Is kidney injury from Cemiplimab reversible?

Partially reversible. Typical onset: Weeks to months after initiation..

How should kidney function be monitored during Cemiplimab therapy?

Urinalysis with protein quantification and microscopy if creatinine rises; Surveillance for concurrent irAEs.

How can kidney injury from Cemiplimab be prevented?

Deprescribe unnecessary AIN-associated medications

Who is at higher risk of kidney injury from Cemiplimab?

Concurrent PPIs/NSAIDs and other AIN-associated drugs; Combination immunotherapy; Lower baseline kidney function; Other concurrent immune-related adverse events.

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Printable monograph

Anti-PD-1 antibody

Cemiplimab

Libtayo · CEMI

Anti-PD-1 antibody · approved 2018 · 11 citations · FAERS AKI reporting ROR 2.07 (95% CI 1.45–2.97, 30 AKI reports)

Up to date· through 2026

Deeply sourced8/9 · 7 signals

Met: 11 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 10y)
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-PD-1 antibody with the checkpoint-class signature of immune-mediated acute interstitial nephritis.

ModerateImmune checkpoint inhibitor (anti-PD-1)

Advanced cutaneous squamous cell carcinomaAdvanced basal cell carcinomaNon-small cell lung cancer

§01

Signature kidney injury

Signature lesion

Acute Interstitial Nephritis

Representative incidence3.6%

Follows the PD-1/PD-L1 class profile: any AKI in roughly 15-17% of patients, with immune-related AIN in a smaller clinically significant subset. As an anti-PD-1 agent it may carry somewhat higher AKI risk than anti-PD-L1 agents, and pharmacovigilance data show an immune-nephropathy signal; cemiplimab-specific renal incidence is not separately quantified. A separate real-world cohort of 1,037 ICI-treated patients supplies the drug-attributable denominator this class otherwise lacks: 18.2% developed AKI of any cause, but only 3.6% (37 patients) had AKI attributed to the checkpoint inhibitor itself — a class figure, not a cemiplimab-specific one.Source: Lumlertgul et al., Eur J Cancer 2023 (class-level ICI-attributed AKI 3.6%; agent-specific AIN rate not separately quantified)

Onset & rechallenge

Time to injuryDelayed (>6 weeks / cumulative)

Weeks to months after initiation.

Distilled from: “Weeks to months after initiation.”

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
tubulointerstitial nephritis is the predominant ICI renal lesion; cemiplimab among agents with higher immune-mediated nephropathy reporting signal PMID 42194777 (opens PubMed in a new tab)
Glomerular Injury / ProteinuriaRarequalitative — no citable incidence
Damage to the filtration barrier — podocyte injury, FSGS and protein leak from VEGF and mTOR blockade.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

3.6%incidence

SeverityModerate

ReversibilityPartially reversible

Evidence11 citations

Nephron map

Glomerulus

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

Deep diveCheckpoint-inhibitor acute interstitial nephritisRelease the brakes on the immune system to fight the cancer and, weeks to months later, the same unleashed T cells can turn on the kidney's interstitium — a delayed, often steroid-responsive nephritis that hides behind a bland urine and a slowly rising creatinine.

Mechanism of kidney injury

PD-1 blockade breaks tubulointerstitial tolerance, producing T-cell-mediated acute (often granulomatous) interstitial nephritis, frequently potentiated by haptenizing co-medications (PPIs, NSAIDs); immune-mediated glomerular lesions occur less often.

Clinical presentation

Subacute creatinine rise, sterile pyuria, white-cell casts, sub-nephrotic proteinuria; commonly with extrarenal immune-related adverse events. Eosinophilia variable.

Management

Hold cemiplimab, exclude prerenal/obstructive and other causes, and treat immune-related AIN with corticosteroids (prednisone ~0.5-1 mg/kg/day with taper); partial-to-full recovery is common, with additional immunosuppression for steroid-refractory disease. Individualize rechallenge after recovery.Lesion-level management framework

Risk factors

Concurrent PPIs/NSAIDs and other AIN-associated drugs
Combination immunotherapy
Lower baseline kidney function
Other concurrent immune-related adverse events

Prevention

Deprescribe unnecessary AIN-associated medications

Anticancer mechanism· how it treats cancer

Human IgG4 monoclonal antibody blocking the PD-1 receptor on T cells, reversing tumor-induced T-cell exhaustion. Used in advanced cutaneous squamous cell carcinoma, basal cell carcinoma, and non-small cell lung cancer.

Note · Renal toxicity is a PD-1/PD-L1 class effect; cited incidence figures are class-level. Dedicated single-agent cemiplimab renal case reports are scarce, so attribution rests primarily on class data and pharmacovigilance signals.

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Clinical depth

Renal dose adjustment

No baseline renal dose adjustment (fixed-dose antibody, not renally cleared). Toxicity-based modification follows irAE grading: withhold for grade 2 nephritis with steroids; permanently discontinue for grade 3-4 or recurrent severe nephritis.

Dialyzability & ESKD dosing

Not dialyzable—IgG4 monoclonal antibody cleared by reticuloendothelial catabolism; not removed by hemodialysis, no supplemental dosing, standard dosing in ESKD.

Differential diagnosis

Distinguish ICI-AIN (late, sterile pyuria, WBC casts, concurrent irAEs, steroid-responsive) from prerenal azotemia, obstruction, and other drug AIN; cystatin C and urine AIN biomarkers (TNF-alpha, IL-9, CXCL9) help confirm AIN and exclude pseudo-AKI. Heavy proteinuria/hematuria suggests a glomerular variant requiring biopsy.

Monitoring

Urinalysis with protein quantification and microscopy if creatinine rises
Surveillance for concurrent irAEs

Key trials & series

Cortazar JASN 2020 multicenter ICI-AKI cohort (class)
Gupta J Immunother Cancer 2021 multicenter ICI-AKI cohort (class)
Lima Immunopharmacol Immunotoxicol 2024 anti-PD-1 vs anti-PD-L1 AKI meta-analysis

Clinical pearls

As an anti-PD-1 agent, cemiplimab may carry a slightly higher AKI risk than the anti-PD-L1 antibodies.
Manage on class principles—biopsy atypical cases since agent-specific data are thin.
A co-prescribed PPI is a frequent co-trigger; deprescribe during the AKI workup.
Urine biomarkers and cystatin C help separate true AIN from pseudo-AKI before steroids.

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 Anti-PD-1 antibody 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

10 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

10 references · 2016–2026 · 3 since 2024

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· 1

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 · LimitedSuccessful Shrinkage of a Giant Cutaneous Squamous Cell Carcinoma with Immunotherapy in a Kidney Transplant Recipient.Eleftheriadis T et al. · Exp Clin Transplant 2023 · PMID 37455472Kidney transplant recipient on cemiplimab developed two episodes of acute renal allograft rejection with doubling of serum creatinine (acute kidney injury), each reversed with intravenous methylprednisolone and temporary immunotherapy interruption.

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.

AbstractRare Case of Fibrillary Glomerulonephritis with Concomitant Acute Interstitial Nephritis Related to Cemiplimab UseASN Kidney Week 2024 2024 · Abstract TH-PO713Concurrent fibrillary glomerulonephritis (randomly arranged 11–17 nm fibrils) and acute interstitial nephritis attributed to the PD-1 inhibitor cemiplimab — a rare glomerular ICI lesion alongside the more typical interstitial nephritis.JournalRenal tubular acidosis and acute kidney injury secondary to cemiplimabRashidi A, Herlitz L, Tariq H · Journal of Onco-Nephrology 2021Renal tubular acidosis with acute kidney injury attributed to the PD-1 inhibitor cemiplimab — widening the cemiplimab renal immune-related-adverse-event spectrum beyond the more typical acute interstitial nephritis. Published in the Journal of Onco-Nephrology (not PubMed-indexed).

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 2,008 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 3.91
Glomerular Injury / ProteinuriaNo disproportionate reporting — This phenotype IS reportable and this agent has enough reports, yet the reporting is not disproportionate — the one genuinely informative negative of the four.

Acute Interstitial Nephritis

ROR 3.9195% CI 1.86–8.22· 7 reports

FAERS outcomes & reporting trend· 20.8% of reports w/ death · 28.4% w/ hospitalization

20.8%

Reported with a death outcome

418 of 2,008 reports

28.4%

Reported with hospitalization

571 of 2,008 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 9 systems · 2,008 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. As of 2026-10-01.

Disproportionality (acute kidney injury):ROR 2.0795% CI 1.45–2.97· 30 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 Injury30

General / constitutional

Fatigue87Pyrexia61Asthenia46Malaise28Pain28

Gastrointestinal

Nausea45Diarrhoea44Vomiting32Colitis30

Respiratory

Dyspnoea63Interstitial Lung Disease46Pneumonitis35

Skin

Rash86Pruritus51

Immune / infection

Pneumonia40Infusion Related Reaction31Sepsis30

Cardiac

Myocarditis49

Endocrine

Hypothyroidism36

Metabolic & electrolyte

Decreased Appetite29

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 Cemiplimab 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

Avelumab

Bavencio · Anti-PD-L1 antibody

Profile

ICI-associated AIN.

AINGLOM

Moderate#1 · 100% phenotype match

Dostarlimab

Jemperli · Anti-PD-1 antibody

Profile

ICI-associated AIN.

AINGLOM

Moderate#2 · 100% phenotype match

Durvalumab

Imfinzi · Anti-PD-L1 antibody

Profile

ICI-associated AIN.

AINGLOM

Moderate#3 · 100% 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#4 · 81% phenotype match

Cosibelimab

Unloxcyt · PD-L1 immune checkpoint inhibitor

Profile

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

AINGLOMLYTE

Moderate#5 · 81% phenotype match

Atezolizumab

Tecentriq · Anti-PD-L1 antibody

Profile

Interstitial nephritis; rare glomerular disease.

AINGLOMCYST

Moderate#6 · 76% phenotype match

Compare Cemiplimab 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.