What kind of kidney injury does Ipilimumab 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, Thrombotic Microangiopathy, Prerenal / Hemodynamic AKI.

How should kidney function be monitored during Ipilimumab therapy?

Urinalysis for proteinuria, pyuria, and hematuria; Surveillance for concurrent immune-related adverse events (skin, GI, hepatic, thyroid, pituitary); Quantify proteinuria (urine protein:creatinine ratio) if glomerular involvement suspected; Electrolytes including potassium and magnesium; Trend creatinine after any drug hold or steroid course to confirm recovery.

How can kidney injury from Ipilimumab be prevented?

Review and minimize concomitant AIN-associated drugs (PPIs, NSAIDs) before and during treatment Maintain euvolemia; reassess RAAS inhibitors and diuretics

Who is at higher risk of kidney injury from Ipilimumab?

Combination ipilimumab + nivolumab therapy (strongest risk for incidence and severity); Concurrent or prior extrarenal immune-related adverse events; Pre-existing hypertension; Concomitant nephritis-associated drugs (PPIs, NSAIDs, antibiotics); RAAS inhibitor or diuretic use (predisposes to prerenal AKI); Pre-existing chronic kidney disease; Higher cumulative checkpoint-inhibitor exposure.

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Printable monograph

CTLA-4 checkpoint inhibitor

Ipilimumab

Yervoy · Ipi

CTLA-4 checkpoint inhibitor · approved 2011 · 13 citations · FAERS AKI reporting ROR 2.84 (95% CI 2.65–3.03, 869 AKI reports)

Up to date· through 2026

Deeply sourced9/9 · 8 signals

Met: 13 citations
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 first-approved CTLA-4 blocker whose kidney signature is immune-mediated acute interstitial nephritis, classically granulomatous, with markedly higher AKI risk when combined with nivolumab.

SevereCTLA-4 checkpoint inhibitor

Unresectable or metastatic melanoma (monotherapy and with nivolumab)Adjuvant treatment of resected stage III melanomaAdvanced renal cell carcinoma (with nivolumab)Metastatic colorectal cancer that is MSI-H/dMMR (with nivolumab)Unresectable malignant pleural mesothelioma (with nivolumab)Metastatic non-small cell lung cancer (with nivolumab +/- chemotherapy)Hepatocellular carcinoma (with nivolumab)Esophageal squamous cell carcinoma (with nivolumab)

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Signature kidney injury

Signature lesion

Acute Interstitial Nephritis

Representative incidence2%

1–2% range across studies

Clinically significant kidney injury from ipilimumab monotherapy is uncommon; renal immune-related adverse events are reported in roughly 1-2% of patients on single-agent checkpoint blockade. The dominant driver of elevated incidence is combination therapy: in real-world ICI cohorts any-cause AKI reaches about 16-17%, but only a minority is true immune-mediated nephritis. The combination of ipilimumab plus nivolumab carries a substantially higher and more severe AKI risk than either single agent. In a pooled analysis of biopsy-proven ICI-related acute tubulointerstitial nephritis, all patients on dual ICI blockade developed stage 3 AKI versus about half on a single agent, and complete renal recovery was less likely with dual blockade.Source: Single-center cohort: 16.5% (51/309) developed AKI, ~2% biopsy/clinically attributed to ICI nephritis (Meraz-Munoz et al., J Immunother Cancer 2020, PMID 32601079); dual-blockade severity from pooled biopsy analysis (Esposito et al., Front Oncol 2023, PMID 37936605).

Onset & rechallenge

Time to injuryVariable / unpredictable

Delayed and variable onset, typically weeks to several months (median ~3 months/91 days), though combination therapy can trigger nephritis after one or two doses or even after discontinuation.

Distilled from: “Delayed and variable: typically weeks to several months after initiation. Median time to AKI in biopsy cohorts was roughly 3 months (about 91 days; ~4 cycles); combination ipilimumab/nivolumab nephritis can appear after only one or two doses, and onset after drug discontinuation has been described.”

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.

Early-detection biomarkers

Urine microscopy with a quantified protein–creatinine ratio — Tubulointerstitial inflammation — the AIN urinary phenotype. In the 13-patient biopsy series that defined checkpoint-inhibitor AKI, pyuria was present in 8 and the median urine protein-to-creatinine ratio was 0.48 g/g (range 0.12–0.98) — sub-nephrotic, which is why a reflex dipstick under-reads it and a quantified ratio is the test to order. Median latency from starting the drug was 91 days. Both findings are non-specific; in that same series the higher-yield warning was extra-renal, an immune-related adverse event elsewhere preceding the AKI in 7 patients. Ipilimumab is named among the series' agents, making this the most CTLA-4-weighted urinary dataset available.PMID 27282937 (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 · Signature3.5%PMID 37263805 (opens PubMed in a new tab)
Acute interstitial nephritis (often granulomatous) is the dominant ipilimumab renal lesion; ICI-attributable AKI pooled ~3.5% (overall AKI during ICI therapy ~16%), and ipilimumab is the highest-risk single agent (adjusted OR 2.18) — biopsy series show AIN as the leading pattern.
Glomerular Injury / ProteinuriaSecondaryno population incidence denominator
Second most common (but uncommon) ICI kidney lesion after AIN; biopsy-confirmed cases include membranous nephropathy and minimal-change/podocytopathy. PMID 32601079 (opens PubMed in a new tab)
Thrombotic MicroangiopathyRareno population incidence denominator
Case-level thrombotic microangiopathy documented in ICI kidney-biopsy cohorts (2 of 12 biopsy-attributed lesions). PMID 32601079 (opens PubMed in a new tab)
Prerenal / Hemodynamic AKIRarequalitative — no citable incidence
Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.
Chronic Interstitial NephropathyRarequalitative — no citable incidence
Slow, cumulative tubulointerstitial scarring — fibrosis, tubular atrophy and glomerulosclerosis with no discrete acute phase. The nitrosourea (carmustine/lomustine) lesion and delayed radioligand (radiation) nephropathy; often irreversible and detected only as a creeping creatinine months to years later.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

2%incidence

SeveritySevere

ReversibilityPartially reversible

Evidence13 citations

Nephron map

Glomerulus

Vasculature / Endothelium

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 lesion is immune-mediated acute (tubulo)interstitial nephritis. CTLA-4 blockade removes a checkpoint on T-cell tolerance, and loss of peripheral tolerance is thought to drive an activated, cytotoxic T-cell infiltrate of the interstitium; biopsies show lymphocytic tubulointerstitial inflammation, frequently with granulomatous features and occasionally vasculitis or thrombotic microangiopathy-like changes. A proposed mechanism is reactivation of drug-specific (e.g., PPI, NSAID) memory T cells once the checkpoint brake is lifted. Less commonly, checkpoint blockade is associated with de novo or relapsing glomerular disease (minimal change disease, membranous nephropathy, pauci-immune/ANCA-type and anti-GBM disease have been reported) and rare thrombotic microangiopathy. Combination with nivolumab amplifies the immune activation and is associated with more frequent and more severe kidney injury. Much AKI in these patients is nonetheless prerenal/hemodynamic rather than drug-immune.

Clinical presentation

Usually a subacute, often asymptomatic rise in serum creatinine found on routine labs. Urinalysis may show sterile pyuria and subnephrotic proteinuria; bland sediment is also common, and eosinophiluria is insensitive. Overt oliguria is unusual but severe, dialysis-requiring AKI occurs, particularly with combination therapy. A concurrent or preceding extrarenal immune-related adverse event (rash, colitis, hepatitis, thyroiditis, hypophysitis) is a key diagnostic clue and was present before AKI onset in a large share of biopsy series. Glomerular involvement may present with nephrotic-range proteinuria, edema, or hematuria.

Management

For immune-mediated nephritis: hold ipilimumab (and nivolumab), exclude prerenal and obstructive causes, and consider kidney biopsy when the diagnosis or lesion is unclear, since management hinges on distinguishing immune nephritis from prerenal AKI. Grade 2-3 nephritis is treated with corticosteroids (e.g., prednisone 0.5-1 mg/kg/day, higher for severe/grade 4) with a slow taper, and discontinuation of offending co-medications (PPIs/NSAIDs). Steroid-refractory cases may need additional immunosuppression. Permanently discontinue for grade 3-4 or recurrent immune-mediated nephritis; cautious rechallenge after resolved low-grade AIN has been done but AKI recurs in a substantial minority (~40% in pooled data). Prerenal AKI is managed with volume optimization and removal of contributing agents, not steroids.Lesion-level management framework

Risk factors

Combination ipilimumab + nivolumab therapy (strongest risk for incidence and severity)
Concurrent or prior extrarenal immune-related adverse events
Pre-existing hypertension
Concomitant nephritis-associated drugs (PPIs, NSAIDs, antibiotics)
RAAS inhibitor or diuretic use (predisposes to prerenal AKI)
Pre-existing chronic kidney disease
Higher cumulative checkpoint-inhibitor exposure

Prevention

Review and minimize concomitant AIN-associated drugs (PPIs, NSAIDs) before and during treatment
Maintain euvolemia; reassess RAAS inhibitors and diuretics

Anticancer mechanism· how it treats cancer

Ipilimumab is a fully human IgG1 monoclonal antibody against cytotoxic T-lymphocyte antigen 4 (CTLA-4), an inhibitory receptor upregulated on activated T cells and constitutively expressed on regulatory T cells. By blocking CTLA-4 engagement of its B7 ligands (CD80/CD86) on antigen-presenting cells, ipilimumab removes an early "checkpoint" brake on T-cell priming in lymph nodes, amplifying antitumor T-cell activation and proliferation and depleting intratumoral regulatory T cells. It was the first immune checkpoint inhibitor to gain FDA approval (2011, advanced melanoma) and is most often used today combined with the PD-1 inhibitor nivolumab.

Note · Ipilimumab monotherapy rarely causes clinically significant kidney injury; the renal story is dominated by combination ipilimumab/nivolumab, where AKI is both more frequent and more severe. The signature lesion is granulomatous-leaning acute interstitial nephritis, distinguishing it somewhat from the more purely lymphocytic AIN of PD-1 monotherapy. This profile reasons from ICI-class biopsy series and cohorts that pool CTLA-4 with PD-1/PD-L1 agents; truly ipilimumab-monotherapy-specific renal incidence figures are limited.

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Clinical depth

Renal dose adjustment

No pharmacokinetic dose adjustment for renal impairment. Ipilimumab is dosed by body weight (e.g., 3 mg/kg in melanoma monotherapy; 1 mg/kg every 3 or 6 weeks in nivolumab combinations) and, as a ~150 kDa IgG1 antibody, is cleared by reticuloendothelial proteolysis rather than the kidney, so mild-to-moderate renal impairment does not meaningfully alter exposure. Data in severe impairment and dialysis are limited. Dose modification is event-driven: hold for grade 2-3 nephritis and permanently discontinue for grade 3-4 or recurrent immune-mediated nephritis.

Dialyzability & ESKD dosing

Not dialyzable. Large IgG1 monoclonal antibodies are not removed by hemodialysis or peritoneal dialysis; dosing timing relative to dialysis is irrelevant. Dialysis is used to support patients with severe ICI-AKI, not to clear the drug.

Differential diagnosis

Distinguish true immune-mediated interstitial nephritis from the more common prerenal/hemodynamic AKI (volume depletion, sepsis, contrast, cardiorenal). Other considerations: concomitant PPI/NSAID/antibiotic-induced AIN (which checkpoint blockade may unmask), tumor-related obstruction, hypercalcemia, tumor lysis, and checkpoint-associated glomerular disease (minimal change, membranous, pauci-immune/anti-GBM) or thrombotic microangiopathy. Concurrent extrarenal immune-related adverse events, sterile pyuria, and granulomatous features on biopsy favor ICI nephritis; bland sediment with a clear hemodynamic trigger favors prerenal. Kidney biopsy is the reference standard when the distinction changes management (steroids vs supportive care).

Monitoring

Urinalysis for proteinuria, pyuria, and hematuria
Surveillance for concurrent immune-related adverse events (skin, GI, hepatic, thyroid, pituitary)
Quantify proteinuria (urine protein:creatinine ratio) if glomerular involvement suspected
Electrolytes including potassium and magnesium
Trend creatinine after any drug hold or steroid course to confirm recovery

Key trials & series

CheckMate 067 (NCT01844505): phase 3 nivolumab + ipilimumab vs nivolumab vs ipilimumab in advanced melanoma; established the combination but with markedly higher grade 3-4 immune-related toxicity
CheckMate 214 (NCT02231749): nivolumab + ipilimumab vs sunitinib in advanced renal cell carcinoma
CheckMate 9LA / CheckMate 743: ipilimumab + nivolumab combinations in NSCLC and pleural mesothelioma

Clinical pearls

Ipilimumab monotherapy rarely hurts the kidney; the renal risk surges when it is paired with nivolumab - dual blockade drives both higher incidence and more stage 3/dialysis-requiring AKI.
The CTLA-4 nephritis lesion leans granulomatous, a histologic tilt distinct from the more purely lymphocytic AIN of PD-1 monotherapy.
ICI nephritis is a delayed, slow-burn diagnosis (median ~3 months) - it does not behave like classic days-after-drug allergic AIN.
An extrarenal immune-related adverse event (rash, colitis, hepatitis, thyroiditis) often precedes the creatinine rise - treat it as a renal early-warning sign.
Co-prescribed PPIs and NSAIDs are frequent cofactors; checkpoint blockade can unmask T-cell reactivity to them, so review and stop them when nephritis is suspected.
Most AKI on these agents is still prerenal/hemodynamic, not drug-immune - reserve high-dose steroids for genuine immune nephritis and consider biopsy when uncertain.

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 CTLA-4 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. 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· 3

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.

CaseB · ModerateSmall-vessel vasculitis leading to severe acute kidney injury after ipilimumab: a case report.Duarte R et al. · Melanoma Res 2024 · PMID 38016155Kidney-biopsy-proven small-vessel vasculitis with arteriolar immune deposition causing severe acute kidney injury following single-agent ipilimumab.CaseB · ModerateIgA Nephropathy Secondary to Ipilimumab Use.Dougherty SC et al. · Case Rep Nephrol Dial 2021 · PMID 34950709Biopsy-proven IgA nephropathy with nephrotic-range proteinuria and dialysis-requiring acute kidney injury arising four weeks after the first cycle of single-agent ipilimumab.CaseC · LimitedNivolumab plus ipilimumab induced endocrinopathy and acute interstitial nephritis in metastatic sarcomatoid renal-cell carcinoma: A case report and review of literature.Hino C et al. · Front Immunol 2022 · PMID 36052087Acute interstitial nephritis (alongside multiple endocrinopathies) attributed to ipilimumab-containing checkpoint-inhibitor therapy for metastatic sarcomatoid RCC.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 42,912 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· 5 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 5.74
Glomerular Injury / Proteinuriacorroborated · ROR 2.12 — on the terms that name the lesion (ROR 3.57)
Chronic Interstitial NephropathyNot queried in FAERS — No MedDRA term set is defined for this phenotype, so FAERS was never asked about it.
Thrombotic MicroangiopathyNo 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.
Prerenal / Hemodynamic AKINot queried in FAERS — No MedDRA term set is defined for this phenotype, so FAERS was never asked about it.

Acute Interstitial Nephritis

ROR 5.7495% CI 5.02–6.57· 217 reports

SIADH / Hyponatremia

ROR 4.0395% CI 3.73–4.35· 652 reports

Electrolyte Disturbance

ROR 3.0995% CI 2.92–3.28· 1,182 reports

Glomerular Injury / Proteinuria

ROR 2.1295% CI 1.78–2.53· 126 reports

Acute Tubular Necrosis

ROR 2.0995% CI 1.54–2.83· 42 reports

FAERS outcomes & reporting trend· 22.3% of reports w/ death · 45.2% w/ hospitalization

22.3%

Reported with a death outcome

9,585 of 42,912 reports

45.2%

Reported with hospitalization

19,401 of 42,912 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 10 systems · 42,912 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 2.8495% CI 2.65–3.03· 869 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

Adrenal Insufficiency937Acute Kidney Injury869

Gastrointestinal

Diarrhoea3,128Colitis2,316Nausea1,385Immune-Mediated Enterocolitis1,121Vomiting1,051

General / constitutional

Pyrexia2,057Fatigue1,695Asthenia730Malaise700Weight Decreased669

Skin

Rash1,805Pruritus926

Respiratory

Dyspnoea1,015Pneumonitis962

Endocrine

Hypophysitis1,074Hypothyroidism840

Metabolic & electrolyte

Decreased Appetite1,117Dehydration682

Immune / infection

Pneumonia979

Nervous system

Headache809

Blood & lymphatic

Anaemia716

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 Ipilimumab 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

Ivonescimab

AK112 (Akeso/Summit) · PD-1 x VEGF bispecific antibody

Profile

Two nephrotoxic pathways in one molecule: VEGF-blockade glomerular injury plus checkpoint-inhibitor interstitial nephritis.

GLOMHTNAIN

Moderate#1 · 77% 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#2 · 76% phenotype match

Pembrolizumab

Keytruda · PD-1 checkpoint inhibitor

Profile

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

AINCINGLOM

Moderate#3 · 62% phenotype match

Nivolumab

Opdivo · PD-1 checkpoint inhibitor

Profile

PD-1 inhibitor; ICI acute interstitial nephritis is the prototype.

AINCINGLOM

Moderate#4 · 60% phenotype match

Trametinib

Mekinist · MEK inhibitor

Profile

MEK inhibitor; hypertension, proteinuria, and combination-therapy AKI.

PREAINGLOM

Moderate#5 · 59% phenotype match

Avelumab

Bavencio · Anti-PD-L1 antibody

Profile

ICI-associated AIN.

AINGLOM

Moderate#6 · 56% phenotype match

Compare Ipilimumab 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 Ipilimumab’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 Ipilimumab; 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 83 clinical records among all 97 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.