How should kidney function be monitored during Cosibelimab therapy?

Urinalysis with microscopy (pyuria, casts) and quantified proteinuria (UPCR/UACR); Assessment for concurrent extrarenal immune-related adverse events; Medication review for PPIs/NSAIDs and other nephrotoxins; Serum electrolytes including potassium and magnesium.

How can kidney injury from Cosibelimab be prevented?

Review and minimize concurrent nephritis-associated drugs (PPIs, NSAIDs) Hold the drug and treat per immune-related adverse event guidelines at first sign of significant creatinine rise

Who is at higher risk of kidney injury from Cosibelimab?

Pre-existing chronic kidney disease; Older age; Concurrent proton pump inhibitor use; Concurrent NSAID use; Concurrent diuretics or ACEI/ARB use; Combination checkpoint blockade (e.g., added CTLA-4 inhibitor); Other extrarenal immune-related adverse events; Prior or concurrent nephritogenic drug exposure.

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Printable monograph

PD-L1 immune checkpoint inhibitor

Cosibelimab

Unloxcyt · PD-L1 inhibitor

PD-L1 immune checkpoint inhibitor · approved 2024 · 5 citations

Up to date· through 2025

Fairly sourced4/9 · 4 signals

Not met: 5 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-L1 blockade for cutaneous SCC — watch for late immune interstitial nephritis

ModeratePD-L1 checkpoint inhibitor era (2020s)

Metastatic cutaneous squamous cell carcinoma (mCSCC) not eligible for curative surgery or radiationLocally advanced cutaneous squamous cell carcinoma (laCSCC) not eligible for curative surgery or radiation

§01

Signature kidney injury

Signature lesion

Acute Interstitial Nephritis

Representative incidence2%

1–3% range across studies

Drug-specific renal data are limited. In the pivotal phase 1 metastatic CSCC cohort (n=78), immune-related adverse events occurred in 23.1% of patients (grade 3 in 2.6%; no grade 4/5), with no nephritis-specific signal reported and a favorable overall safety profile. By class, immune-mediated nephritis/AKI with checkpoint inhibitors is uncommon: a 2023 systematic review and meta-analysis of 27 studies (24,048 patients) found a pooled all-cause AKI incidence of ~5.7%, with clinically significant immune-mediated nephritis substantially lower (roughly 1-3%), and anti-PD-L1 agents tending toward the lower end of that range versus CTLA-4 or combination regimens.Source: Class-level estimate from Liu et al., Front Immunol 2023 (PMID 37313406): pooled ICI-associated AKI incidence 5.7%; drug-specific phase 1 safety from Clingan et al., J Immunother Cancer 2023 (PMID 37848259).

Onset & rechallenge

Time to injuryDelayed (>6 weeks / cumulative)

Weeks to months; pooled ICI median ~3–4 months (~108 days).

Distilled from: “Delayed and variable — typically weeks to months after initiation. Pooled ICI data place median time to AKI at roughly 3-4 months (~108 days), though onset ranges from a few weeks to after treatment discontinuation.”

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 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).
Glomerular Injury / ProteinuriaRareno population incidence denominator
Case-level; glomerular lesions (2 membranous nephropathy, 2 minimal change disease) among 12 biopsy/nephrologist-attributed ICI nephrotoxicity cases. PMID 32601079 (opens PubMed in a new tab)

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

2%incidence

SeverityModerate

ReversibilityPartially reversible

Evidence5 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

The dominant renal mechanism is immune-related: PD-L1 blockade reactivates self-reactive effector T cells and breaks peripheral tolerance, producing a CD4/CD8 T-cell-rich acute (tubulo)interstitial nephritis. Contributing mechanisms described for the PD-1/PD-L1 axis include loss of tolerance to self renal antigens, reactivation of T cells previously primed by nephritogenic co-medications (PPIs, NSAIDs, antibiotics), and increased PD-L1 expression by tubular epithelium. Less commonly, immune dysregulation can produce glomerular lesions (e.g., podocytopathy/minimal-change-like or other immune-complex glomerulonephritis) and electrolyte disturbances. There is no appreciable direct tubular toxicity from the antibody itself.

Clinical presentation

Typically an asymptomatic, often delayed rise in serum creatinine detected on routine labs. Sterile pyuria, subnephrotic proteinuria, white-cell casts, and eosinophilia may be present but are inconsistent; classic allergic-AIN features (rash, fever, eosinophilia) are frequently absent. Concurrent extrarenal immune-related adverse events (dermatitis, colitis, thyroiditis, hepatitis) raise suspicion. Glomerular involvement, when it occurs, may present with new or worsening proteinuria.

Management

Per checkpoint-inhibitor immune-related adverse event guidance: for grade 2 nephritis (creatinine 2.0-3.0x baseline, CTCAE v5.0) hold cosibelimab and start corticosteroids (prednisone ~0.5-1 mg/kg/day); for grade 3-4 (creatinine >3.0x baseline or >4.0 mg/dL, or dialysis-requiring) permanently discontinue and give methylprednisolone 1-2 mg/kg/day with slow taper over at least 4-6 weeks. Exclude pre-renal, obstructive, and other causes; involve nephrology and consider kidney biopsy when the diagnosis is uncertain or steroids fail. Steroid-refractory cases may warrant additional immunosuppression (e.g., mycophenolate). Rechallenge only after recovery and careful risk-benefit discussion.Lesion-level management framework

Risk factors

Pre-existing chronic kidney disease
Older age
Concurrent proton pump inhibitor use
Concurrent NSAID use
Concurrent diuretics or ACEI/ARB use
Combination checkpoint blockade (e.g., added CTLA-4 inhibitor)
Other extrarenal immune-related adverse events
Prior or concurrent nephritogenic drug exposure

Prevention

Review and minimize concurrent nephritis-associated drugs (PPIs, NSAIDs)
Hold the drug and treat per immune-related adverse event guidelines at first sign of significant creatinine rise

Anticancer mechanism· how it treats cancer

Cosibelimab is a fully human IgG1 monoclonal antibody that binds programmed death-ligand 1 (PD-L1), blocking its interaction with the PD-1 and B7-1 (CD80) receptors and thereby restoring T-cell anti-tumor activity. Unlike effector-silenced anti-PD-L1 antibodies, it retains a functional Fc domain and can additionally engage antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity against PD-L1-expressing tumor cells.

Note · Cosibelimab (Unloxcyt; cosibelimab-ipdl) received first FDA approval in December 2024 and is the first anti-PD-L1 therapy approved for advanced cutaneous SCC. Drug-specific nephrotoxicity literature is essentially absent; this profile reasons from the registrational phase 1 safety data and from the broader PD-1/PD-L1 checkpoint-inhibitor nephrotoxicity literature.

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Clinical depth

Renal dose adjustment

No starting-dose adjustment for renal impairment is established; as a ~150 kDa IgG1 monoclonal antibody, cosibelimab is not cleared by the kidney, and mild-to-moderate renal impairment is not expected to alter exposure. Dosing is a fixed flat regimen (1200 mg IV every 3 weeks). Management of nephrotoxicity is by holding or discontinuing the drug and immunosuppression rather than dose reduction. Data in severe renal impairment or dialysis are lacking.

Dialyzability & ESKD dosing

Not dialyzable. Large therapeutic monoclonal antibodies are not removed by hemodialysis or peritoneal dialysis owing to their size; no dosing change is anticipated for patients on dialysis, though formal data are absent.

Differential diagnosis

Distinguish immune-mediated AIN from pre-renal azotemia (volume depletion, cancer-related), obstruction, contrast- or chemotherapy-associated ATN, hypercalcemia, and tumor-related causes. Concurrent PPI/NSAID-induced AIN can be hard to separate and may be synergistic. New proteinuria suggests a glomerular immune lesion. The delayed timing, sterile pyuria/white-cell casts, and accompanying extrarenal irAEs favor checkpoint-inhibitor AIN; kidney biopsy is the reference standard when feasible.

Monitoring

Urinalysis with microscopy (pyuria, casts) and quantified proteinuria (UPCR/UACR)
Assessment for concurrent extrarenal immune-related adverse events
Medication review for PPIs/NSAIDs and other nephrotoxins
Serum electrolytes including potassium and magnesium

Key trials & series

NCT03212404 — pivotal open-label, multicenter phase 1 study; metastatic CSCC cohort ORR 47.4% (Clingan et al., J Immunother Cancer 2023)
Locally advanced CSCC cohort of the same phase 1 program supporting FDA approval (2024)

Clinical pearls

Renal toxicity is a class effect, not drug-specific: expect immune-mediated AIN, not direct tubular injury.
Anti-PD-L1 agents like cosibelimab generally carry lower nephritis risk than CTLA-4 or combination checkpoint regimens.
ICI-AIN is often a delayed, asymptomatic creatinine rise — surveillance labs, not symptoms, usually make the diagnosis.
Always review for PPIs and NSAIDs: they are common AIN co-culprits that potentiate checkpoint-inhibitor nephritis.
Corticosteroids are the mainstay; many cases recover at least partially, but late or severe presentations can leave residual CKD.

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-L1 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

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

Evidence accrual

5 references · 2020–2025 · 4 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 Cosibelimab 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 · 100% phenotype match

Checkpoint inhibitors (pembrolizumab · nivolumab · ipilimumab)

Immune checkpoint inhibitor

Profile

Acute interstitial nephritis with long latency.

AINGLOMLYTE

Moderate#2 · 85% phenotype match

Avelumab

Bavencio · Anti-PD-L1 antibody

Profile

ICI-associated AIN.

AINGLOM

Moderate#3 · 81% phenotype match

Cemiplimab

Libtayo · Anti-PD-1 antibody

Profile

ICI-associated AIN.

AINGLOM

Moderate#4 · 81% phenotype match

Dostarlimab

Jemperli · Anti-PD-1 antibody

Profile

ICI-associated AIN.

AINGLOM

Moderate#5 · 81% phenotype match

Durvalumab

Imfinzi · Anti-PD-L1 antibody

Profile

ICI-associated AIN.

AINGLOM

Moderate#6 · 81% phenotype match

Compare Cosibelimab 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.