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.
15signature agents
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· 6Mild· 7
Agents’ overall reversibility
Often irreversible· 1Partially reversible· 2Variable· 7Reversible· 5
Agents’ onset window
How soon each agent’s kidney toxicity typically appears — a whole-drug tempo, not specific to this lesion.
Subacute (weeks)· 10Delayed (weeks–months)· 1Variable· 4
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