Is kidney injury from Immune Checkpoint Inhibitors reversible?

Reversible. Typical onset: Delayed — median ~14 weeks after starting therapy..

How should kidney function be monitored during Immune Checkpoint Inhibitors therapy?

Check serum creatinine before every infusion — ICI-AIN often presents as an asymptomatic creatinine rise weeks to months into therapy, classically later than skin/GI/thyroid irritis; Screen urinalysis for new pyuria/sterile leukocyturia and sub-nephrotic proteinuria; eosinophiluria is insensitive and should not be relied on; Review the concurrent med list at each visit for PPIs, NSAIDs, and antibiotics — these are strongly associated with ICI-AIN and are potential confounding AIN triggers to stop; Track for concurrent extra-renal immune-related adverse events (colitis, hepatitis, thyroiditis, dermatitis), which frequently co-occur and support an immune-mediated etiology; Monitor creatinine response within days to 1-2 weeks of starting corticosteroids; failure to improve should prompt biopsy reconsideration and steroid escalation.

How can kidney injury from Immune Checkpoint Inhibitors be prevented?

Review and avoid concurrent AIN-causing drugs

Who is at higher risk of kidney injury from Immune Checkpoint Inhibitors?

Combination ICI therapy; Lower baseline eGFR; Concurrent PPI / AIN-associated drugs.

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Printable monograph

Immune checkpoint inhibitor

Immune Checkpoint Inhibitors

Keytruda · Opdivo · Yervoy · ICI

Immune checkpoint inhibitor · approved 2014 · 8 citations

Recent· through 2023

Fairly sourced5/9 · 5 signals

Met: 8 citations
Not met: 12+ references
Not met: Accrued over 10+ years (span: 7y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Met: Current through 2023
Not met: Real-world FAERS signal

Describes how this page is sourced, not how dangerous the drug is. Thinly sourced means fewer of the sourcing signals are met — not that the agent is kidney-safe. A rule-based summary, not a formal certainty appraisal.

Release the immune brakes and the interstitium pays — weeks to months later.

ModerateImmune checkpoint inhibitor

MelanomaNSCLCRenal cellMany others

§01

Signature kidney injury

Signature lesion

Acute Interstitial Nephritis

Representative incidence3%

2–5% range across studies

ICI-associated AKI ~2–5% (higher with combination therapy); ~93% of biopsies show interstitial nephritis.Source: Cortazar et al., JASN 2020

Onset & rechallenge

Time to injuryDelayed (>6 weeks / cumulative)

Delayed — a median of about 14 weeks after starting therapy.

Distilled from: “Delayed — median ~14 weeks after starting therapy.” · PMID 31896554 (opens PubMed in a new tab)

RechallengeCase-by-case

In the multicenter ICI-AKI cohort ~22% were rechallenged and ~23% of those developed recurrent AKI — feasible but an individualized, co-managed decision. PMID 31896554 (opens PubMed in a new tab)

§02

Renal toxicities, ranked

This agent's kidney lesions ordered by prominence — the #1 signature lesion first, then secondary and rare patterns. Cited incidence is shown where a citable figure exists; otherwise the tier stands qualitatively.

Acute Interstitial Nephritis#1 · Signaturequalitative — no citable incidence
Immune-mediated inflammation of the renal interstitium — the signature kidney injury of checkpoint inhibitors.
Glomerular Injury / ProteinuriaSecondaryqualitative — no citable incidence
Damage to the filtration barrier — podocyte injury, FSGS and protein leak from VEGF and mTOR blockade.
Electrolyte DisturbanceSecondaryqualitative — no citable incidence
Renal electrolyte derangement — magnesium/potassium/calcium wasting (cisplatin, anti-EGFR antibodies) or retention (FGFR-inhibitor hyperphosphatemia, tumor-lysis hyperkalemia/hyperphosphatemia).

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

3%incidence

SeverityModerate

ReversibilityReversible

Evidence8 citations

Nephron map

Glomerulus

Distal Tubule / Collecting Duct

InterstitiumSupporting tissue around the tubules

Acute Interstitial Nephritis

Immune-mediated inflammation of the renal interstitium — the signature kidney injury of checkpoint inhibitors.

§03

Kidney injury

Mechanism of kidney injury

Loss of self-tolerance is thought to let T cells attack the renal tubulointerstitium — an immune-related adverse event proposed to be driven by reactivation of drug-specific T cells. The long latency distinguishes it from classic drug-induced AIN.

Clinical presentation

AKI with modest sterile pyuria and sub-nephrotic proteinuria; eosinophilia is frequently ABSENT. Other immune-related adverse events (rash, colitis, thyroiditis) may coexist.

Management

Hold ICI and give corticosteroids (prednisone 0.5–1 mg/kg, tapered); biopsy if unclear. Rechallenge is possible but recurs in roughly 20-25% of reported cases.Lesion-level management framework

Risk factors

Combination ICI therapy
Lower baseline eGFR
Concurrent PPI / AIN-associated drugs

Prevention

Review and avoid concurrent AIN-causing drugs

Anticancer mechanism· how it treats cancer

Pembrolizumab, nivolumab and ipilimumab block PD-1, PD-L1 or CTLA-4, restoring anti-tumor T-cell activity. Melanoma, NSCLC, renal cell and many others.

Note · The most common immunotherapy-related kidney lesion.

§04

Clinical depth

Renal dose adjustment

As large monoclonal antibodies (anti-PD-1, anti-PD-L1, anti-CTLA-4) cleared by reticuloendothelial proteolysis rather than the kidney, ICIs require no dose adjustment for renal impairment and the labels specify no CrCl-based modification. Management of nephrotoxicity is immunologic, not pharmacokinetic: per ASCO/NCCN/KDIGO, hold the drug for grade 2+ AKI and start corticosteroids (typically prednisone ~0.5-1 mg/kg/day, higher for severe cases), with permanent discontinuation for grade 3-4 or recurrent nephritis.

Dialyzability & ESKD dosing

Not dialyzable — IgG-class antibodies are far too large to cross dialysis membranes, and renal replacement does not alter exposure, so no peri-HD timing adjustment is needed. ICIs have been used in patients on hemodialysis without PK-based dose changes, though outcome data are limited; ICI-AIN itself can progress to dialysis-requiring AKI in a minority, which is often reversible with timely steroids.

Differential diagnosis

ICI-AIN is a T-cell-mediated interstitial nephritis; distinguish it from prerenal azotemia (low FeNa, volume-responsive), ATN from concurrent platinum/contrast (granular casts, earlier onset), and drug-induced AIN from a co-prescribed PPI/NSAID/antibiotic — though these often coexist and the ICI may unmask tolerance to a companion drug. Delayed onset (often 8-16 weeks, sometimes months), sterile pyuria/sub-nephrotic proteinuria, accompanying extra-renal irAEs, and steroid responsiveness favor ICI-AIN; kidney biopsy remains the reference standard when the picture is atypical or steroids are being committed to.

Monitoring

Check serum creatinine before every infusion — ICI-AIN often presents as an asymptomatic creatinine rise weeks to months into therapy, classically later than skin/GI/thyroid irritis
Screen urinalysis for new pyuria/sterile leukocyturia and sub-nephrotic proteinuria; eosinophiluria is insensitive and should not be relied on
Review the concurrent med list at each visit for PPIs, NSAIDs, and antibiotics — these are strongly associated with ICI-AIN and are potential confounding AIN triggers to stop
Track for concurrent extra-renal immune-related adverse events (colitis, hepatitis, thyroiditis, dermatitis), which frequently co-occur and support an immune-mediated etiology
Monitor creatinine response within days to 1-2 weeks of starting corticosteroids; failure to improve should prompt biopsy reconsideration and steroid escalation

Key trials & series

CheckMate 067 (nivolumab +/- ipilimumab in melanoma) — defined the higher immune-related toxicity burden of combination CTLA-4/PD-1 blockade, including nephritis, versus monotherapy
KEYNOTE-189 / KEYNOTE-407 (pembrolizumab-chemotherapy in NSCLC) — registrational combination trials in which AKI/nephritis was more frequent with the ICI-plus-platinum-pemetrexed arms, highlighting combination nephrotoxicity
Cortazar et al., Kidney Int 2016 — first multicenter clinicopathologic series of ICI-associated AKI establishing acute interstitial nephritis as the dominant lesion and steroid responsiveness
Cortazar et al., J Am Soc Nephrol 2020 — large multicenter ICI-AKI cohort defining risk factors (PPI use, combination ICI, lower baseline eGFR) and that most patients recover renal function with steroids

Clinical pearls

AIN is by far the dominant ICI renal lesion; glomerular lesions (minimal change, pauci-immune/ANCA GN, podocytopathies) and electrolyte disorders occur but are much less common
Onset is characteristically delayed — typically weeks to several months after starting therapy, later than most other irAEs — so a 'late' creatinine bump should still trigger an ICI-AIN workup
Concomitant PPIs are a reproducible risk factor and a frequent companion AIN trigger; deprescribing an unnecessary PPI is both diagnostic and therapeutic
Most patients have at least partial renal recovery with prompt corticosteroids, and many can be successfully rechallenged with the ICI, though recurrence risk is real and is higher when nephritis was severe
Combination anti-CTLA-4 plus anti-PD-1 carries a higher nephritis rate than PD-1/PD-L1 monotherapy; baseline lower eGFR also raises risk

irAE atlasImmune-related adverse events of checkpoint blockade, indexed by organ

27 grade-indexed syndromes across 11 organ systems, written for checkpoint blockade as a class rather than per agent — where a rate differs between anti-PD-1, anti-PD-L1, anti-CTLA-4 and combination therapy, the card names the class it was measured in.

Beyond the kidney — non-renal toxicities· 5 organ systems

Class-level context for the major non-renal toxicities of the Immune checkpoint inhibitor class.

Endocrine

Thyroiditis, hypophysitis, diabetes

Thyroiditis, hypophysitis, type-1 diabetes

Gastrointestinal

Diarrhea, colitis, mucositis, perforation

Immune colitis

Hepatic / Liver

Transaminitis, hepatitis, VOD/SOS

Immune hepatitis

Pulmonary

Pneumonitis, ILD, effusions, hypertension

Pneumonitis

Dermatologic

Rash, HFS, SJS/TEN, vitiligo

Rash, vitiligo, rarely SJS/TEN

§05

References

5 primary references — trials, cohorts, mechanism, and reviews. Single-patient case reports are listed separately below, graded by strength. Citation metadata via PubMed / NLM.

Evidence accrual

5 references · 2016–2022 · 3 since 2020

Primary (non–case-report) references per year — a proxy for how actively the agent's renal literature is accruing. Recent years are highlighted. Reflects curation depth, not a systematic bibliometric count.

Case reports — ranked by strength· 3

Single-patient and small-series reports, graded by evidentiary strength — A Strong (biopsy-proven plus a series and/or positive rechallenge), B Moderate, and C Limited (a single clinically-diagnosed case). Strongest first. Grades are inferred automatically from each report's abstract and journal — a heuristic ranking aid, not a formal quality appraisal.

CaseA · StrongNivolumab-induced acute tubular injury: A case report.Yang HH et al. · Clin Case Rep 2023 · PMID 36911644Biopsy-proven acute tubular injury (not the usual interstitial nephritis) after nivolumab, with creatinine rise recurring on rechallenge and a positive lymphocyte transformation test.CaseB · ModerateImmune Checkpoint Inhibitor-Associated Sarcoidosis Reaction in the Kidney: Case Report.Charkviani M et al. · Kidney Med 2023 · PMID 37122393Kidney biopsy-proven sarcoid-like noncaseating granulomas causing stage 3 AKI with hypercalcemia and hyponatremia after nivolumab/ipilimumab for renal cell carcinoma.CaseC · LimitedPembrolizumab-Induced Anti-GBM Glomerulonephritis: A Case Report.El Yamani N et al. · Kidney Med 2023 · PMID 37415622Rare crescentic anti-glomerular basement membrane glomerulonephritis with severe AKI progressing to dialysis after pembrolizumab for cervical squamous cell carcinoma.

Conference abstracts & journal reports· 2 non-PubMed

Non-PubMed sources — conference abstracts (e.g. ASN Kidney Week, badged Abstract) and case reports from non-indexed field journals (e.g. Journal of Onco-Nephrology, badged Journal). Included for completeness; weigh below peer-reviewed PubMed citations.

JournalMinimal change disease and acute interstitial nephritis in a patient with Hodgkin's lymphoma treated with nivolumabChemaly ER, et al. · Journal of Onco-Nephrology 2020Minimal change disease with concurrent acute interstitial nephritis in a Hodgkin lymphoma patient on the PD-1 inhibitor nivolumab — a combined glomerular (podocytopathy) and interstitial checkpoint-inhibitor lesion. Journal of Onco-Nephrology (not PubMed-indexed).JournalA case of pembrolizumab induced distal renal tubular acidosisAtiq SO, Gokhale T, Atiq Z, Holmes R, Sparks MA · Journal of Onco-Nephrology 2021Distal renal tubular acidosis attributed to the PD-1 inhibitor pembrolizumab — a tubular checkpoint-inhibitor effect distinct from the usual interstitial nephritis. Journal of Onco-Nephrology (not PubMed-indexed).

Guidelines & consensus· 22

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.

ASONDiagnosis and management of immune checkpoint inhibitor-associated nephrotoxicity: a position statement from the American Society of Onco-nephrologyKidney Int 2025 · PMID 39455026ICI-AKI most commonly presents as acute interstitial nephritis; nephrology consultation and kidney biopsy should be considered for stage 2 or higher AKI or suspected glomerular disease, but where biopsy is not feasible, prompt empiric corticosteroids (prednisone ~1 mg/kg/day) should be started for clinically suspected ICI-AKI since early steroids improve renal recovery, with cautious individualized consideration of ICI rechallenge after recovery.ASCOManagement of Immune-Related Adverse Events in Patients Treated With Immune Checkpoint Inhibitor Therapy: ASCO Guideline UpdateJ Clin Oncol 2021 · PMID 34724392For grade 2 or higher ICI-related nephritis/AKI, hold the ICI, exclude alternative causes, and initiate corticosteroids (prednisone 0.5-1 mg/kg/day for grade 2, 1-2 mg/kg/day for grade 3-4) tapered over 4-6 weeks once creatinine improves; permanently discontinue for grade 4 toxicity.ESMOManagement of toxicities from immunotherapy: ESMO Clinical Practice Guideline for diagnosis, treatment and follow-upAnn Oncol 2022 · PMID 36270461For ICI-related AKI, exclude alternative etiologies and stop concomitant nephrotoxins (PPIs, NSAIDs); ESMO permits continuing the ICI for stage 1 AKI with monitoring, but recommends withholding the ICI and starting corticosteroids for stage 2 or higher nephritis, escalating immunosuppression for steroid-refractory disease.SITCSociety for Immunotherapy of Cancer (SITC) clinical practice guideline on immune checkpoint inhibitor-related adverse eventsJ Immunother Cancer 2021 · PMID 34172516Grade ICI-related AKI by CTCAE; for persistent grade 2 or higher renal toxicity, discontinue the ICI, exclude other causes, and treat with corticosteroids with a taper begun once creatinine improves toward grade 1, considering kidney biopsy and additional immunosuppression for refractory cases.IC-OSImmune Checkpoint Inhibitor-Associated Cardiovascular Toxic Effects: International Cardio-Oncology Society Position StatementJAMA Oncol 2026 · PMID 41231466Concerns for myocarditis continue to dominate the spectrum of CV toxic effects in patients receiving ICI therapy. Recommendations for management vary according to severity. Multidisciplinary collaborations remain key for managing acute toxic effects and future cancer treatment decisions, including ICI rechallenge.EULAREULAR points to consider for the diagnosis and management of rheumatic immune-related adverse events due to cancer immunotherapy with checkpoint inhibitorsAnn Rheum Dis 2021 · PMID 32327425Oncologists should be encouraged to consult rheumatologists promptly for assessment when rheumatic musculoskeletal and systemic signs or symptoms are suspected due to immunotherapy, and rheumatologists should provide facilitated access for such patients.ASCOManagement of Immune-Related Adverse Events in Patients Treated With Immune Checkpoint Inhibitor Therapy: American Society of Clinical Oncology Clinical Practice GuidelineJ Clin Oncol 2018 · PMID 29442540Withhold the checkpoint inhibitor and start corticosteroids for grade 2 or higher immune-related renal toxicity after excluding other causes of AKI, with steroid taper as renal function recovers and permanent discontinuation for severe (grade 4) events.PUMCH Expert PanelClinical recommendations on diagnosis and treatment of immune checkpoint inhibitor-induced renal immune-related adverse eventsThorac Cancer 2020 · PMID 32232975Screen and monitor with serum creatinine, urinalysis/sediment, and 24-hour urine protein; strongly recommend kidney biopsy to confirm ICI-related ATIN and exclude other AKI causes, withdraw nephrotoxins (PPIs, NSAIDs), and initiate corticosteroids when a grade 2 or higher renal irAE is highly suspected, with multidisciplinary decisions on ICI withdrawal and rechallenge.ADQIImmune Checkpoint Inhibitor-Associated Acute Kidney Injury: A Report from the 34th Acute Disease Quality Initiative (ADQI) Consensus ConferenceJ Am Soc Nephrol 2026 · PMID 42536415AKI occurs in up to 20% of ICI-treated patients with ICI-AKI accounting for roughly 2-5% of cases, and acute tubulointerstitial nephritis dominates (80-90% of biopsies); no clinical feature reliably separates ICI-AKI from other causes, so kidney biopsy remains the diagnostic gold standard and emerging biomarkers are not yet ready for routine use. Early glucocorticoid initiation (within 3 days of diagnosis) is associated with higher rates of kidney recovery, and recurrent ICI-AKI occurs in fewer than 20% of rechallenged patients, supporting cautious rechallenge in selected patients with individualized multidisciplinary decisions for transplant recipients and other high-risk groups.

General onco-nephrology references

ADQIThe nephrotoxic effects of anti-cancer therapies: consensus report of the 34th Acute Disease Quality Initiative workgroupNat Rev Nephrol 2026 · PMID 41361704Provides expert-based statements (modified Delphi) on preventing and managing cisplatin/platinum-associated AKI, including isotonic IV hydration, attention to volume status and concomitant nephrotoxins, and incorporates evidence that IV magnesium supplementation may reduce cisplatin-associated AKI; emphasizes risk stratification and standardized AKI definitions.SIRMSIRM-SIN-AIOM: appropriateness criteria for evaluation and prevention of renal damage in the patient undergoing contrast medium examinations-consensus statements from Italian College of Radiology (SIRM), Italian College of Nephrology (SIN) and Italian Association of Medical Oncology (AIOM)Radiol Med 2022 · PMID 35303246Recommends eGFR-based renal risk assessment and pre/post-contrast isotonic saline or sodium bicarbonate hydration; advises maintaining a 5-7 day interval between iodinated contrast administration and cisplatin in cancer patients to reduce additive nephrotoxicity.KDIGOKDIGO Controversies Conference on onco-nephrology: understanding kidney impairment and solid-organ malignancies, and managing kidney cancerKidney Int 2020 · PMID 33126977Identifies platinum compounds (especially cisplatin) as leading cytotoxic causes of acute tubular injury, AKI, and electrolyte/magnesium wasting; calls for interdisciplinary onco-nephrology care, accurate GFR estimation, and individualized drug dosing in patients with reduced kidney function.KDIGOKDIGO Controversies Conference on onco-nephrology: kidney disease in hematological malignancies and the burden of cancer after kidney transplantationKidney Int 2020 · PMID 33276867Addresses chemotherapy-associated AKI/CKD in hematologic cancer, GFR estimation and chemotherapy dosing in patients with reduced kidney function, and management priorities and research gaps for onco-nephrology care.ADDIKDIntegrating International Consensus Guidelines for Anticancer Drug Dosing in Kidney Dysfunction (ADDIKD) into everyday practiceEClinicalMedicine 2025 · PMID 40290844Provides GRADE-based, drug-specific dose-adjustment recommendations for anticancer agents in kidney dysfunction (illustrated for methotrexate, cisplatin, carboplatin and nivolumab); the recommendations build on Part 1's standardised CKD-EPI eGFR assessment rather than Cockcroft-Gault creatinine clearance.ADDIKDAligning kidney function assessment in patients with cancer to global practices in internal medicineEClinicalMedicine 2025 · PMID 40290845Three consensus recommendations: assess kidney function by GFR (measured GFR or CKD-EPI eGFR), classify it using KDIGO categories, and use this uniform approach to dose anticancer drugs — moving cancer medicine away from Cockcroft-Gault estimated creatinine clearance.ADDIKDA methodology for determining dosing recommendations for anticancer drugs in patients with reduced kidney functionEClinicalMedicine 2025 · PMID 40290846Establishes that, where RCT evidence is lacking, anticancer drug dosing recommendations in kidney dysfunction should be derived by critically appraising observational literature via GRADE combined with structured international multidisciplinary consensus voting.KDIGODiagnosis, evaluation, and management of acute kidney injury: a KDIGO summary (Part 1)Crit Care 2013 · PMID 23394211Defines/stages AKI by serum creatinine and urine output; emphasizes avoiding nephrotoxins, maintaining euvolemia/perfusion, dose-adjusting drugs to kidney function, and monitoring high-risk patients — the framework applied to nephrotoxic anti-cancer agents.KDIGOExecutive summary of the KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease: known knowns and known unknownsKidney Int 2024 · PMID 38519239Evaluate and risk-stratify CKD, manage to delay progression and its complications, and practise explicit medication management and drug stewardship — the framework the atlas's G1–G5 eGFR banding and every renal dose-adjustment recommendation sit inside. Because the guideline excludes dialysis and transplant recipients by its own statement of scope, its recommendations do not carry to those settings, where this atlas's dialyzability and post-transplant guidance rests on other sources.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.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 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.

Where Immune Checkpoint Inhibitors sits in nephrotoxicity space — each dot is an anti-cancer agent, positioned so neighbors share a kidney-injury phenotype. Its 6 closest are filled and lead to a numbered marker, matching the numbered cards below.

Position is a 2-D projection (MDS) of each agent's injury signature, nephron target, severity, and class, so two dots can sit close on the page while differing on an axis the projection flattened — the numbered ranking is computed from the full metric, not from the distance you see. Open the full map.

Phenotype-similar agents· the numbered markers on the map above

Toripalimab

Loqtorzi · PD-1 immune checkpoint inhibitor

Profile

First FDA-approved drug for nasopharyngeal carcinoma; renal risk is class-typical immune-mediated interstitial nephritis.

AINLYTEGLOM

Moderate#1 · 85% phenotype match

Cosibelimab

Unloxcyt · PD-L1 immune checkpoint inhibitor

Profile

PD-L1 blockade for cutaneous SCC — watch for late immune interstitial nephritis

AINGLOMLYTE

Moderate#2 · 85% phenotype match

Avelumab

Bavencio · Anti-PD-L1 antibody

Profile

ICI-associated AIN.

AINGLOM

Moderate#3 · 73% phenotype match

Cemiplimab

Libtayo · Anti-PD-1 antibody

Profile

ICI-associated AIN.

AINGLOM

Moderate#4 · 73% phenotype match

Dostarlimab

Jemperli · Anti-PD-1 antibody

Profile

ICI-associated AIN.

AINGLOM

Moderate#5 · 73% phenotype match

Durvalumab

Imfinzi · Anti-PD-L1 antibody

Profile

ICI-associated AIN.

AINGLOM

Moderate#6 · 73% phenotype match

Compare Immune Checkpoint Inhibitors with its nearest agents

Nearest agents by kidney-injury phenotype (shared injuries, nephron target, severity, class) — a similarity approximation, not a claim of shared drug identity or mechanism.

Kidney risk across Checkpoint inhibitors

Same-class agents ordered by their documented kidney-injury profile — atlas severity, an acute-kidney-injury FAERS signal, and how many injury types each is documented to cause. Agents nearer the top carry the lighter documented renal profile.

A comparison of documented kidney-injury data within one drug class — not a substitution recommendation. Efficacy, indication, and non-renal toxicity differ between these agents and are out of scope here. Educational only, not medical advice.

Who studies this

The leading contributors to Immune Checkpoint Inhibitors’s clinical kidney literature on PubMed, ranked by a blend of publication volume and citation impact — filtered toward clinical work via the PubMed Humans heading and clinical publication types (trials, cohorts, case reports, guidelines, reviews). Names link to that author’s work on Immune Checkpoint Inhibitors; the PMIDs beside each name are up to three of their most recent papers on it, not the full count.

Ranked by a 50/50 blend of publication volume and a position-weighted, capped Relative Citation Ratio (NIH iCite) on this agent’s renal literature; the citation count shown is the raw total, not the ranking score — counted over the 247 clinical records among the 300 most-relevant of 530 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.