What kind of kidney injury does Relatlimab cause?

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

How should kidney function be monitored during Relatlimab therapy?

Urinalysis if creatinine rises (pyuria/WBC casts/tubular proteinuria); Surveillance for extrarenal immune-related adverse events.

How can kidney injury from Relatlimab be prevented?

Review and minimize concomitant AIN-associated drugs Patient education on irAE symptoms

Who is at higher risk of kidney injury from Relatlimab?

Combination checkpoint blockade (relatlimab + nivolumab); Concurrent AIN-associated drugs (PPIs, NSAIDs, antibiotics); Prior immune-related adverse events; Pre-existing CKD.

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Printable monograph

Immune checkpoint inhibitor (anti-LAG-3)

Relatlimab

Opdualag · Rela

Immune checkpoint inhibitor (anti-LAG-3) · approved 2022 · 7 citations · FAERS AKI reporting ROR 2.66 (95% CI 1.37–5.14, 9 AKI reports)

Up to date· through 2026

Fairly sourced6/9 · 6 signals

Met: 7 citations
Not met: 12+ references
Not met: Accrued over 10+ years (span: 6y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Met: Current through 2026
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.

An anti-LAG-3 checkpoint inhibitor whose kidney risk is the class lesion — immune-mediated acute interstitial nephritis, amplified in combination with nivolumab.

ModerateImmune checkpoint inhibitor (anti-LAG-3)

Unresectable or metastatic melanoma (with nivolumab)

§01

Signature kidney injury

Signature lesion

Acute Interstitial Nephritis

LAG-3-specific renal literature is thin: dedicated searches return no relatlimab AKI cohort or case series, and the pivotal RELATIVITY-047 trial reported aggregate grade 3/4 treatment-related adverse events (about 18.9% with the combination vs 9.7% with nivolumab alone) without an isolated nephritis rate. The renal signal is therefore class-based — immune checkpoint inhibitors cause acute interstitial nephritis, the dominant lesion in 80–90%+ of biopsied ICI-AKI cases, with combination immunotherapy a recognized risk factor.Source: Tawbi et al., NEJM 2022 (RELATIVITY-047); Cortazar et al., JASN 2020 (ICI-AKI biopsy series)

Onset & rechallenge

Time to injuryDelayed (>6 weeks / cumulative)

Typically weeks to months after initiation (long ICI-AIN latency).

Distilled from: “Delayed — typically weeks to months after initiation (long latency is characteristic of ICI-AIN).”

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)

Long-term outlook & thresholds

Renal recoveryOften partial recovery

Class-level checkpoint-inhibitor AKI recovery: in a 138-patient multicenter ICI-AKI cohort, complete, partial, and no recovery of kidney function occurred in roughly 40%, 45%, and 15% of patients respectively. Two covariates carried a better renal prognosis — treatment with steroids, and the PRESENCE of a concomitant tubulointerstitial-nephritis-causing medication (69% of patients were on one). The second is an observational association, not an intervention: the cohort analysed no effect of stopping that drug, and the likeliest reading is that a competing culprit makes the ICI a less certain cause. Rechallenge is feasible in selected patients but recurrent AKI occurs in about a quarter.PMID 31896554 (opens PubMed in a new tab)

CKD trajectory.: Roughly 15% of patients have no renal recovery, leaving residual chronic kidney disease, and recovery is often incomplete (partial recovery in ~45%) — a class-level pattern across checkpoint inhibitors. A separate single-center cohort of 1,037 ICI-treated patients sharpens the comparison: complete kidney recovery was less common after ICI-attributed AKI than after AKI from other causes (54% versus 79%, p=0.01), and ICI-AKI reached higher AKI stages.PMID 37499561 (opens PubMed in a new tab)
Dialysis / RRT.: Severe checkpoint-inhibitor AKI can require dialysis, though most ICI-attributed AKI is not dialysis-requiring.

Long-term outcome and threshold data distilled from the agent's cited literature — educational, not a substitute for the primary sources.

Recovery across agents

§02

Renal toxicities, ranked

This agent's defining kidney lesion — its #1 signature. 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.

§03

Kidney injury

Mechanism of kidney injury

By analogy to the established immune-checkpoint-inhibitor mechanism, LAG-3 blockade (combined with PD-1 blockade) disrupts peripheral immune tolerance and permits T-cell-mediated tubulointerstitial inflammation — acute interstitial nephritis. Multicenter ICI-AKI series show acute tubulointerstitial nephritis as the predominant biopsy lesion (>80–90%), often with a long latency and frequently potentiated by concomitant AIN-associated drugs (PPIs, NSAIDs). Combination checkpoint blockade (as in Opdualag) increases the risk relative to single-agent PD-1 therapy. A direct relatlimab-specific renal lesion has not been separately characterized.

Clinical presentation

A subacute creatinine rise (often weeks to months into therapy), sometimes with sterile pyuria, white-cell casts, low-grade tubular proteinuria and occasionally eosinophilia; eosinophiluria is insensitive. Extrarenal immune-related adverse events may coexist. Nephrotic-range proteinuria is uncommon and suggests an alternative glomerular irAE.

Management

Hold the drug and exclude alternative causes; treat suspected ICI-AIN with corticosteroids (early initiation improves renal recovery in multicenter cohorts), with biopsy when feasible to confirm. Discontinue contributing AIN-associated drugs. Rechallenge decisions are individualized, weighing recurrence risk; corticosteroid duration influences recurrence.Lesion-level management framework

Risk factors

Combination checkpoint blockade (relatlimab + nivolumab)
Concurrent AIN-associated drugs (PPIs, NSAIDs, antibiotics)
Prior immune-related adverse events
Pre-existing CKD

Prevention

Review and minimize concomitant AIN-associated drugs
Patient education on irAE symptoms

Anticancer mechanism· how it treats cancer

Monoclonal antibody against lymphocyte-activation gene-3 (LAG-3), an inhibitory immune checkpoint on T cells. Blocking LAG-3 restores T-cell activation; given as a fixed-dose combination with the anti-PD-1 antibody nivolumab (Opdualag) for unresectable or metastatic melanoma.

Note · Relatlimab-specific renal data are thin — the AIN signature is inferred from the broader ICI class literature (where acute tubulointerstitial nephritis dominates) and from the combination's higher overall irAE rate. No relatlimab-specific AIN incidence has been quantified.

§04

Clinical depth

Renal dose adjustment

No renal dose adjustment is established (monoclonal antibody, not renally cleared); mild–moderate impairment does not require change. The actionable step is holding the drug and steroid treatment for immune-mediated AIN rather than dose modification.

Dialyzability & ESKD dosing

The IgG antibodies are not dialyzable and are cleared by proteolysis; no ESKD dose change is expected. Dialysis supports severe AKI management, not drug removal.

Differential diagnosis

ICI-associated acute interstitial nephritis (subacute creatinine rise, sterile pyuria/WBC casts, long latency, steroid-responsive) vs prerenal AKI vs a glomerular irAE (heavy proteinuria) vs drug AIN from co-medications; biopsy and the temporal/medication context discriminate, and combination therapy raises pre-test probability.

Monitoring

Urinalysis if creatinine rises (pyuria/WBC casts/tubular proteinuria)
Surveillance for extrarenal immune-related adverse events

Key trials & series

RELATIVITY-047 (Tawbi NEJM 2022) — pivotal phase 2/3 combination trial
Cortazar JASN 2020 and Gupta J Immunother Cancer 2021 — multicenter ICI-AKI biopsy series (class evidence)

Clinical pearls

Latency is long — a creatinine rise weeks to months in, often with sterile pyuria, should trigger drug-hold and nephrology referral, not just dose-reduction.

Where it strikes· nephron segments & injury signatures

Nephron segments

Interstitium

Supporting tissue around the tubules

Injury signatures

Acute Interstitial Nephritis

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 (anti-LAG-3) 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 · 2020–2023 · 3 since 2021

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· 2

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.

CaseC · LimitedImmune checkpoint inhibitor-associated lymphocytic colitis in a patient with metastatic melanoma.Matar R et al. · BMJ Case Rep 2026 · PMID 42156103Case of immune checkpoint inhibitor-associated lymphocytic colitis in a melanoma patient on nivolumab/relatlimab — an extrarenal immune-related adverse event that illustrates the combination's propensity for immune-mediated toxicity.CaseC · LimitedTreatment of metastatic melanoma with anti-PD-1 and anti-LAG-3 in a kidney transplant recipient.Patel JD et al. · Immunotherapy 2025 · PMID 40119495Nivolumab/relatlimab in a kidney transplant recipient caused rapid renal allograft rejection, with LAG-3 expression positive in the renal graft tissue.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 472 of them for this agent. Nobody counts the patients who were fine, so none of these numbers is an incidence, a risk, or a rate: they describe what gets reported, shaped by a drug's fame, its indication, and who was watching. How these numbers work.

Reporting odds ratio (ROR) — is kidney injury named in this agent's reports more often than in every other drug's? Above 1 means yes, disproportionately.
Renal phenotypes — the same question asked separately for each kind of kidney injury, so the ratios differ from the overall one and from each other.
Outcomes — a share of this agent's own reports, not of patients: how many were filed as involving a death or a hospitalization. Not a case-fatality rate.

FAERS reported renal phenotypes· 1 signal

Only significant signals appear (95% CI lower bound above 1) — a phenotype missing here was tested and did not reach significance, except Prerenal / Hemodynamic AKI, Pseudo-AKI, Renal Cysts, Chronic Interstitial Nephropathy — outside the clinician-reviewed MedDRA term map, never queried — and ATN and AIN, queried but biopsy-bound: real cases are filed as generic “acute kidney injury”, so their absence is not a negative. As of 2026-10-01.

What reporting says about this profile's documented lesions

Acute Interstitial Nephritiscorroborated · ROR 11.98

Acute Interstitial Nephritis

ROR 11.9895% CI 4.96–28.92· 5 reports

FAERS outcomes & reporting trend· 20.1% of reports w/ death · 21.8% w/ hospitalization

20.1%

Reported with a death outcome

95 of 472 reports

21.8%

Reported with hospitalization

103 of 472 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 11 systems · 472 reports

Bars rank systems by summed reaction-term mentions (a report counts once per term it names) — an ordinal “more vs less reported” cue, not a tally of distinct reports. Renal & urinary first. Showing the top 10 of 11 classified systems; 1 lower-ranked system is not drawn. As of 2026-10-01.

Disproportionality (acute kidney injury):ROR 2.6695% CI 1.37–5.14· 9 AKI reports ·AKI is reported disproportionately more often than for other drugs (CI entirely above 1) — a hypothesis-generating signal, not proof of causation.

Renal & urinary

Acute Kidney Injury9

General / constitutional

Fatigue17Myasthenia Gravis12Weight Decreased9Pain7Back Pain6

Cardiac

Myocarditis19Troponin Increased7Immune-Mediated Myocarditis6

Gastrointestinal

Colitis12Diarrhoea12Abdominal Pain6

Immune / infection

Immune-Mediated Myositis9Infusion Related Reaction8

Skin

Rash13

Musculoskeletal

Muscular Weakness7Arthralgia6

Endocrine

Hypothyroidism9

Metabolic & electrolyte

Decreased Appetite8

Respiratory

Dyspnoea8

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 Relatlimab 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

Bicalutamide

Casodex · Nonsteroidal antiandrogen

Profile

Hepatically cleared, kidney-neutral, no renal dose adjustment; only rare idiosyncratic interstitial nephritis.

AIN

Mild#1 · 81% phenotype match

Checkpoint inhibitors (pembrolizumab · nivolumab · ipilimumab)

Immune checkpoint inhibitor

Profile

Acute interstitial nephritis with long latency.

AINGLOMLYTE

Moderate#2 · 65% phenotype match

Avelumab

Bavencio · Anti-PD-L1 antibody

Profile

ICI-associated AIN.

AINGLOM

Moderate#3 · 62% phenotype match

Cemiplimab

Libtayo · Anti-PD-1 antibody

Profile

ICI-associated AIN.

AINGLOM

Moderate#4 · 62% phenotype match

Dostarlimab

Jemperli · Anti-PD-1 antibody

Profile

ICI-associated AIN.

AINGLOM

Moderate#5 · 62% phenotype match

Durvalumab

Imfinzi · Anti-PD-L1 antibody

Profile

ICI-associated AIN.

AINGLOM

Moderate#6 · 62% phenotype match

Compare Relatlimab 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.