. A dedicated phase II study (BRIDGE) in myeloma patients with moderate or severe renal impairment characterized melphalan exposure across renal function and supported a reduced 30 mg dose for moderate impairment, with no new safety signals but substantial treatment-emergent toxicity (including deaths in a heavily pretreated population). As a melphalan-delivery system, its renal liabilities mirror the alkylator class (myelosuppression, and the alkylator-associated risk of tubular injury at high exposure).ModerateCatumaxomabCytokine-release symptoms within hours of each intraperitoneal infusion; any prerenal AKI follows the inflammatory/volume insult.No characteristic intrinsic nephrotoxicity. The dominant treatment-related toxicity is cytokine-release-related (pyrexia, nausea, vomiting, chills, fatigue) plus intraperitoneal-administration effects (abdominal pain); transient transaminase rises and lymphopenia are common but usually clinically minor. Cytokine release with fever, GI losses, and large-volume ascites/paracentesis creates a setting for prerenal/hemodynamic AKI rather than a direct renal lesion. Drug-specific renal incidence is not quantified.ModerateFotemustineDelayed — weeks to months, and cumulative with repeated cycles; chronic interstitial injury may appear after prolonged exposure.Renal toxicity is generally reported as mild within fotemustine regimens, but, consistent with the nitrosourea class, delayed tubulointerstitial injury/ATN can occur; in one combination study renal toxicity was mild yet possibly contributed to two deaths. Drug-specific incidence is not well quantified and is often confounded by co-administered cisplatin.ModerateNimustine (ACNU)Delayed and cumulative — typically over months of repeated cycles, mirroring the nitrosourea class.Drug-specific human renal-toxicity data for nimustine are thin; renal risk is asserted largely at the class level. Like other nitrosoureas, cumulative dosing is associated with delayed tubulointerstitial injury and CKD, but a reliable nimustine-specific incidence is not established. Dose-limiting toxicity in practice is hematologic (delayed myelosuppression).ModerateDoxifluridineVariable; class-level TMA typically after prolonged cumulative exposure.No drug-specific nephrotoxicity incidence is established. Renal risk is inferred at the fluoropyrimidine-class level (rare TMA/HUS); direct doxifluridine renal injury reports are sparse.ModerateCarmofur (HCFU)Variable; class-level TMA after cumulative exposure.No established drug-specific renal incidence. Renal risk is class-level (rare fluoropyrimidine TMA/HUS). Carmofur's characteristic serious toxicity is leukoencephalopathy, not nephrotoxicity.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.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.No denominator-based rate; pharmacovigilance shows vemurafenib > dabrafenib. Mild creatinine elevation common, serious AKI uncommon.MildMelphalanDays after high-dose administration.High-dose intravenous melphalan can cause hyponatremia/SIADH; in a small high-dose series most patients showed declining sodium, but this is reported at case/series level rather than as a large quantified rate. Notably, melphalan PK is not adversely affected by renal failure, so transplant in renal impairment is feasible with dose reduction.MildTemozolomideDuring cycles of therapy; variable.Generally renally well tolerated; renal clearance of the parent drug is a minor elimination pathway and dedicated PubMed searches for temozolomide nephrotoxicity/SIADH return essentially no indexed series. Hyponatremia/SIADH is an occasional, case/toxicity-table-level event, and rare acute interstitial nephritis has been reported in combination contexts.MildDecitabineEarly after a treatment cycle (days) for tumor lysis; TMA over weeks.Tumor lysis syndrome with AKI is a recognized but uncommon complication when bulky/proliferative disease responds; renal incidence specific to decitabine is not well quantified (case-level). Rare biopsy-proven renal thrombotic microangiopathy has been reported.MildHydroxyureaVery early (within 12-24 hours of high-dose treatment).Acute tumor lysis syndrome from hydroxyurea is rare and reported at case level, almost exclusively with high-dose cytoreduction of leukemias carrying a high blast burden. Standard-dose hydroxyurea is not characteristically nephrotoxic.MildNelarabineEarly after treatment initiation (days).Tumor lysis syndrome with attendant AKI is a labeled risk when bulky T-ALL responds rapidly; drug-specific renal incidence is not well quantified (case-level). The dose-limiting and most feared toxicity is neurologic, not renal.MildOsimertinibReported within roughly the first weeks to a few months of therapy (around two months in several published cases).Syndrome of inappropriate antidiuretic hormone (SIADH)-type hyponatremia is described at the case level; occasional acute kidney injury and rare proteinuria are reported. Not quantified as a discrete renal endpoint in randomized data, where overall renal adverse events are uncommon.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 across renal-function subgroups, including dialysis. The principal renal hazard is tumor lysis syndrome (TLS), which is uncommon and case-level in myeloma.MildThalidomideTumor lysis within days of initiation in high-burden disease; bradycardia over weeks of dosing.Thalidomide is not a direct nephrotoxin; the principal renal hazard is tumor lysis syndrome, which is uncommon in myeloma and reported at the case level. Sinus bradycardia is a recognized dose-related non-renal effect that, with the drug’s sedative/hypotensive properties, can compound prerenal physiology. Venous thromboembolism is the other dominant class toxicity.MildCrizotinibCreatinine rise often within weeks and reverses on discontinuation; cysts develop and grow over months.Crizotinib commonly causes a reversible rise in serum creatinine and is distinctively associated with the development and progression of complex renal cysts. Peripheral edema and electrolyte disturbances (including hypophosphatemia and hypokalemia) are reported. In real-world ALK-inhibitor cohorts, creatinine-based AKI/CKD events are frequent but mostly mild and reversible; frank kidney failure is uncommon.MildLorlatinibMetabolic effects and edema appear within weeks of starting therapy.Lorlatinib is characterized by prominent metabolic effects - hypercholesterolemia and hypertriglyceridemia occur in the majority of patients (the leading grade 3/4 toxicity in the CROWN trial) - plus peripheral edema. Direct renal toxicity is limited and, like other ALK inhibitors, creatinine elevations are generally mild and reversible. Renal effects are not well quantified specifically for lorlatinib.MildRucaparibWithin the first weeks of treatment.Early reversible serum-creatinine elevation is common and partly drug-specific: rucaparib is a recognized inhibitor of renal cation transporters, and a pooled meta-analysis found markedly higher odds of creatinine rise vs placebo across the class, but grade >=3 renal events were rare (<1%).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.MildDaratumumabTumor lysis (if any) early; renal benefit accrues over treatment as paraprotein/free light chains fall.Direct nephrotoxicity is uncommon; tumor lysis can occur with high tumor burden. Crucially, daratumumab-based regimens IMPROVE outcomes (PFS, and OS in relapsed disease) in myeloma patients with renal insufficiency, including dialysis-dependent patients, and can drive renal recovery.MildIsatuximabTumor lysis (if any) early; renal benefit over the treatment course.Direct nephrotoxicity is uncommon; tumor lysis can occur with high tumor burden. In the ICARIA-MM and IKEMA renal-impairment subgroups, isatuximab regimens remained effective and produced renal responses; real-world data show inferior PFS with eGFR <60 but persistent benefit.MildPalbociclibOften within the first 1-2 cycles (median onset roughly 30-35 days); creatinine plateaus and reverses after dose hold or discontinuation.A reversible rise in serum creatinine is common, but true structural kidney injury is uncommon. CDK4/6 inhibitors block the proximal-tubule transporters that secrete creatinine, producing a 'pseudo-AKI' picture. In a single-centre cohort, 17.5% of palbociclib-treated patients met creatinine-based AKI criteria, and when cystatin C was available, 73% of those events proved to be pseudo-AKI rather than a true GFR decline.MildRibociclibFirst cycles (median onset roughly 6 weeks for the creatinine signal); reversible on hold or discontinuation. QTc effects are dose- and concentration-dependent and seen early.Like other CDK4/6 inhibitors, ribociclib produces a frequent, reversible creatinine rise via inhibition of tubular creatinine secretion (pseudo-AKI ~14% in a class-effect analysis); clinically meaningful structural AKI is uncommon. A retrospective cohort of palbociclib/ribociclib patients found a >=20% creatinine-clearance decline in about 23%.MildEtoposideTLS typically within hours to a few days of starting cytotoxic therapy in sensitive tumors; exposure-related myelosuppression accrues over cycles.Etoposide is renally cleared (~30-40% as unchanged drug, so dose-adjust in renal impairment) and is a frequent component of regimens for bulky, rapidly proliferating tumors that can trigger tumor lysis syndrome (TLS). Direct etoposide nephrotoxicity is not a recognized signal; TLS-related AKI risk depends on tumor burden and tumor type rather than a per-drug rate.MildVincristineDays after dosing, often within the first 1-2 cycles; resolves after the drug is withheld.Vincristine-associated SIADH with hyponatremia is a recognized but uncommon, largely case-level adverse effect; a global pharmacovigilance analysis estimated a reporting rate of about 1.3 per 100,000 treated patients, with a possible over-representation in Asian patients. FAERS disproportionality analysis also flags inappropriate ADH secretion as a vinca-class signal.MildVinblastineDays after administration, generally within the first cycles.As a vinca alkaloid, vinblastine can cause SIADH with hyponatremia; this is a recognized class effect reported at case level rather than as a quantified rate. Rare Raynaud phenomenon and other vascular events (especially in germ-cell regimens) are also described.MildVinorelbineDays after dosing, sometimes after several cycles (one report after three cycles).SIADH with hyponatremia is reported with vinorelbine at case level; FAERS pharmacovigilance analysis of vinca alkaloids flags inappropriate ADH secretion as a shared signal. Quantitative incidence is not established.MildIbandronateAcute when it occurs (days), related to dose and infusion rate; antiresorptive electrolyte effects within the first days.Lower renal risk than zoledronate or pamidronate. In a 2-year phase III breast-cancer trial, adverse renal events with IV ibandronate were ~4% versus ~4.5% with placebo — essentially at background. Bisphosphonates as a class can cause toxic ATN (zoledronate) or collapsing FSGS (pamidronate), but ibandronate is the renal-safety outlier within the class.MildEnzalutamideHypertension emerges over weeks to months of therapy.Hypertension is the dominant renovascular signal. A 2024 JAMA Oncology meta-analysis of androgen-receptor signaling inhibitors found a markedly increased risk of grade ≥3 hypertension (relative risk ~2.25); an earlier meta-analysis showed the same for enzalutamide specifically. Direct intrinsic kidney injury is uncommon; rare hyponatremia appears mainly in combination regimens.MildTamoxifenFlare hypercalcemia within the first days to weeks; hyponatremia case-level and variable.Direct nephrotoxicity is not a feature. Tumor-flare hypercalcemia occurs early in patients with osteolytic bone metastases (about 13% — 12 of 93 — in one hypercalcemic breast-cancer series). Euvolemic hyponatremia (SIADH-type) is reported only at the case level.MildLeuprolideMonths to years (metabolic/cardiovascular and skeletal).No characteristic direct nephrotoxicity. Androgen-deprivation therapy is associated with metabolic syndrome, insulin resistance, dyslipidemia and increased cardiovascular disease, which raise long-term renovascular risk; a large matched cohort (n≈19,079) found CKD to be an independent risk factor for ADT-associated fracture, and preclinical models show GnRH-agonist-induced metabolic syndrome and atherosclerosis.MildPirtobrutinibEarly after initiation in high-burden disease (first cycle); TLS is usually a single early event.Direct nephrotoxicity is not characteristic. Tumor lysis syndrome is an identified risk when rapidly debulking high-burden lymphoid malignancy; renal-specific incidence is low and not well quantified. BTK inhibitors as a class are also associated with hypertension and bleeding/atrial fibrillation (non-renal).MildLazertinibDuring therapy; case-level and variable.Hyponatremia is a recognized signal of third-generation EGFR TKIs (an osimertinib-class effect); for lazertinib specifically the renal/sodium data are limited and not well quantified. EGFR blockade also causes electrolyte wasting (hypomagnesemia, hypokalemia), and combination with amivantamab adds to these effects.MildRepotrectinibEarly after initiation; stable thereafter (a step change, not a progressive decline).An apparent rise in serum creatinine is described that often reflects inhibition of tubular creatinine secretion rather than a true fall in GFR (pseudo-AKI). Genuine intrinsic nephrotoxicity is not a characteristic feature and is not well quantified. This pattern is increasingly recognized across kinase inhibitors (e.g., ALK TKIs, where most creatinine-based eGFR changes do not require treatment change).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.MildSunvozertinibElectrolyte changes can appear within the first weeks to months of therapy; hypomagnesemia risk rises with treatment duration.No established AKI rate. As with the EGFR-inhibitor class, the renal-relevant signal is electrolyte disturbance — particularly hypomagnesemia (renal Mg wasting) and diarrhea-driven losses, with a hyponatremia/SIADH-like pattern possible — rather than structural nephron injury. WU-KONG6 reported diarrhea and skin/EGFR-pathway toxicities as dominant; renal-specific events are not quantified.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.MildMomelotinibAny tumor-lysis risk is early; otherwise no defined renal onset.No established intrinsic nephrotoxicity. As a JAK-inhibitor-class agent, dominant toxicities are hematologic (thrombocytopenia), infection, and (notably) peripheral neuropathy; renal injury is not a defining signal. Tumor-lysis at initiation and prerenal factors are the indirect renal considerations.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.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.MildLurbinectedinVariable across cycles (not tightly defined) — monitor with each dose.Not directly tubulotoxic; clinically significant AKI is rare and arises from rhabdomyolysis or tumor lysis. Rhabdomyolysis was formally recognized post-approval (FDA FAERS) and as an isolated phase 1 dose-limiting toxicity; the trial rate is not quantified. The dominant toxicity is hematologic (grade >=3 neutropenia ~41%) with frequent transaminase elevations.MildCladribineTumor-lysis AKI is acute (24-72 h); high-dose sensorimotor neuropathy is delayed (weeks).At standard hairy-cell-leukemia doses cladribine is renally quiet; clinically significant nephrotoxicity is uncommon and dose-related, worst at historical high investigational doses. The dominant renal hazard is tumor lysis syndrome in bulky/leukocytotic disease, reported at the case level rather than as a population incidence.MildMobocertinibDiarrhea early (within the first week); AKI follows. Prerenal AKI is typically reversible with early volume repletion and diarrhea control.Diarrhea is near-universal: any-grade ~83% (up to ~93% pooled), grade >=3 ~20-21%, with median onset ~5 days. AKI is predominantly prerenal; a real-world cohort reported grade >=3 renal failure in ~6%. Precise drug-attributable AKI and QT rates are not robustly quantified beyond class warnings.MildMitoxantroneTumor lysis hours to days post-infusion.Direct nephrotoxicity is low and not quantified; the principal renal risk is tumor lysis syndrome when used in bulky/rapidly proliferating hematologic malignancies. Benign blue-green discoloration of urine/sclera is expected (the anthracenedione chromophore), not injury.MildIdarubicinHours to days after starting induction.Minimal intrinsic nephrotoxicity; the dominant renal threat is tumor lysis syndrome in acute leukemia. In one inv(16) AML induction cohort tumor-lysis AKI occurred in ~6%, with some requiring hemodialysis; a general drug-specific AKI rate is not quantified.MildVismodegibMuscle spasms within the first weeks-to-months; hyponatremia is sporadic and variable in timing.Muscle spasms are near-universal (~64-71%), with dysgeusia and alopecia close behind; hyponatremia is reported but uncommon and not precisely quantified for an SIADH mechanism. Direct kidney injury is rare.MildGlasdegibMuscle spasms and QT changes within early cycles; prerenal/electrolyte issues track intercurrent illness and intake.Muscle spasms, QT prolongation, cytopenias, edema, nausea and mucositis are the labeled toxicities; the FDA notes a use limitation in severe renal impairment (a renal-impairment trial was a post-marketing requirement). Direct nephrotoxicity is not a defined signal, and AKI is largely secondary (dehydration, sepsis, tumor lysis).MildMidostaurinTumor lysis early in induction; prerenal/electrolyte issues track intercurrent illness; edema across treatment.Given with intensive chemotherapy, the dominant toxicities are cytopenias, nausea/vomiting, mucositis, edema and QT changes; tumor lysis is a treatment-related (largely chemotherapy-driven) hazard. A midostaurin-specific direct nephrotoxicity is not described, and AKI is multifactorial (volume loss, sepsis, TLS).MildAsciminibHypertension can emerge across treatment; pancreatitis often early.Hypertension and pancreatitis (with amylase/lipase elevations) are recognized toxicities; thrombocytopenia/neutropenia are common. Asciminib has a notably cleaner profile than prior TKIs, and direct nephrotoxicity is not a defined signal — renal effects are largely hypertension-mediated.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 notable labeled toxicities; nausea/diarrhea contribute to volume shifts. Direct nephrotoxicity is not a defined signal and AKI, when it occurs, is secondary (fluid shifts, GI losses, mastocytosis mediator release).MildTazemetostatTumor lysis, if it occurs, is early after response; prerenal effects track intercurrent GI toxicity.Tazemetostat is generally well tolerated with low direct organ toxicity; the noted boxed risk is secondary T-cell lymphoma/myeloid malignancy. Tumor lysis is an uncommon, treatment-related concern in responding lymphoma. A discrete AKI rate is not quantified and direct nephrotoxicity is low.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.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.MildChlorambucilHyponatremia, when reported, has occurred during ongoing dosing, including with low doses; timing is variable.Chlorambucil has minimal direct nephrotoxicity. Drug-associated SIADH with hyponatremia is reported only rarely, in isolated case reports; tumor lysis is uncommon given its indolent-disease indications and gradual cytoreduction. No reliable incidence figure exists.MildBicalutamideIf AIN occurs, typically subacute over weeks of exposure (idiosyncratic).Bicalutamide is largely kidney-neutral. Pharmacokinetics are unaffected by renal impairment and no renal dose adjustment is required. Acute interstitial nephritis is, at most, a rare idiosyncratic case-report-level event; no meaningful incidence rate is established.Mild