What kind of kidney injury does Nivolumab cause?

Acute Interstitial Nephritis — Immune-mediated inflammation of the renal interstitium — the signature kidney injury of checkpoint inhibitors. Other reported patterns: Chronic Interstitial Nephropathy, Glomerular Injury / Proteinuria, Acute Tubular Necrosis, Thrombotic Microangiopathy, SIADH / Hyponatremia.

How should kidney function be monitored during Nivolumab therapy?

Urinalysis with microscopy for pyuria and proteinuria; urine protein-to-creatinine ratio if proteinuria detected; Assessment for concurrent extrarenal immune-related adverse events; Review of concomitant AIN-associated medications (PPIs, NSAIDs, antibiotics).

How can kidney injury from Nivolumab be prevented?

No proven pharmacologic prophylaxis; vigilance and early recognition are the mainstay Review and, where feasible, deprescribe nonessential AIN-associated co-medications (notably PPIs) before and during treatment

Who is at higher risk of kidney injury from Nivolumab?

Combination checkpoint blockade (nivolumab plus ipilimumab); Concomitant proton pump inhibitor use; Lower baseline eGFR / pre-existing CKD; Concurrent use of other AIN-associated drugs (NSAIDs, antibiotics); Concomitant extrarenal immune-related adverse events; Diabetes mellitus.

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Printable monograph

PD-1 checkpoint inhibitor

Nivolumab

Opdivo · Nivo

PD-1 checkpoint inhibitor · approved 2014 · 10 citations · FAERS AKI reporting ROR 2.75 (95% CI 2.63–2.88, 1,893 AKI reports)

Up to date· through 2026

Deeply sourced8/9 · 7 signals

Met: 10 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.

The PD-1 blocker that breaks renal immune tolerance, producing late-onset acute tubulointerstitial nephritis as its signature kidney lesion.

ModeratePD-1 checkpoint inhibitor

Metastatic melanoma (monotherapy and with ipilimumab)Non-small cell lung cancerRenal cell carcinomaHodgkin lymphomaHead and neck squamous cell carcinomaUrothelial carcinomaHepatocellular carcinomaGastric, esophageal, and gastroesophageal junction cancersMicrosatellite-instability-high / mismatch-repair-deficient colorectal cancer

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Signature kidney injury

Signature lesion

Acute Interstitial Nephritis

Representative incidence3.5%

Clinically significant ICI-attributed AKI is uncommon but not rare. A 2023 systematic review/meta-analysis of real-world data (18 studies, ~12,000 ICI-treated patients) found a pooled incidence of all-cause AKI during ICI therapy of about 16%, but AKI specifically attributed to the ICI of roughly 3.5%. Risk is higher with combination ICI regimens (e.g., nivolumab-ipilimumab) than with PD-1 monotherapy. Among biopsied ICI-AKI, acute tubulointerstitial nephritis is the dominant lesion (>90%); glomerular lesions and thrombotic microangiopathy are reported but uncommon.Source: Xie et al., Eur J Intern Med 2023

Onset & rechallenge

Time to injuryDelayed (>6 weeks / cumulative)

Median ~14 weeks (IQR 6–37) in a 138-patient multicenter cohort, 91 days in the original series; ranges weeks to many months and can follow discontinuation.

Distilled from: “Characteristically delayed compared with other drug-induced AIN: median time from ICI initiation to AKI was about 14 weeks (IQR 6-37) in a 138-patient multicenter cohort, and 91 days in the original series; onset ranges from weeks to many months and can follow drug discontinuation.” · PMID 31896554 (opens PubMed in a new tab)

RechallengeCase-by-case

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

Long-term outlook & thresholds

Renal recoveryOften partial 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. Steroid treatment and the PRESENCE of a concomitant tubulointerstitial-nephritis-causing medication were each associated with a better renal prognosis — the latter an observational association the cohort reports, not an effect of stopping that drug, which it did not analyze. 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; recovery is often incomplete (partial recovery in ~45%).
Dialysis / RRT.: Severe cases can require dialysis, though most ICI-attributed AKI is not dialysis-requiring.

Early-detection biomarkers

Urinary NGAL and KIM-1 — Subclinical proximal tubular injury preceding a measurable serum-creatinine rise. Emerging tubular-injury markers: in an experimental model, the COMBINATION of an immune checkpoint inhibitor and cisplatin produced subclinical tubular damage detectable through urinary albumin, NGAL and KIM-1 before overt AKI, while ICI exposure alone produced an inflammatory signature (TNF-α, IL-9, CD8, CD3) rather than a tubular-marker rise — so these markers flag the combined nephrotoxic hit earlier than creatinine. Preclinical/class-level evidence, not nivolumab-specific human validation.PMID 40902411 (opens PubMed in a new tab)

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 was the dominant lesion in 93% of the 60 biopsied immune-checkpoint-inhibitor-associated AKI patients in a 138-patient multicenter cohort (a biopsy-lesion proportion, not a treated-population incidence) — the signature nivolumab renal lesion. Class-wide ICI-AKI incidence runs ~2-5%. PMID 31896554 (opens PubMed in a new tab)
Chronic Interstitial NephropathySecondaryno population incidence denominator
Chronic tubulointerstitial scarring as the sequela of incomplete recovery: complete kidney recovery occurred in only 40%, partial in 45%, and none in 15% of ICI-AKI patients. PMID 31896554 (opens PubMed in a new tab)
Acute Tubular NecrosisSecondaryno population incidence denominator
Minority histologic pattern — AIN dominates 93% of ICI-AKI biopsies, with ATN and other lesions making up the ~7% remainder. PMID 31896554 (opens PubMed in a new tab)
Glomerular Injury / ProteinuriaRareno population incidence denominator
Case-level; biopsy/nephrology-attributed glomerular lesions (2 membranous nephropathy, 2 minimal change disease) among 12 attributed ICI nephrotoxicity cases. PMID 32601079 (opens PubMed in a new tab)
Thrombotic MicroangiopathyRareno population incidence denominator
Case-level; thrombotic microangiopathy documented in 2 of 12 biopsy/nephrology-attributed ICI nephrotoxicity cases. PMID 32601079 (opens PubMed in a new tab)
SIADH / HyponatremiaRarequalitative — no citable incidence
Rare true SIAD at case level; most ICI hyponatremia is hypophysitis or adrenalitis mimicking SIADH.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

3.5%incidence

SeverityModerate

ReversibilityPartially reversible

Evidence10 citations

Nephron map

Glomerulus

Vasculature / Endothelium

Proximal Tubule

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

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.Appears in 1 documented synergy combination

Mechanism of kidney injury

The signature mechanism is loss of T-cell tolerance rather than direct tubular toxicity. PD-1 blockade is thought to reactivate drug-specific or self-reactive T cells, producing a delayed-type hypersensitivity acute tubulointerstitial nephritis (ATIN) with a dense CD4/CD8 T-cell interstitial infiltrate, sometimes granulomatous. A widely cited hypothesis is that checkpoint inhibition abrogates established tolerance to long-used concomitant drugs (proton pump inhibitors, NSAIDs, antibiotics), which then act as the nephritogenic antigen; case reports document AIN with positive drug lymphocyte stimulation tests to a PPI used safely for years before nivolumab. Less commonly, immune dysregulation manifests as glomerular disease (minimal change disease, FSGS, pauci-immune/ANCA-associated GN, immune-complex GN) or thrombotic microangiopathy. Reported tubular findings include karyomegalic, regenerating (Ki-67-positive) epithelium and, rarely, acute tubular injury.

Clinical presentation

Usually an asymptomatic rise in serum creatinine detected on routine monitoring, often with sterile pyuria and subnephrotic proteinuria; the classic allergic-AIN triad (rash, fever, eosinophilia) is frequently absent. Concurrent extrarenal immune-related adverse events (colitis, hepatitis, dermatitis, thyroiditis) occur in a substantial minority and support an immune etiology. When glomerular disease supervenes, nephrotic-range proteinuria and edema may dominate. Severe cases can require dialysis.

Management

Hold nivolumab and exclude alternative causes of AKI (volume depletion, obstruction, contrast, other drugs). Discontinue contributing AIN-associated co-medications, especially PPIs. Per oncology/nephrology guidance, treat grade >=2 ICI-AKI with corticosteroids (typically prednisone ~1 mg/kg/day, with IV methylprednisolone pulses for severe disease), tapered over 4-6+ weeks; most patients are steroid-treated and steroids are associated with better renal recovery. Kidney biopsy is advised when the diagnosis is uncertain, to confirm ATIN versus a glomerular lesion or TMA that would change management. In a 138-patient multicenter cohort, complete, partial, and no recovery occurred in roughly 40%, 45%, and 15% respectively; rechallenge is feasible in selected patients but recurrent AKI occurs in about a quarter.Lesion-level management framework

Risk factors

Combination checkpoint blockade (nivolumab plus ipilimumab)
Concomitant proton pump inhibitor use
Lower baseline eGFR / pre-existing CKD
Concurrent use of other AIN-associated drugs (NSAIDs, antibiotics)
Concomitant extrarenal immune-related adverse events
Diabetes mellitus

Prevention

No proven pharmacologic prophylaxis; vigilance and early recognition are the mainstay
Review and, where feasible, deprescribe nonessential AIN-associated co-medications (notably PPIs) before and during treatment

Anticancer mechanism· how it treats cancer

Fully human IgG4 monoclonal antibody against programmed cell death protein 1 (PD-1) on T cells. By blocking PD-1 engagement with its ligands PD-L1/PD-L2, nivolumab releases the inhibitory brake on tumor-reactive T cells, restoring cytotoxic antitumor immunity. The same loss of peripheral T-cell tolerance that drives efficacy underlies its off-target immune-related adverse events.

Note · Incidence figures and the ATIN-dominant histology derive largely from retrospective multicenter cohorts and a meta-analysis pooling several PD-1/PD-L1/CTLA-4 agents; nivolumab-specific lesions (karyomegalic AIN, acute tubular injury, MCD/FSGS) rest on case reports and small series and should be read as hedged signals rather than established frequencies.

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Clinical depth

Renal dose adjustment

As a monoclonal antibody, nivolumab requires no baseline renal dose adjustment; pharmacokinetics are not meaningfully altered by mild-to-moderate renal impairment and it is dosed as a flat or weight-based IV regimen. The relevant adjustment is immunologic, not pharmacokinetic: hold or permanently discontinue based on AKI grade per immune-related adverse event protocols rather than CrCl banding.

Dialyzability & ESKD dosing

Not dialyzable. As a ~146 kDa IgG4 antibody it is not removed by hemodialysis, and ESKD/dialysis does not require dose change. Patients on dialysis or with a kidney transplant can receive nivolumab, though transplant recipients carry a substantial risk of allograft rejection from checkpoint blockade.

Differential diagnosis

Distinguish ICI-ATIN from prerenal azotemia (low FeNa, volume-responsive), acute tubular necrosis from sepsis/contrast/ischemia, and obstruction. Pyuria, white-cell casts, subnephrotic proteinuria, and concurrent extrarenal irAEs favor ATIN; the delayed onset (weeks to months) helps separate it from classic rapid allergic AIN. Nephrotic-range proteinuria points to a superimposed glomerular lesion (minimal change disease, FSGS, ANCA-associated or immune-complex GN). Schistocytes, thrombocytopenia, and hemolysis suggest thrombotic microangiopathy. A concomitant culprit drug (PPI/NSAID) may coexist and must be deprescribed; biopsy resolves ambiguous cases.

Monitoring

Urinalysis with microscopy for pyuria and proteinuria; urine protein-to-creatinine ratio if proteinuria detected
Assessment for concurrent extrarenal immune-related adverse events
Review of concomitant AIN-associated medications (PPIs, NSAIDs, antibiotics)

Key trials & series

Cortazar et al. 2020 (JASN) — 138-patient multicenter ICI-AKI cohort defining risk factors, ATIN dominance (93% of biopsies), and recovery/mortality outcomes
Cortazar et al. 2016 (Kidney Int) — first clinicopathologic series establishing ICI-AKI as predominantly acute tubulointerstitial nephritis
Xie et al. 2023 (Eur J Intern Med) — systematic review/meta-analysis quantifying AKI incidence (~3.5% ICI-attributed) and risk factors

Clinical pearls

AIN here is a tolerance-failure phenomenon: PD-1 blockade can unmask hypersensitivity to a co-medication (classically a PPI) the patient tolerated for years — always review and stop the PPI.
Onset is characteristically late (median ~14 weeks) — unlike most drug-induced AIN, so a normal creatinine early in therapy does not exclude later ICI-AKI.
The classic allergic triad (rash/fever/eosinophilia) is usually absent; sterile pyuria with a creatinine rise is the more reliable clue.
Concurrent extrarenal immune-related adverse events strongly support an immune cause and, in cohort data, predict worse renal recovery.
Steroids and stopping a concomitant AIN-causing drug are each associated with better renal recovery; consider biopsy when a glomerular lesion or TMA is plausible.
True SIAD is reported with nivolumab (melanoma, no paraneoplastic confound) but is rare — most checkpoint-inhibitor hyponatremia is hypophysitis or adrenalitis biochemically mimicking SIADH, so screen cortisol and thyroid function first.

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 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

10 primary references — trials, cohorts, mechanism, and reviews. 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.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 96,645 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· 7 signals

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 6.11
Glomerular Injury / Proteinuriacorroborated · ROR 3.04 — on the terms that name the lesion (ROR 4.4)
SIADH / Hyponatremiacorroborated · ROR 2.99 — on the terms that name the lesion (ROR 2.99)
Acute Tubular Necrosiscorroborated · ROR 1.66
Thrombotic Microangiopathycorroborated · ROR 1.35
Chronic Interstitial NephropathyNot queried in FAERS — No MedDRA term set is defined for this phenotype, so FAERS was never asked about it.

Acute Interstitial Nephritis

ROR 6.1195% CI 5.60–6.67· 513 reports

Glomerular Injury / Proteinuria

ROR 3.0495% CI 2.76–3.36· 403 reports

SIADH / Hyponatremia

ROR 2.9995% CI 2.82–3.18· 1,092 reports

Electrolyte Disturbance

ROR 2.6395% CI 2.52–2.74· 2,264 reports

Fanconi Syndrome

ROR 2.5695% CI 1.98–3.30· 60 reports

Acute Tubular Necrosis

ROR 1.6695% CI 1.32–2.08· 75 reports

Thrombotic Microangiopathy

ROR 1.3595% CI 1.10–1.65· 96 reports

FAERS outcomes & reporting trend· 25.6% of reports w/ death · 40.6% w/ hospitalization

25.6%

Reported with a death outcome

24,759 of 96,645 reports

40.6%

Reported with hospitalization

39,271 of 96,645 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 10 systems · 96,645 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 2.7595% CI 2.63–2.88· 1,893 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 Injury1,893Adrenal Insufficiency1,399

Gastrointestinal

Diarrhoea5,251Nausea3,182Colitis2,280Vomiting2,084Immune-Mediated Enterocolitis1,472

General / constitutional

Fatigue4,195Pyrexia3,721Asthenia2,101Weight Decreased1,857Malaise1,560

Respiratory

Dyspnoea2,692Pneumonitis2,190Interstitial Lung Disease1,668

Skin

Rash3,093Pruritus1,790

Metabolic & electrolyte

Decreased Appetite2,911

Immune / infection

Pneumonia2,471

Endocrine

Hypothyroidism2,112

Blood & lymphatic

Anaemia1,770

Musculoskeletal

Arthralgia1,513

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 Nivolumab 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

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#1 · 72% 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#2 · 72% phenotype match

Pembrolizumab

Keytruda · PD-1 checkpoint inhibitor

Profile

PD-1 inhibitor; ICI interstitial nephritis, varied glomerular lesions.

AINCINGLOM

Moderate#3 · 70% phenotype match

Tislelizumab

Tevimbra · PD-1 immune checkpoint inhibitor

Profile

A PD-1 blocker whose kidney risk is the class-typical rare immune-mediated interstitial nephritis.

AINPRETMA

Moderate#4 · 60% phenotype match

Ipilimumab

Yervoy · CTLA-4 checkpoint inhibitor

Profile

CTLA-4 inhibitor; immune (often granulomatous) interstitial nephritis.

AINCINGLOM

Severe#5 · 60% phenotype match

Atezolizumab

Tecentriq · Anti-PD-L1 antibody

Profile

Interstitial nephritis; rare glomerular disease.

AINGLOMCYST

Moderate#6 · 59% phenotype match

Compare Nivolumab with its nearest agents

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

Kidney risk across Checkpoint inhibitors

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

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

Who studies this

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

Ranked by a 50/50 blend of publication volume and a position-weighted, capped Relative Citation Ratio (NIH iCite) on this agent’s renal literature; the citation count shown is the raw total, not the ranking score — counted over the 155 clinical records among all 184 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.