The Injury Atlas Does the kidney recover? Cross-drug outcomesRepresentative per-agent crystal / obstructive nephropathy 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.
XTAL
Crystal / Obstructive Nephropathy
Intratubular precipitation of drug or metabolite — high-dose methotrexate and tumor lysis crystals.
46agents
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· 2Moderate· 27Mild· 17
Agents’ overall reversibility
Partially reversible· 6Variable· 7Reversible· 33
Agents’ onset window
How soon each agent’s kidney toxicity typically appears — a whole-drug tempo, not specific to this lesion.
Hyperacute (<24 h)· 1Acute (days)· 39Subacute (weeks)· 3Variable· 3
Real-world reporting for this lesion
FAERS across all lesions →Agents with a disproportionate FAERS reporting signal for crystal / obstructive nephropathy (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.
7Corroborated
Documented in the atlas profile and carrying a FAERS signal — the strongest claim the atlas makes.
31Documented, 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.
42Not 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.
0Reported 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.
AbirateroneAcalabrutinibBendamustineBevacizumabBicalutamideCabazitaxelCapecitabineCarboplatinCisplatinCladribineDarolutamideDenosumabEnfortumab vedotinEnzalutamideEverolimusGemcitabineHydroxyureaIbandronateIbrutinibImatinibIrinotecanLanreotideLeuprolideMethotrexate (high-dose)Mitomycin CNaxitamabNilotinibNintedanibNiraparibOctreotidePacritinibPamidronatePexidartinibPolatuzumab vedotinRadium-223 dichlorideRegorafenibRelacorilantRibociclibRituximabRuxolitinibSelumetinibSonidegibTamoxifenTisotumab vedotinTopotecanTretinoin (ATRA)Trifluridine/tipiracilVandetanibZoledronic acid
49 agents with a significant XTAL reporting signal.
Management approach
Full framework →Prevent precipitation; for established high-dose methotrexate toxicity, glucarpidase rapidly cleaves circulating drug.
Drug-level levers
- Hold further methotrexate until clearance and renal recovery.
- For tumor-lysis urate nephropathy, prophylaxis is the key lever.
Pharmacologic toolkit
- Hydration + urinary alkalinization — Vigorous IV hydration and urine alkalinization keep methotrexate soluble.
- Leucovorin rescue — High-dose leucovorin guided by serial methotrexate levels.
- Glucarpidase — For delayed methotrexate clearance / AKI: recombinant carboxypeptidase-G2 cleaves plasma methotrexate, usually allowing recovery without dialysis.
- Rasburicase (tumor lysis) — For urate crystal nephropathy from tumor lysis, with hydration; also manage hyperphosphatemia.
When to biopsy
Not indicated — the diagnosis is clinical and biochemical (drug levels, uric acid, urine crystals).
Monitoring
- · Serial methotrexate levels, creatinine, urine pH
- · Uric acid, phosphate, potassium (tumor lysis)
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 crystal / obstructive nephropathy.
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.
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.Intl. Expert PanelConsensus Guideline for Use of Glucarpidase in Patients with High-Dose Methotrexate Induced Acute Kidney Injury and Delayed Methotrexate ClearanceOncologist 2018 · PMID 29079637For HDMTX infusions <=24 h, glucarpidase may be indicated when the methotrexate concentration is >30 uM at 36 h, >10 uM at 42 h, or >5 uM at 48 h together with a significantly elevated serum creatinine (indicating HDMTX-induced AKI); administer optimally within 48-60 h of infusion start, as it is far less effective beyond 60 h.
Cited incidence across agents
Where the literature gives a representative crystal / obstructive nephropathy figure, the agents ranked highest first. Hover a dot for its cited note.
Offending agents
Signature offenders
18Agents for which crystal / obstructive nephropathy is the defining renal lesion.
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, grade 3/4 laboratory TLS fell to 3.1% (MURANO), with clinical TLS rarer still, and structured protocols can drive it near zero.SevereSonrotoclaxEarly and dose-timed. Tumor lysis clusters around the initial ramp-up doses and the first full target dose — the window of maximal, synchronous cytoreduction — typically developing within about 12–72 hours of an effective dose. Kidney injury therefore concentrates in the first days of treatment and at each dose escalation, with risk falling once the bulk of disease has been debulked and full dosing is tolerated. This front-loaded timing is the entire rationale for the stepwise ramp-up.No clean, drug-specific published incidence of sonrotoclax acute kidney injury exists as a discrete endpoint; the renal risk is inferred from the tumor-lysis physiology that defines potent BCL-2 inhibition. The precedent is venetoclax, where laboratory and clinical tumor lysis syndrome were frequent enough — including early fatal cases — that a mandatory ramp-up schedule, risk-stratified prophylaxis, and inpatient monitoring became standard of care (Tambaro & Wierda, Lancet Haematol 2020). Because sonrotoclax is more potent than venetoclax and induces apoptosis faster, its tumor-lysis potential is at least as high, which is precisely why its development and label built in a stepwise dose ramp-up from the outset. Reported drug-specific AKI rates should not be overstated until mature peer-reviewed trial safety data are published. Reported rate: tumor lysis syndrome in 7% — 125 patients with BTK-inhibitor-pretreated relapsed/refractory mantle cell lymphoma enrolled in the global phase I/II… (Eyre 2026, PMID 42385124).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.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.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.ModerateCytarabineHours to days after initiating therapy in high-burden disease.Intrinsic tubular nephrotoxicity is uncommon; the major renal risk is AKI from tumor lysis syndrome during leukemia/lymphoma cytoreduction, reported at case and series level including fatal TLS. Direct cytarabine-nephrotoxicity primary literature is genuinely sparse.ModerateFludarabineTLS within days of starting therapy; systemic toxicity accrues with impaired clearance.Direct nephrotoxicity is uncommon; the chief renal risks are tumor-lysis-syndrome AKI during cytoreduction and increased systemic toxicity when the renally cleared drug accumulates in renal impairment. About 60% of the active metabolite 2-F-ara-A is renally eliminated, so renal function directly drives exposure. Reported rate: tumor lysis syndrome in 0.33% — 6,137 patients with intermediate- or high-risk advanced chronic lymphocytic leukemia treated with fludarabine 20-40… (Cheson 1998, PMID 9667245).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.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).ModerateDecitabineEarly 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.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.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).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.MildMitoxantroneTumor lysis hours to days post-infusion.Direct nephrotoxicity is low and not quantified; the principal renal risk is tumor lysis syndrome when used in bulky/rapidly proliferating hematologic malignancies. Benign blue-green discoloration of urine/sclera is expected (the anthracenedione chromophore), not injury.MildIdarubicinHours to days after starting induction.Minimal intrinsic nephrotoxicity; the dominant renal threat is tumor lysis syndrome in acute leukemia. In 114 consecutive adult AML patients receiving induction, fulminant tumor lysis with acute renal failure occurred in 6.1% (95% CI 2.5-12.2), most of whom required hemodialysis; five of those seven patients had inv(16), so risk in that subgroup is substantially higher than the cohort-wide rate. That cohort used cytarabine-daunorubicin induction, so the figure reflects anthracycline-based induction generally — an idarubicin-specific AKI rate is not quantified.Mild
Also associated
28Agents that cause crystal / obstructive nephropathy as a secondary pattern alongside a different signature lesion.
CAR-T Cell TherapyAcute — within the CRS window (first days–weeks).AKI ~5–33% across cohorts (commonly ~10–30%), mostly mild and reversible.ModerateClofarabineEarly, typically within the first treatment cycle (days).A systemic inflammatory response syndrome (SIRS) / capillary-leak syndrome with associated AKI was reported in roughly 4% of treated children in the registration program; hypotension was among the most common grade 3 or greater adverse events in the pivotal phase II trial. Precise renal incidence is not well quantified and most AKI data are case-level. Reported rate: renal insufficiency in 6% — Adults with relapsed and/or refractory non-Hodgkin lymphoma receiving SINGLE-AGENT clofarabine (1-h IV daily x5, q28d)… (Nabhan 2011, PMID 21425150).ModerateBlinatumomabEarly, typically during the first days of an infusion cycle (CRS) or with rapid tumor cytoreduction (TLS), concentrated around initiation and dose step-up.Acute kidney injury is predominantly secondary to cytokine release syndrome (CRS) and tumor lysis syndrome (TLS) rather than a direct drug effect; renal injury is described mainly at the case/series level and is not robustly quantified as a primary endpoint. By analogy to immune-effector-cell therapies, AKI is generally low-grade and rapidly reversible when the syndrome is controlled.ModerateElranatamabEarly, concentrated around the two-step priming doses and the first full doses.Cytokine release syndrome is common with elranatamab (about 58% in the pivotal MagnetisMM-3 trial, largely grade 1-2 with the two-step priming regimen); CRS-associated acute kidney injury, and occasionally tumor-lysis-related injury, are emerging case-level signals that are not separately well quantified, superimposed on frequent myeloma kidney disease.ModerateMosunetuzumabEarly — during cycle 1 step-up dosing, coincident with CRS (first days to ~2 weeks).No direct tubular nephrotoxic signal. AKI is a downstream/case-level consequence of cytokine release syndrome (CRS, ~44% any-grade, almost all grade 1-2 and concentrated in cycle 1) and tumor lysis syndrome; renal-specific incidence is not quantified. Reported rate: tumor lysis syndrome in 0.9% — 218 patients with relapsed/refractory non-Hodgkin lymphoma, including 90 with relapsed/refractory follicular lymphoma,… (Matasar 2024, PMID 38195322).ModerateEpcoritamabEarly — during cycle 1 step-up dosing with CRS.No direct tubular signal. AKI is case-level and downstream of CRS (~50% any-grade, predominantly grade 1-2 with subcutaneous step-up dosing) and tumor lysis; renal incidence is not separately quantified — emerging data. Reported rate: clinical tumor lysis syndrome in 5% — 42 patients with Richter transformation (Kater 2026, PMID 41380698).ModerateGlofitamabEarly — concentrated around cycle 1 step-up dosing and the first full dose.No direct tubular signal. AKI is case-level, downstream of CRS (~63% any-grade, grade >=3 in ~4% after obinutuzumab pretreatment and step-up dosing) and tumor lysis; renal incidence not separately quantified — emerging data.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.ModerateRevumenibDuring early treatment as leukemic differentiation and lysis occur (first days–weeks).Differentiation syndrome and tumor lysis syndrome are on-target risks identified during development (differentiation syndrome carries a boxed warning). Resulting AKI is hemodynamic (capillary leak, fluid shifts) and/or crystal/metabolic (TLS); renal-specific incidence is not separately well quantified. QTc prolongation is an additional class effect.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).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%.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.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.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.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.ModerateBrentuximab vedotinEarly — tumor lysis in the first cycle(s) of bulky disease.Direct nephrotoxicity is minimal. Tumor lysis syndrome occurs at low rates (<=5% in anaplastic large-cell lymphoma experience) and is the principal pathway to AKI/electrolyte disturbance; renal-specific incidence is not quantified.MildPolatuzumab vedotinEarly — tumor lysis during initial cycles of bulky disease.Renal data are limited; direct nephrotoxicity is not a prominent trial signal. AKI is case-level and chiefly tumor-lysis- or volume-mediated. Renal-specific incidence is not quantified.MildPomalidomideTumor lysis typically within days of starting therapy in high-burden disease.Pomalidomide pharmacokinetics are not substantially altered by renal impairment - it is extensively metabolized hepatically, with <5% renal excretion of unchanged drug - and pooled trial data show a similar safety profile and dosing through moderate renal impairment (CrCl 30 to <60). Dialysis patients are the exception - the label reports about 38% higher AUC and 64% more serious adverse events there, with a reduced starting dose given after the session. The principal renal hazard is tumor lysis syndrome (TLS), which is uncommon and case-level in myeloma.MildThalidomideTumor lysis within days of initiation in high-burden disease; bradycardia over weeks of dosing.Thalidomide is not a direct nephrotoxin; the principal renal hazard is tumor lysis syndrome, which is uncommon in myeloma and reported at the case level. Sinus bradycardia is a recognized dose-related non-renal effect that, with the drug’s sedative/hypotensive properties, can compound prerenal physiology. Venous thromboembolism is the other dominant class toxicity.MildAcalabrutinibTumor lysis early (first cycle); hypertension over weeks–months.Hypertension occurs but is less frequent than with ibrutinib (~15% vs ~26% in a matched real-world cohort; ELEVATE-RR confirmed lower hypertension and atrial fibrillation head-to-head). One single-center cardio-oncology cohort still found ~49% new/worsened hypertension by sensitive criteria. Tumor lysis is the principal route to AKI; direct nephrotoxicity is case-level.MildZanubrutinibTumor lysis early (first cycle); otherwise renal function typically stable.Direct nephrotoxicity is not a prominent signal. Cardiovascular toxicity (atrial fibrillation, hypertension) is lower than ibrutinib in pooled and head-to-head (ASPEN, ALPINE) analyses. Tumor lysis can occur with rapid cytoreduction of bulky CLL/lymphoma; renal events are case-level and not well quantified.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.MildLinvoseltamabDays — coincident with step-up dosing and CRS in the first 1-2 weeks; CRS in LINKER-MM1 occurred predominantly during step-up dosing.No drug-specific renal toxicity signal was reported in the LINKER-MM1 registrational program; AKI is not a labeled or characteristic adverse event. Any kidney injury is expected to be indirect and infrequent, mediated chiefly by cytokine release syndrome (CRS), infection/sepsis, and (early) tumor lysis. By class analogy to CAR-T and other immune-effector therapies, AKI occurs in roughly 5-21% of T-cell-redirection recipients, is usually mild (KDIGO stage 1) and transient with recovery in ~79% within a month, and tracks with higher-grade CRS. No linvoseltamab-specific incidence is published.Mild