The Injury Atlas Does the kidney recover? Cross-drug outcomesRepresentative per-agent glomerular injury / proteinuria 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.
GLOM
Glomerular Injury / Proteinuria
Damage to the filtration barrier — podocyte injury, FSGS and protein leak from VEGF and mTOR blockade.
59agents
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· 6Moderate· 38Mild· 15
Agents’ overall reversibility
Often irreversible· 2Partially reversible· 19Variable· 15Reversible· 23
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)· 2Subacute (weeks)· 27Delayed (weeks–months)· 18Variable· 11
Real-world reporting for this lesion
FAERS across all lesions →Agents with a disproportionate FAERS reporting signal for glomerular injury / proteinuria (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.
36Corroborated
Documented in the atlas profile and carrying a FAERS signal — the strongest claim the atlas makes.
11Documented, 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.
19Not 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.
18Reported 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.
5-FluorouracilAfatinibAtezolizumabAxitinibBelzutifanBevacizumabBicalutamideBortezomibBusulfanCabozantinibCapecitabineCarboplatinCarmustine (BCNU)CetuximabChlorambucilCisplatinCobimetinibCyclophosphamideCytarabineDactinomycin (actinomycin D)DasatinibDinutuximabDocetaxelDoxorubicinDurvalumabErlotinibEtoposideEverolimusFludarabineFruquintinibGefitinibGemcitabineIbandronateIfosfamideImatinibIpilimumabIrinotecanLenvatinibLomustine (CCNU)LorlatinibMelphalanMethotrexate (high-dose)Mitomycin CMogamulizumabNintedanibNivolumabOxaliplatinPaclitaxelPamidronatePanitumumabPazopanibPembrolizumabPemetrexedPenpulimabPentostatinRamucirumabRegorafenibRituximabSirolimusSorafenibSunitinibTemozolomideTemsirolimusThalidomideThiotepaTopotecanTrametinibTrifluridine/tipiracilVandetanibVemurafenibVinorelbineZiv-afliberceptZoledronic acid
73 agents with a significant GLOM reporting signal.
Management approach
Full framework →Reduce proteinuria with RAAS blockade and blood-pressure control; hold or dose-reduce for heavy or worsening protein leak.
Drug-level levers
- Hold for nephrotic-range proteinuria or a rapidly rising UPCR; resume at a reduced dose after improvement.
- Dose-reduce for moderate proteinuria.
- Switch out of class if proteinuria is severe or persistent.
Pharmacologic toolkit
- RAAS blockade — ACE inhibitor or ARB to lower proteinuria and treat coexisting hypertension.
- Blood-pressure control — Tight control limits further glomerular stress.
When to biopsy
Consider for nephrotic-range proteinuria, hematuria, or atypical features to define the glomerular lesion (e.g., collapsing FSGS, TMA) and inform whether to continue therapy.
Monitoring
- · Urine protein/creatinine ratio at baseline and periodically
- · Blood pressure
- · Creatinine / eGFR and albumin
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 glomerular injury / proteinuria.
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.
KDIGOExecutive summary of the KDIGO 2025 Clinical Practice Guideline for the Management of Immunoglobulin A Nephropathy (IgAN) and Immunoglobulin A Vasculitis (IgAV)Kidney Int 2025 · PMID 40975525Encourages liberal kidney biopsy and stricter proteinuria control (<0.5 g/d, ideally <0.3 g/d) with RAAS blockers, SGLT2 inhibitors, and targeted-release budesonide — the framework for IgA-dominant glomerular lesions, including those triggered by immune-modulating cancer therapy.KDIGOExecutive summary of the KDIGO 2024 Clinical Practice Guideline for the Management of ANCA-Associated VasculitisKidney Int 2024 · PMID 38388147Updates immunosuppressive induction (rituximab/cyclophosphamide), incorporates avacopan and lower-dose or glucocorticoid-sparing regimens — the management framework for drug- and checkpoint-inhibitor-associated ANCA/pauci-immune glomerulonephritis.KDIGOExecutive summary of the KDIGO 2024 Clinical Practice Guideline for the Management of Lupus NephritisKidney Int 2024 · PMID 38182299Updates first-line lupus nephritis therapy to combination immunosuppression with the addition of belimumab or a calcineurin inhibitor (voclosporin) — informs management of immune-complex/lupus-like glomerulonephritis encountered with immunotherapy.KDIGOExecutive summary of the KDIGO 2021 Guideline for the Management of Glomerular DiseasesKidney Int 2021 · PMID 34556300Provides the staging/treatment framework for drug-associated glomerular lesions (e.g., bisphosphonate- and interferon-related collapsing FSGS, VEGF-inhibitor podocytopathy/proteinuria), including immunosuppression and supportive RAAS-blockade strategies.ASCO / CCORole of Bone-Modifying Agents in Metastatic Breast Cancer: An American Society of Clinical Oncology-Cancer Care Ontario Focused Guideline UpdateJ Clin Oncol 2017 · PMID 29035643Endorses denosumab 120 mg SC q4w, pamidronate 90 mg IV q3-4w, or zoledronic acid 4 mg IV q12w or q3-4w; nitrogen bisphosphonates require renal function monitoring and dose/interval adjustment for impaired clearance, whereas denosumab needs no renal dose adjustment (with hypocalcemia risk in CKD).UK Consensus PanelUsing bevacizumab to treat metastatic cancer: UK consensus guidelinesBr J Hosp Med (Lond) 2010 · PMID 21135762Assess and monitor blood pressure and proteinuria during bevacizumab therapy; treat emergent hypertension to standard targets and interrupt/discontinue the drug for uncontrolled hypertension, nephrotic-range proteinuria or other severe vascular toxicity.
Cited incidence across agents
Where the literature gives a representative glomerular injury / proteinuria figure, the agents ranked highest first. Hover a dot for its cited note.
Offending agents
Signature offenders
15Agents for which glomerular injury / proteinuria is the defining renal lesion.
Interferon-αSubacute — weeks to months of therapy.Rare; best characterized by an 11-case biopsy series, disproportionately in Black patients (APOL1).SeverePamidronateSubacute to delayed — months to years of therapy (15–48 months in the Markowitz 2001 series).Not well quantified; the histopathologic pattern comes from case series, notably at higher-than-approved doses. Reported rate: renal deterioration in 7.7% — Patients with multiple myeloma or metastatic breast cancer receiving 1-hour intravenous pamidronate infusions, British… (de 2006, PMID 17156591).SevereBevacizumabWeeks to months; dose-dependent.In a 72-trial meta-analysis (21,902 bevacizumab cases vs 20,608 controls), all-grade proteinuria was 18% (95% CI 11.7–26.6%) and high-grade 2.4% (1.8–3.2%); all-grade hypertension was 25.3% (21.5–29.5%). Relative to controls the risk ratios were 3.37 for all-grade and 5.49 for high-grade proteinuria. A separate 16-trial meta-analysis put high-grade proteinuria at 2.2% and nephrotic syndrome at RR 7.78, with renal cell carcinoma carrying the highest cumulative incidence (10.2%).ModerateSirolimusVariable—weeks to months after initiation or dose escalation; proteinuria characteristically emerges or worsens within months after calcineurin-inhibitor withdrawal/conversion.New or worsening proteinuria occurs in a substantial minority of treated patients in transplant cohorts (more pronounced after conversion from a calcineurin inhibitor than with de novo use), but oncology-specific renal incidence is not well quantified and is described largely at the case and small-series level. Acute renal dysfunction (e.g., delayed graft recovery) is recognized but variable. Reported rate: proteinuria in 23.1% — 18 of 78 kidney, pancreas and islet transplant recipients given sirolimus de novo or after conversion, 5 of the 18 (27.8%) reaching nephrotic range; a transplant-immunosuppression figure, not an oncology one (Franco 2007, PMID 17362756).ModerateDasatinibProteinuria can appear within weeks to months and increases with treatment duration and exposure.Dasatinib causes significantly more albuminuria than other TKIs. In a pharmacokinetic cohort, dasatinib users had higher urine albumin-creatinine ratios and about 10% showed severely increased albuminuria (UACR >300 mg/g) versus none on other TKIs, with the degree of proteinuria correlating with plasma exposure. Nephrotic-range proteinuria with biopsy-proven glomerular injury (FSGS, podocyte foot-process effacement, endothelial injury) is reported in cases.ModerateIvonescimabVEGF-pathway proteinuria/hypertension typically within the first weeks-to-cycles; checkpoint-inhibitor AIN usually delayed, often 8-16 weeks (range days to >1 year).Renal-specific data are immature for this newly approved agent; no dedicated nephrotoxicity series exists. In registrational trials, grade >=3 VEGF-related adverse events (a class category encompassing proteinuria, hypertension, and hemorrhage) occurred in roughly 3% of patients (HARMONi-A: 5/161, 3.1%) — against 4/161 (2.5%) in the chemotherapy-alone arm of the same trial, a one-patient difference that is not separable from background. Grade >=3 immune-related adverse events (the checkpoint-inhibitor category that includes AIN) occurred in ~6-9% across trials, though kidney-specific irAE rates were not separately tabulated. Clinically significant AKI was uncommon.ModeratePazopanibProteinuria and hypertension typically emerge within weeks to a few months of starting therapy; TMA case reports describe onset within the first weeks to ~2 months.Proteinuria is common but usually low-grade, and reported any-grade rates span roughly 15% to 80% depending on the population and how proteinuria was ascertained. In a pooled secondary analysis of two phase III trials of pazopanib or sunitinib in metastatic RCC (n=1392, Sorich 2016), any-grade proteinuria occurred in 15.0% and grade 3/4 in 3.7% — a trial adverse-event figure covering both agents, not a pazopanib-specific rate. In a single-center first-line mRCC cohort, proteinuria was reported in 80% of the pazopanib-treated patients (Land 2016), most grade 1-2 and managed with continued monitoring at the same dose. Assume proteinuria is the expectation rather than the exception on pazopanib and schedule urine protein monitoring accordingly. Hypertension is one of the most frequent class effects, with severe (grade 3-4) hypertension a recognized class risk. Thrombotic microangiopathy is rare and largely case-level; biopsy-proven renal-limited and systemic TMA/TTP-like presentations have been reported.ModerateEverolimusSubacute — proteinuria typically emerges over the first weeks to months of therapy; thrombotic microangiopathy usually appears within weeks to months, often in the setting of concurrent calcineurin-inhibitor or anti-VEGF exposure.Proteinuria is a class effect of mTOR inhibitors, and with systematic monitoring it is close to universal. A retrospective review of 129 first-line metastatic renal-cell patients found any-grade proteinuria in 81% overall and in 96% of the everolimus arm (44 patients) — the highest of the three regimens compared, against 80% on pazopanib and 64% on bevacizumab. Almost all of it was minor: the study's grade 3-4 proteinuria (24%, 6 patients) occurred entirely in the bevacizumab group, none in the everolimus arm, and 35 of the everolimus patients (80%) simply continued at the same dose under monitoring. So the striking number is detection, not injury — heavy proteinuria and overt podocytopathy remain uncommon, and most nephrotic-range and biopsy-proven FSGS data are still extrapolated from the sirolimus/transplant literature. A phase II trial combining everolimus with bevacizumab reported grade 3-4 proteinuria of 25%, which reflects the added anti-VEGF effect and overstates everolimus alone. Thrombotic microangiopathy is rare and drawn mainly from case reports, typically with concomitant calcineurin-inhibitor or anti-VEGF exposure.ModeratemTOR InhibitorsWeeks–months.Everolimus commonly causes all-grade proteinuria, with high-grade uncommon; mTOR-inhibitor proteinuria/FSGS is well described. Temsirolimus case-level only.MildDoxorubicinSubacute in models (over weeks); clinical events rare and variable.Adriamycin nephropathy is the canonical rodent model of podocyte injury and focal segmental glomerulosclerosis (FSGS); clinically significant glomerular disease from therapeutic dosing in patients is rare and largely case-level. Separately, doxorubicin — especially the pegylated liposomal formulation — is an increasingly recognized but underreported cause of kidney-limited thrombotic microangiopathy (a vascular/endothelial lesion), described in biopsy-proven case reports and drug-induced-TMA series.MildErlotinibWeeks to months after starting therapy; proteinuria/creatinine typically improve over weeks after discontinuation in reported cases.Glomerular disease (including minimal-change-type nephrotic syndrome) and acute kidney injury are reported rarely, at the case level; pharmacovigilance data show measurable disproportionality signals for AKI/renal failure (and rare TMA) but no robust trial-based incidence. Reported rate: proteinuria in 3% — Erlotinib-MONOTHERAPY comparator arm of 4 randomized controlled trials in EGFR-mutation-positive advanced NSCLC (Deng 2022, PMID 35985780).MildGefitinibWeeks to months after initiation in reported cases; proteinuria resolves over weeks to months after stopping the drug.Nephrotic syndrome (minimal-change disease and secondary membranous nephropathy patterns) and rare acute renal failure are reported only as isolated cases; not quantified in clinical-trial datasets.MildBelantamab mafodotinVariable; renal events reported during prolonged therapy. Ocular toxicity is often detectable within the first cycles.Renal-specific data are emerging and sparse; direct nephrotoxicity is not an established signal. In myeloma, AKI more often reflects the underlying disease (cast nephropathy, hypercalcemia, volume status) than the ADC. A case of focal segmental glomerulosclerosis after belantamab mafodotin (confounded by severe COVID-19) has been reported. The defining toxicity is ocular keratopathy (71-77% in DREAMM-2).MildOlverembatinibVariable; proteinuria and hypertension, when they occur with multi-kinase TKIs, typically emerge over weeks to months of therapy.Renal-specific data are sparse. In the Chinese phase 1/2 program (n=165) proteinuria was among the common treatment-related adverse events, though grade and exact rate were not separately quantified; clinically significant AKI was not a prominent signal. Direct nephrotoxicity appears low overall.MildTemsirolimusSubacute — typically weeks to months into weekly dosing; not firmly characterized for temsirolimus.Not firmly quantified for temsirolimus specifically. Proteinuria is the recognized mTOR-inhibitor glomerular signal, but for temsirolimus it is documented mostly at the class/case level rather than in drug-specific renal endpoints (everolimus proteinuria runs high yet is usually grade 1-2 — e.g., 96% all-grade in one first-line mRCC cohort). In the pivotal temsirolimus ARCC trial, metabolic lab abnormalities (hyperglycemia, hyperlipidemia, hypophosphatemia) dominated and frank nephrotoxicity was uncommon; drug-specific AKI and nephrotic syndrome appear only in case reports. Reported rate: grade >=3 hypophosphatemia in 5% — 82 East Asian (Sun 2012, PMID 22844126).Mild
Also associated
44Agents that cause glomerular injury / proteinuria as a secondary pattern alongside a different signature lesion.
GemcitabineDelayed — months of cumulative exposure.Estimates span three orders of magnitude by ascertainment. The only figure with a real denominator is the manufacturer safety-database review: 12 cases against 78,800 patient exposures, a crude 0.015% (range 0.008–0.078%). The product characteristics give 0.01%. Against that, a single center reported 2.7% — four of its five cases on nab-paclitaxel/gemcitabine, where a pharmacokinetic interaction is suspected. Historically high mortality: of 23 cases with reported outcome in the literature tally, 11 died within a few weeks, death directly attributed to HUS in two.SevereMitomycin CDelayed — after cumulative dosing, sometimes after therapy ends.Dose-dependent, generally 4–15%; nearly every case in the landmark 85-patient registry had received a cumulative total dose above 60 mg. >50% historical mortality.SevereCarfilzomibVariable — frequently early (first cycles), but TMA can also appear later, sometimes after a treatment break and re-escalation.Renal complications are common and a recognized class concern: in a 114-patient real-world cohort, ~17% had carfilzomib-attributable renal events (TMA ~5%, albuminuria >1 g/day ~6%, otherwise-unexplained grade >=3 AKI ~5%), occurring mostly early and unpredictably. On the prospective CARDAMON trial 8 patients experienced TMA (6 of 8 hypertensive at presentation, 7 of 8 with AKI); after a protocol amendment adding aggressive hypertension management, carfilzomib step-up dosing at the start of maintenance and dexamethasone premedication, the rate fell from 4.2 to 1.6 events per 1,000 patient-cycles with no further maintenance events. Pharmacovigilance (FAERS) shows carfilzomib carries by far the strongest TMA signal among proteasome inhibitors.SevereIpilimumabDelayed and variable: typically weeks to several months after initiation. Median time to AKI in biopsy cohorts was roughly 3 months (about 91 days; ~4 cycles); combination ipilimumab/nivolumab nephritis can appear after only one or two doses, and onset after drug discontinuation has been described.Clinically significant kidney injury from ipilimumab monotherapy is uncommon; renal immune-related adverse events are reported in roughly 1-2% of patients on single-agent checkpoint blockade. The dominant driver of elevated incidence is combination therapy: in real-world ICI cohorts any-cause AKI reaches about 16-17%, but only a minority is true immune-mediated nephritis. The combination of ipilimumab plus nivolumab carries a substantially higher and more severe AKI risk than either single agent. In a pooled analysis of biopsy-proven ICI-related acute tubulointerstitial nephritis, all patients on dual ICI blockade developed stage 3 AKI versus about half on a single agent, and complete renal recovery was less likely with dual blockade.SevereVEGFR Tyrosine Kinase InhibitorsHypertension within days–weeks; proteinuria over weeks–months.Hypertension ~17–50%; proteinuria 8–73% across agents (the cited review's ranges; it reports no single pooled proteinuria rate).ModerateImmune Checkpoint InhibitorsDelayed — median ~14 weeks after starting therapy.ICI-associated AKI ~2–5% (higher with combination therapy); ~93% of biopsies show interstitial nephritis.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).ModerateRamucirumabWithin the first one to two cycles (weeks).Hypertension and proteinuria are common class effects; nephrotic syndrome is a less frequent but reported event, sometimes after only 1-2 doses and typically accompanied by hypertension.ModerateZiv-afliberceptWithin weeks to a few months of therapy.Hypertension and proteinuria are common class effects; in the registrational VELOUR trial, grade 3-4 hypertension and proteinuria were more frequent with aflibercept plus FOLFIRI than with FOLFIRI alone. Nephrotic-range proteinuria and renal thrombotic microangiopathy are documented, including with the ophthalmic formulation, indicating a direct VEGF-trap mechanism. A meta-analysis of 15 trials (4,451 patients) put the summary all-grade hypertension incidence at 42.4%.ModerateLenvatinibWithin the first weeks of therapy (hypertension early; proteinuria over weeks).Hypertension is among the most common adverse events; in the SELECT thyroid-cancer trial hypertension occurred in about 68% (grade >=3 ~42%) and proteinuria in roughly 31%. In KEYNOTE-B61 (lenvatinib plus pembrolizumab) grade 3-4 hypertension occurred in ~23%. Proteinuria is a frequent renal AE with lenvatinib.ModerateCabozantinibWithin weeks of starting therapy.Hypertension and proteinuria are common; in pivotal RCC trials (e.g., METEOR, CABOSUN) hypertension was among the most frequent adverse events with grade >=3 rates around 15-28%. Cabozantinib is one of the TKIs most often associated with proteinuria, with case reports of nephrotic syndrome. Reported rate: grade >=3 hypertension in 15% — Adults with advanced/metastatic clear-cell renal cell carcinoma previously treated with >=1 VEGFR tyrosine-kinase… (Choueiri 2016, PMID 27279544).ModerateRegorafenibWithin the first weeks of therapy.Hypertension is common and frequently grade 3. Pooling 3,813 patients across the cardiovascular-event literature puts all-grade hypertension at 36.8% (95% CI 29.8-43.8%) and high-grade at 9.9% (7.4-12.4%), against controls a relative risk of 4.10 all-grade and 5.82 high-grade. An earlier, smaller meta-analysis of 1,069 patients from five trials (750 on regorafenib) ran higher at 44.4% (30.8-59.0%) all-grade and 12.5% (5.2-27.1%) high-grade, with wider intervals; the CORRECT trial itself reported about 28% (grade 3 ~7%). Proteinuria also occurs as a VEGF-pathway class effect, but is not separately quantified for this agent.ModerateVandetanibWithin the first weeks of therapy.In the pivotal phase III ZETA trial, any-grade hypertension occurred in about 32% of vandetanib-treated patients versus 5% with placebo; proteinuria occurs as an antiangiogenic class effect.ModerateTivozanibWithin the first weeks of therapy.In the phase III TIVO-3 trial, hypertension was the most common grade 3-4 treatment-related adverse event, occurring in about 20% of tivozanib-treated patients; proteinuria occurs as a VEGFR class effect but is comparatively less prominent.ModerateAtezolizumabTypically weeks to a few months after initiation (median time to checkpoint-inhibitor AKI is on the order of 3-4 months, characteristically later than classic drug AIN).Across the checkpoint-inhibitor class, any acute kidney injury occurs in roughly 15-17% of treated patients in cohort studies, while clinically significant immune-related AKI (most often acute interstitial nephritis) affects a smaller subset (commonly a few percent). Meta-analysis suggests anti-PD-L1 agents like atezolizumab carry somewhat lower AKI risk than anti-PD-1 agents; PD-L1-specific rates are not precisely separated. A separate real-world cohort of 1,037 ICI-treated patients supplies the drug-attributable denominator this class otherwise lacks: 18.2% developed AKI of any cause, but only 3.6% (37 patients) had AKI attributed to the checkpoint inhibitor itself — a class figure, not an atezolizumab-specific one.ModerateDurvalumabWeeks to several months after starting therapy.As with the PD-1/PD-L1 class, any AKI occurs in roughly 15-17% of treated patients, with immune-related AIN representing a smaller, clinically significant fraction (a few percent). Anti-PD-L1 agents trend toward lower AKI risk than anti-PD-1 agents; durvalumab-specific rates are not separately well quantified. A separate real-world cohort of 1,037 ICI-treated patients supplies the drug-attributable denominator this class otherwise lacks: 18.2% developed AKI of any cause, but only 3.6% (37 patients) had AKI attributed to the checkpoint inhibitor itself — a class figure, not a durvalumab-specific one.ModerateAvelumabWeeks to months after initiation.Immune-related nephritis follows the PD-1/PD-L1 class pattern: any AKI in roughly 15-17% of patients and clinically significant immune-related AIN in a smaller subset. Anti-PD-L1 agents trend toward lower AKI risk than anti-PD-1 agents; avelumab-specific renal incidence is not separately quantified and rests on class-level pharmacovigilance and meta-analysis data. A separate real-world cohort of 1,037 ICI-treated patients supplies the drug-attributable denominator this class otherwise lacks: 18.2% developed AKI of any cause, but only 3.6% (37 patients) had AKI attributed to the checkpoint inhibitor itself — a class figure, not an avelumab-specific one.ModerateCemiplimabWeeks to months after initiation.Follows the PD-1/PD-L1 class profile: any AKI in roughly 15-17% of patients, with immune-related AIN in a smaller clinically significant subset. As an anti-PD-1 agent it may carry somewhat higher AKI risk than anti-PD-L1 agents, and pharmacovigilance data show an immune-nephropathy signal; cemiplimab-specific renal incidence is not separately quantified. A separate real-world cohort of 1,037 ICI-treated patients supplies the drug-attributable denominator this class otherwise lacks: 18.2% developed AKI of any cause, but only 3.6% (37 patients) had AKI attributed to the checkpoint inhibitor itself — a class figure, not a cemiplimab-specific one.ModerateDostarlimabWeeks to months after initiation.Consistent with the PD-1/PD-L1 class: any AKI in roughly 15-17% of treated patients, with immune-related AIN in a smaller clinically significant subset. As a newer anti-PD-1 agent, dostarlimab-specific renal incidence is not separately quantified. A separate real-world cohort of 1,037 ICI-treated patients supplies the drug-attributable denominator this class otherwise lacks: 18.2% developed AKI of any cause, but only 3.6% (37 patients) had AKI attributed to the checkpoint inhibitor itself — a class figure, not a dostarlimab-specific one.ModerateTrastuzumab emtansine (T-DM1)Variable; reported after initiation, over weeks to months of therapy.Renal toxicity is rare and case-level. FDA adverse-event analyses flagged renal events with trastuzumab-based therapy, and biopsy-proven cases (collapsing focal segmental glomerulosclerosis; TMA-like microvascular injury) have been reported. Incidence is not quantified.ModerateBortezomibRare adverse renal events can occur at any point during therapy, from weeks to several months after initiation; the beneficial light-chain reduction is often rapid.Bortezomib is generally renal-friendly and often improves renal function in myeloma by rapidly reducing light-chain-driven cast nephropathy; it requires no renal dose adjustment. Thrombotic microangiopathy and glomerular microangiopathy are rare, case-level events, and pharmacovigilance shows a far weaker TMA signal than carfilzomib.ModerateSelpercatinibHypertension within the first weeks to months; creatinine changes early.Hypertension is among the most common adverse events in LIBRETTO-001 (a frequent grade >=3 event), and a reversible serum-creatinine increase is also recognized. A single-center hereditary-MTC series found hypertension in ~26% on selective RET inhibitors. Reported rate: grade >=3 hypertension in 19.7% — 837 patients with RET-activated advanced/metastatic solid tumors receiving selpercatinib monotherapy (20 mg QD to 240… (Raez 2024, PMID 39471424).ModerateIbrutinibHypertension develops over weeks–months (can be early); tumor lysis is early (first cycle); glomerular/interstitial lesions are case-level over weeks to months.New or worsened hypertension is common (~26% in a real-world CLL cohort comparing it with acalabrutinib; higher with longer follow-up). AKI at CLL presentation and with tumor lysis is well described. Drug-attributable AKI from interstitial nephritis or glomerular endotheliosis is case-level.ModerateDatopotamab deruxtecan (Dato-DXd)Not well characterized (recent approval); by class analogy a subacute tubular pattern during cumulative dosing.Renal signal is theoretical and not yet quantified, extrapolated from the ADC class. In TROPION-PanTumor01 and the phase III TROPION-Breast01 the dominant toxicities were mucosal (stomatitis ~50%) and ocular events, nausea, and interstitial lung disease; grade ≥3 treatment-related adverse events were lower than chemotherapy (~21%), and kidney-specific events were not prominent.ModerateFruquintinibWithin weeks of starting therapy (hypertension often earliest).Hypertension and proteinuria are characteristic VEGFR-TKI class effects; in the FRESCO-2 safety analysis hypertension was the most frequent treatment-related adverse event of special interest, occurring in 28.9% of fruquintinib-treated patients all-grade and 10.7% at grade ≥3, with proteinuria also reported (1.3% of patients required a dose reduction for it). Renal-specific TMA is rare but described across the VEGF-inhibitor class.ModerateTislelizumabDelayed: commonly weeks to several months after initiation (often 8-12+ weeks); can occur after multiple cycles or after a single dose, and rarely after drug discontinuation.Drug-specific renal data are sparse: the registrational ESCC trials (RATIONALE-302, RATIONALE-306) did not report nephritis as a notable adverse event, and no tislelizumab-specific biopsy series exists. Reasoning from the PD-1 class, immune-mediated acute interstitial nephritis (the class signature) is uncommon at roughly 1-3% of treated patients, while any-cause AKI in real-world ICI cohorts is far higher (16-17%) but mostly prerenal/non-immune rather than true ICI-nephritis.ModerateToripalimabDelayed; PD-1-related AIN characteristically appears 3-10 months after initiation (later than CTLA-4 agents), though it can occur at any point during or after treatment.Drug-specific renal data are limited; reasoning from the PD-1 class is required. Across PD-1/PD-L1 agents, clinically significant immune-related AKI (predominantly AIN) occurs in roughly 1-5% of patients, with attributable PD-L1-related AKI under 1% in one large cohort but pooled estimates as high as ~3-5% with platinum co-therapy. In the JUPITER-02 registrational trial, immune-related adverse events were more frequent with toripalimab (54.1% vs 21.7%) and grade ≥3 irAEs occurred in 9.6%, but kidney-specific irAEs were not individually quantified.ModerateCosibelimabDelayed and variable — typically weeks to months after initiation. Pooled ICI data place median time to AKI at roughly 3-4 months (~108 days), though onset ranges from a few weeks to after treatment discontinuation.Drug-specific renal data are limited. In the pivotal phase 1 metastatic CSCC cohort (n=78), immune-related adverse events occurred in 23.1% of patients (grade 3 in 2.6%; no grade 4/5), with no nephritis-specific signal reported and a favorable overall safety profile. By class, immune-mediated nephritis/AKI with checkpoint inhibitors is uncommon: a 2023 systematic review and meta-analysis of 27 studies (24,048 patients) found a pooled all-cause AKI incidence of ~5.7%, with clinically significant immune-mediated nephritis substantially lower (roughly 1-3%), and anti-PD-L1 agents tending toward the lower end of that range versus CTLA-4 or combination regimens.ModeratePenpulimabVariable and often delayed: ICI-associated AIN commonly emerges weeks to several months after initiation (median around 3-4 months), and can appear after multiple cycles or even after discontinuation. Chemotherapy-related ATN in the combination regimen tends to occur earlier, peri-infusion.Penpulimab-specific renal data are limited. In the pivotal first-line phase 3 trial (penpulimab plus chemotherapy), grade >=3 immune-related adverse events occurred in only 4.1% of patients, and renal events were not separately prominent; the most common toxicities were hematologic. By class, immune checkpoint inhibitor-associated AKI (predominantly acute tubulointerstitial nephritis) occurs in roughly 2-5% of patients on PD-1 monotherapy, with higher rates when combined with nephrotoxic chemotherapy. Platinum (cisplatin) and gemcitabine in the registrational backbone independently contribute ATN and (rarely) thrombotic microangiopathy risk, so observed kidney injury in this regimen is often multifactorial.ModerateSugemalimabDelayed — typically weeks to months after initiation; in the multicenter ICI-AKI cohort median time from checkpoint-inhibitor start to AKI was about 14 weeks (IQR 6-37), later than most other drug-induced AIN.No sugemalimab-specific renal-injury incidence has been published; the GEMSTONE registrational trials reported no nephritis among the most common grade 3-4 treatment-related adverse events (which were dominated by myelosuppression and immune-mediated pneumonitis). By extrapolation from the PD-1/PD-L1 checkpoint-inhibitor class, immune-related AKI occurs in roughly 2-5% of treated patients (higher with combination checkpoint blockade), with clinically significant/biopsy-confirmed acute interstitial nephritis being the dominant lesion. A separate real-world cohort of 1,037 ICI-treated patients supplies the drug-attributable denominator this class otherwise lacks: 18.2% developed AKI of any cause, but only 3.6% (37 patients) had AKI attributed to the checkpoint inhibitor itself — a class figure, not a sugemalimab-specific one.ModerateSunitinibHypertension typically appears early (within the first treatment cycle/weeks); proteinuria develops over weeks to months, and biopsy-proven TMA in case series presented on average around 2 years (range ~7-36 months) into therapy.In a systematic review/meta-analysis of 4,999 patients across 13 trials, all-grade hypertension occurred in ~21.6% and high-grade hypertension in ~6.8% of sunitinib-treated patients, with a significantly increased risk of renal dysfunction versus controls (RR ~1.36); risk varied by tumor type and dosing schedule. Proteinuria is common but less consistently quantified, and severe glomerular lesions (thrombotic microangiopathy, nephrotic-range proteinuria) are reported mainly at the case-series level. Reported figures are class-consistent with other VEGF-pathway inhibitors.ModerateAxitinibHypertension typically emerges early, frequently within days to the first few weeks of starting therapy. Proteinuria tends to develop over weeks of continued exposure and is dose-related. Severe glomerular lesions (TMA, nephrotic syndrome) are usually later and more variable in timing.Hypertension is the dominant and best-quantified renal-relevant signal. In the randomized phase III AXIS trial, treatment-emergent all-causality hypertension occurred in 40.4% of axitinib-treated patients (vs 29.0% with sorafenib), with grade 3 hypertension in 15.3% and grade 4 in 0.3%. A real-world VEGFR-TKI cohort in metastatic RCC similarly found hypertension to be the single most common anti-angiogenesis-related adverse event (about 48.6% in TKI-naive patients across the class). Proteinuria is the next most common renal effect; across the VEGF-inhibitor class mild/asymptomatic proteinuria is reported in roughly 21% to 63% of patients, with heavy (nephrotic-range) proteinuria in up to about 6.5% of RCC patients, and axitinib-specific proteinuria rates have been higher in some populations (e.g., Japanese cohorts). Thrombotic microangiopathy and other glomerular lesions (FSGS-like injury, podocytopathy, hyaline occlusive glomerular microangiopathy) are reported at the severe, biopsy-level end of the spectrum but are not precisely quantified for axitinib specifically.ModerateNivolumabCharacteristically delayed compared with other drug-induced AIN: median time from ICI initiation to AKI was about 14 weeks (IQR 6-37) in a 138-patient multicenter cohort, and 91 days in the original series; onset ranges from weeks to many months and can follow drug discontinuation.Clinically significant ICI-attributed AKI is uncommon but not rare. A 2023 systematic review/meta-analysis of real-world data (18 studies, ~12,000 ICI-treated patients) found a pooled incidence of all-cause AKI during ICI therapy of about 16%, but AKI specifically attributed to the ICI of roughly 3.5%. Risk is higher with combination ICI regimens (e.g., nivolumab-ipilimumab) than with PD-1 monotherapy. Among biopsied ICI-AKI, acute tubulointerstitial nephritis is the dominant lesion (>90%); glomerular lesions and thrombotic microangiopathy are reported but uncommon.ModeratePembrolizumabDelayed and highly variable, typically weeks to months after initiation; multicenter cohorts reported median onsets around 14-16 weeks. Can occur after a single dose or after many months, and may recur on rechallenge.In real-world cohorts of patients receiving immune checkpoint inhibitors, any AKI is common (roughly 16-18%), but AKI attributable to the checkpoint inhibitor itself (ICPi-AKI) is less frequent. A single-center cohort reported AKI in 16.5% of ICI-treated patients with checkpoint-attributable nephrotoxicity in a minority, while a larger real-world study found ICPi-AKI in about 3.6%. Acute interstitial nephritis is the dominant biopsy lesion (>80% in the largest multicenter series). These figures are pooled across PD-1/PD-L1/CTLA-4 agents rather than pembrolizumab-specific.ModerateTrametinibVariable. Pyrexia-associated AKI tends to appear early, tracking the febrile syndrome that often begins within the first weeks to few months of dabrafenib/trametinib. The rare biopsy-proven interstitial nephritis and glomerulonephritis cases have presented later — generally around 2 to 6 months into therapy.The renal signal from trametinib itself is modest. In an FDA Adverse Event Reporting System (FAERS) disproportionality analysis, trametinib carried a statistically significant but low acute-kidney-injury reporting odds ratio of 1.32 (95% CI 1.11-1.56) — well below vemurafenib's — and at mean steady-state plasma concentrations trametinib produced no measurable cytotoxicity in cultured proximal-tubular, glomerular endothelial or glomerular epithelial cells (Sanagawa, Anticancer Drugs 2021). Most of the quantified AKI burden comes from combination use: in a single-center retrospective cohort of 199 patients receiving dabrafenib/trametinib, 42 (21%) met an AKI definition (1.5x creatinine rise) within 12 months, and roughly a quarter of those episodes (about 5% of the whole cohort) occurred during a treatment-induced pyrexia syndrome (Seethapathy, Nephrol Dial Transplant 2022). Biopsy-proven interstitial nephritis and glomerular lesions are rare and reported only as individual cases; kidney impairment was rarely reported in the pivotal monotherapy trial.ModerateSorafenibHypertension typically emerges within the first few weeks of treatment; proteinuria develops over weeks to months of continued exposure. Nephrotic syndrome and thrombotic microangiopathy are variable, generally appearing after weeks to months but occasionally sooner.Hypertension is the dominant renal-vascular signal: a systematic review/meta-analysis of 9 trials (4,599 patients) reported an all-grade incidence of 23.4% (95% CI 16.0-32.9%) and high-grade (grade 3-4) incidence of 5.7% (Wu 2008), and a larger meta-analysis of 93 trials (20,494 patients) gave concordant figures of 21.3% all-grade and 5.9% high-grade, with higher rates in renal-cell and thyroid cancer and rising incidence with longer treatment duration (Yang 2017). Proteinuria is a VEGF-pathway class effect: across VEGF-signaling inhibitors mild/asymptomatic proteinuria is reported in roughly 21-63% and heavy (nephrotic-range) proteinuria in up to about 6.5% of renal-cell carcinoma patients (Izzedine 2009); drug-specific quantitative proteinuria data for sorafenib alone are more limited. Nephrotic-range proteinuria and renal-limited thrombotic microangiopathy are documented but uncommon.ModerateNintedanibOver months of therapy in reported cases.Renal effects are uncommon; proteinuria and rare biopsy-proven renal thrombotic microangiopathy have been reported, consistent with VEGF-pathway inhibition. Renal incidence is not well quantified (case-level), and much of the published renal experience comes from pulmonary-fibrosis rather than oncology cohorts.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.MildAdagrasibEarly — within the first weeks of therapy.Renal effects are usually mild: a creatinine rise (partly from inhibited tubular creatinine secretion) plus prerenal AKI from GI losses. The KRYSTAL-1 registrational program reported renal-related lab changes; a dedicated PubMed-indexed pseudo-AKI/albuminuria study for adagrasib does not yet exist, so the precise incidence is unquantified.MildPaclitaxelInfusion reactions occur during or shortly after administration (typically first/second exposure); any prerenal AKI follows the hemodynamic instability.Paclitaxel has low direct nephrotoxicity. Hypersensitivity/infusion reactions - historically attributed to the Cremophor EL (polyoxyethylated castor oil) vehicle via complement activation, with newer evidence for IgE-mediated reactions - and associated fluid shifts can transiently compromise renal perfusion, but structural kidney injury is uncommon and not well quantified.MildIbandronateAcute when it occurs (days), related to dose and infusion rate; antiresorptive electrolyte effects within the first days.Lower renal risk than zoledronate or pamidronate. In a 2-year phase III breast-cancer trial, adverse renal events with IV ibandronate were ~4% versus ~4.5% with placebo — essentially at background. Bisphosphonates as a class can cause toxic ATN (zoledronate) or collapsing FSGS (pamidronate), but ibandronate is the renal-safety outlier within the class. Reported rate: serum creatinine increase >=44.2 micromol/l in 2% — Women with breast cancer and bone metastases receiving intravenous ibandronate 6 mg every 3-4 weeks for up to 6 months,… (von 2008, PMID 18334511).MildCetuximabDevelops insidiously over weeks to months of therapy and is cumulative — the nadir deepens the longer treatment continues, so the largest deficits typically appear after several months. Reversible: renal magnesium handling recovers over weeks (usually within about 4-8 weeks) after cetuximab is stopped.Hypomagnesemia is an on-target class effect. In the defining prospective cohort (Tejpar, Lancet Oncol 2007), 95/98 patients (97%) developed a declining serum magnesium slope on EGFR-antibody therapy. Cetuximab-specific pooled data give an any-grade incidence of ~36% (Cao, Chemotherapy 2010; 19 trials, 95% CI 22-54%), with grade 3-4 hypomagnesemia — a CTCAE serum-magnesium threshold, not a symptom rate — in roughly 5-6%; a pooled analysis of randomized anti-EGFR antibody trials (cetuximab and panitumumab together) reports an overall any-grade incidence of 17% across the class (Petrelli, Expert Opin Drug Saf 2011). Versus control, the relative risk is ~3.9 for cetuximab specifically and ~5.83 across anti-EGFR antibodies (Petrelli, Expert Opin Drug Saf 2011). Magnesium falls cumulatively, deepening with treatment duration.MildPanitumumabDevelops over weeks of therapy and is cumulative, deepening with treatment duration and repeated every-2-week dosing. Recovery after discontinuation is typically slow — over several weeks to a couple of months — as distal-tubule magnesium handling gradually normalizes; hypomagnesemia can persist or transiently worsen shortly after the last dose.Hypomagnesemia is the signature renal-tubular toxicity and one of panitumumab's most frequent adverse effects. Any-grade rates cluster around 30-40% across RAS/KRAS wild-type mCRC trials, with grade 3-4 hypomagnesemia in roughly 3-7%; it is dose- and duration-related and deepens with cumulative exposure (Van Cutsem, J Clin Oncol 2007, established it as a frequent toxicity of the registration monotherapy trial). Rates are consistently HIGHER than with cetuximab: a pooled analysis put the relative risk of hypomagnesemia at ~12.6 for panitumumab versus ~3.9 for cetuximab (Petrelli, Expert Opin Drug Saf 2011), and in the head-to-head ASPECCT trial grade 3-4 hypomagnesemia was 7% with panitumumab versus 3% with cetuximab (Price, Lancet Oncol 2014).MildIobenguane I-131Biphasic — modest, often transient creatinine changes within weeks of a therapeutic dose; the characteristic radiation nephropathy is delayed, typically appearing 6-12 months or later after cumulative renal irradiation, sometimes years out.Reported renal toxicity is uncommon and usually low-grade. In a dosimetry-guided high-activity 131I-MIBG cohort, 3 of 14 patients (21%) had transient grade 1 renal toxicity (Maric 2023, small single-center series using conventional 131I-MIBG). In the registrational high-specific-activity trial (Azedra, n=68 dosed), renal failure was not among the most common treatment-emergent events — nausea, myelosuppression and fatigue dominated — and clinically significant (grade >=3) nephrotoxicity was rare. The kidney concern is driven less by acute events than by the delayed, cumulative absorbed radiation dose, so headline incidence figures come from small cohorts and should be read as low-grade signal rather than a robust rate.Mild