How should kidney function be monitored during Retifanlimab therapy?

Urinalysis with protein and sediment when creatinine rises; Serum electrolytes including sodium, potassium, magnesium; Surveillance for concurrent immune-related adverse events (TSH, LFTs, symptoms).

How can kidney injury from Retifanlimab be prevented?

Review and deprescribe non-essential PPIs and NSAIDs before and during therapy Treat concurrent immune-related adverse events promptly

Who is at higher risk of kidney injury from Retifanlimab?

Concomitant proton pump inhibitors; Concomitant NSAIDs or recent nephritogenic antibiotics; Combination with CTLA-4 blockade or other immunotherapy; Prior immune-related adverse events; Pre-existing chronic kidney disease or lower baseline eGFR.

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Printable monograph

PD-1 immune checkpoint inhibitor

Retifanlimab

Zynyz · PD-1 inhibitor

PD-1 immune checkpoint inhibitor · approved 2023 · 6 citations

Up to date· through 2025

Fairly sourced5/9 · 5 signals

Met: 6 citations
Not met: 12+ references
Not met: Accrued over 10+ years (span: 5y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Met: Current through 2025
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.

PD-1 blockade — kidney injury is immune-mediated interstitial nephritis, not direct tubular toxicity.

Moderatecheckpoint-immunotherapy

Metastatic or recurrent locally advanced Merkel cell carcinoma (accelerated approval, 2023)Locally recurrent or metastatic squamous cell carcinoma of the anal canal, first-line with carboplatin-paclitaxel (POD1UM-303)

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Signature kidney injury

Signature lesion

Acute Interstitial Nephritis

Representative incidence2%

1–3% range across studies

Renal immune-related adverse events are uncommon with PD-1 monotherapy. Across the checkpoint-inhibitor class, checkpoint-attributed AKI occurs in roughly 2-5% of treated patients (a 2023 meta-analysis of 24,048 patients pooled it at 5.7%) and biopsy-confirmed immune-related AIN in approximately 1-3%, with higher rates when combined with CTLA-4 blockade or nephritogenic co-medications (PPIs, NSAIDs). Any-cause AKI in real-world ICI cohorts runs far higher (~16-17%) but is mostly prerenal or non-immune rather than true ICI-nephritis. Retifanlimab's registrational program did not flag nephritis as a prominent signal; in the phase III POD1UM-303 anal-cancer trial the dominant grade ≥3 events were chemotherapy-driven cytopenias (neutropenia 35%, anemia 20%), not renal events.Source: Class-level AIN/AKI incidence extrapolated from ICI nephrotoxicity literature (PMID 33162990); retifanlimab-specific safety from POD1UM-303 (PMID 40517007) and POD1UM-202 (PMID 35816951), where renal events were not a leading toxicity.

Onset & rechallenge

Time to injuryDelayed (>6 weeks / cumulative)

Weeks to several months (median ~3 months); can occur after discontinuation.

Distilled from: “Usually delayed — weeks to several months after initiation (median ~3 months for ICI-AIN), but can occur at any point including after discontinuation.”

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

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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 · Signatureno population incidence denominator
Acute tubulointerstitial nephritis is the signature ICI renal lesion — dominant in 93% of the 60 biopsied patients in a 138-patient multicenter ICI-AKI cohort (a biopsy-lesion proportion, not a treated-population incidence). PMID 31896554 (opens PubMed in a new tab)
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).
Prerenal / Hemodynamic AKIRarequalitative — no citable incidence
Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

2%incidence

SeverityModerate

ReversibilityPartially reversible

Evidence6 citations

Nephron map

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.

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Kidney injury

Mechanism of kidney injury

Kidney injury is immune-mediated, not a direct toxic effect on tubular cells. PD-1/PD-L1 blockade abrogates peripheral tolerance, allowing reactivation of effector T cells directed against self or drug-hapten antigens within the renal interstitium, producing a T-cell–rich acute tubulointerstitial nephritis. Tubular epithelial PD-L1 expression appears permissive: biopsy series show AIN arises only where tubular PD-L1 and interstitial PD-1–positive inflammatory cells coexist (PMID 35755033, PMID 33552089). Concomitant PPIs, NSAIDs, and antibiotics are frequent co-triggers via the same loss-of-tolerance mechanism.

Clinical presentation

Typically a subacute, often asymptomatic rise in serum creatinine weeks to months into therapy. Urinalysis may show sterile pyuria and subnephrotic proteinuria; eosinophiluria is insensitive. Fever, rash, or eosinophilia accompany a minority. Concurrent extrarenal immune-related adverse events (thyroiditis, colitis, hepatitis, dermatitis) raise suspicion. Hyponatremia and mild electrolyte disturbances may co-occur.

Management

Withhold retifanlimab for grade 2 and permanently discontinue for grade 3-4 or recurrent immune-mediated nephritis per label guidance. Exclude prerenal, obstructive, and competing causes; discontinue offending co-medications (PPIs, NSAIDs). For immune-related AIN, start corticosteroids (prednisone ~0.5-1 mg/kg/day, up to 1-2 mg/kg for severe disease) with a slow taper over 4-6+ weeks; consider kidney biopsy to confirm AIN versus ATN before committing to prolonged steroids. Most patients recover at least partial function; steroid dose and chronicity on biopsy did not predict recovery in one cohort, whereas lower serum sodium did (PMID 37547603). Rechallenge is case-by-case after full recovery.Lesion-level management framework

Risk factors

Concomitant proton pump inhibitors
Concomitant NSAIDs or recent nephritogenic antibiotics
Combination with CTLA-4 blockade or other immunotherapy
Prior immune-related adverse events
Pre-existing chronic kidney disease or lower baseline eGFR

Prevention

Review and deprescribe non-essential PPIs and NSAIDs before and during therapy
Treat concurrent immune-related adverse events promptly

Anticancer mechanism· how it treats cancer

Retifanlimab is a humanized, hinge-stabilized IgG4κ monoclonal antibody that binds programmed cell death protein 1 (PD-1) on T cells and blocks its engagement by PD-L1/PD-L2. This releases the inhibitory checkpoint that tumors exploit, restoring cytotoxic T-cell recognition and killing of malignant cells. The crystal structure (PMID 39632294) shows the epitope partially overlaps the ligand-binding site, reshaping the PD-1 BC, C'D, and FG loops to occlude PD-L1 docking.

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Clinical depth

Renal dose adjustment

No dose adjustment for mild-to-moderate renal impairment; retifanlimab is a monoclonal antibody cleared by reticuloendothelial catabolism, not renal excretion. No studied data in severe impairment or dialysis. Dosing is flat (500 mg IV every 4 weeks), not weight- or GFR-based. Renal management is toxicity-driven (withhold/discontinue) rather than pharmacokinetic dose reduction.

Dialyzability & ESKD dosing

Not dialyzable. As a ~150 kDa IgG4 monoclonal antibody it is not removed by hemodialysis or peritoneal dialysis; no supplemental dosing needed around dialysis sessions.

Differential diagnosis

Distinguish immune-related AIN from prerenal azotemia (volume depletion, chemotherapy-associated emesis/diarrhea in the anal-cancer regimen), contrast or platinum-related ATN from concurrent carboplatin, obstruction, and drug-induced AIN from co-prescribed PPIs/NSAIDs/antibiotics. Biopsy is the discriminator: ICI-AIN shows T-cell–rich interstitial infiltrate with tubular PD-L1 positivity, versus tubular necrosis in ATN. TMA and glomerular lesions are rare with PD-1 agents and should prompt a search for alternative causes.

Monitoring

Urinalysis with protein and sediment when creatinine rises
Serum electrolytes including sodium, potassium, magnesium
Surveillance for concurrent immune-related adverse events (TSH, LFTs, symptoms)

Key trials & series

POD1UM-303/InterAACT-2 (NCT04472429) — phase III, first-line anal SCC, retifanlimab + carboplatin-paclitaxel improved PFS (9.3 vs 7.4 mo, HR 0.63); PMID 40517007
POD1UM-202 (NCT03597295) — phase II, previously treated advanced anal SCC, ORR 13.8%; PMID 35816951
POD1UM-201 — phase II in metastatic Merkel cell carcinoma, basis for accelerated approval

Clinical pearls

AIN is often clinically silent; a subacute creatinine rise weeks-to-months in, with sterile pyuria, is the classic clue.
Always hunt for a concomitant PPI or NSAID — they are frequent co-triggers and the easiest modifiable risk factor.
The antibody is renally inert pharmacokinetically: no GFR-based dose adjustment and not dialyzable; manage the kidney by withholding/steroids, not dose reduction.
Lower serum sodium at the time of biopsy has been associated with better renal recovery in ICI-AIN — a counterintuitive prognostic signal.

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 PD-1 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

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References

6 primary references — trials, cohorts, mechanism, and reviews. Citation metadata via PubMed / NLM.

Evidence accrual

6 references · 2020–2025 · 3 since 2023

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.

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 Retifanlimab 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

Checkpoint inhibitors (pembrolizumab · nivolumab · ipilimumab)

Immune checkpoint inhibitor

Profile

Acute interstitial nephritis with long latency.

AINGLOMLYTE

Moderate#1 · 61% phenotype match

Amivantamab

Rybrevant · EGFR-MET bispecific antibody

Profile

EGFR-mediated electrolyte (magnesium) wasting; an emerging acute interstitial nephritis signal is also clinician-flagged.

LYTEAIN

Moderate#2 · 61% phenotype match

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#3 · 61% phenotype match

Cosibelimab

Unloxcyt · PD-L1 immune checkpoint inhibitor

Profile

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

AINGLOMLYTE

Moderate#4 · 61% phenotype match

Penpulimab

Penpulimab (AK105) · PD-1 immune checkpoint inhibitor

Profile

Fc-silent PD-1 blocker for nasopharyngeal carcinoma — class-typical, infrequent immune interstitial nephritis

AINATNLYTE

Moderate#5 · 60% phenotype match

Sugemalimab

Cejemly · PD-L1 immune checkpoint inhibitor

Profile

A full-length anti-PD-L1 antibody whose kidney is its immune system: rare but real autoimmune interstitial nephritis.

AINATNLYTE

Moderate#6 · 60% phenotype match

Compare Retifanlimab 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.