What kind of kidney injury does Pembrolizumab 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, Electrolyte Disturbance, Thrombotic Microangiopathy, Hemorrhagic Cystitis.

How should kidney function be monitored during Pembrolizumab therapy?

Serum electrolytes and bicarbonate (for RTA/hypokalemia); Urinalysis with protein quantification when AKI or edema develops; Surveillance for concurrent extrarenal immune-related adverse events.

How can kidney injury from Pembrolizumab be prevented?

Review and discontinue non-essential PPIs and other AIN-associated drugs before/during therapy

Who is at higher risk of kidney injury from Pembrolizumab?

Concurrent proton pump inhibitor use; Lower baseline eGFR / pre-existing CKD; Other (extrarenal) immune-related adverse events; Concomitant NSAIDs or antibiotics (potential hapten triggers); Combination checkpoint blockade (e.g., added CTLA-4 inhibitor).

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Printable monograph

PD-1 checkpoint inhibitor

Pembrolizumab

Keytruda · Pembro

PD-1 checkpoint inhibitor · approved 2014 · 15 citations · FAERS AKI reporting ROR 3.31 (95% CI 3.18–3.45, 2,447 AKI reports)

Up to date· through 2026

Deeply sourced9/9 · 8 signals

Met: 15 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 archetypal checkpoint-inhibitor kidney injury: a delayed, often PPI-associated acute interstitial nephritis that usually responds to drug withdrawal and steroids.

ModeratePD-1 checkpoint inhibitor

MelanomaNon-small cell lung cancerRenal cell carcinomaHead and neck squamous cell carcinomaUrothelial carcinomaMSI-high / dMMR solid tumorsHodgkin lymphomaTriple-negative breast cancer

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Signature kidney injury

Signature lesion

Acute Interstitial Nephritis

Representative incidence3.6%

In real-world cohorts of patients receiving immune checkpoint inhibitors, any AKI is common (roughly 16-18%), but AKI attributable to the checkpoint inhibitor itself (ICPi-AKI) is less frequent. A single-center cohort reported AKI in 16.5% of ICI-treated patients with checkpoint-attributable nephrotoxicity in a minority, while a larger real-world study found ICPi-AKI in about 3.6%. Acute interstitial nephritis is the dominant biopsy lesion (>80% in the largest multicenter series). These figures are pooled across PD-1/PD-L1/CTLA-4 agents rather than pembrolizumab-specific.Source: Lumlertgul, Eur J Cancer 2023

Onset & rechallenge

Time to injuryDelayed (>6 weeks / cumulative)

Typically weeks to months; multicenter cohort medians ~14–16 weeks; can follow a single dose or many months out and may recur on rechallenge.

Distilled from: “Delayed and highly variable, typically weeks to months after initiation; multicenter cohorts reported median onsets around 14-16 weeks. Can occur after a single dose or after many months, and may recur on rechallenge.”

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

About two-thirds of patients recover kidney function after checkpoint-inhibitor AKI; corticosteroids are the mainstay for moderate-to-severe disease, and earlier initiation (within ~3 days of AKI) is associated with higher odds of renal recovery.PMID 34625513 (opens PubMed in a new tab)

CKD trajectory.: In a separate single-center cohort of 1,037 ICI-treated patients, those whose AKI was ICI-attributed reached higher AKI stages and were less likely to recover kidney function completely than patients with AKI from other causes (54% versus 79%, p=0.01) — so some are left with residual CKD.PMID 37499561 (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 · Signature1.77%PMID 30746132 (opens PubMed in a new tab)
Pembrolizumab-related nephropathy in 12/676 treated patients (1.77%); acute interstitial nephritis (with acute tubular injury) the dominant biopsy lesion. Class-wide, ICI-related AKI runs ~3% with AIN the recurrent histology.
Electrolyte DisturbanceSecondaryqualitative — no citable incidence
Renal electrolyte derangement — magnesium/potassium/calcium wasting (cisplatin, anti-EGFR antibodies) or retention (FGFR-inhibitor hyperphosphatemia, tumor-lysis hyperkalemia/hyperphosphatemia).
Glomerular Injury / ProteinuriaSecondaryno population incidence denominator
Glomerular lesions (minimal change disease, membranous nephropathy) reported in biopsy series of ICI-related AKI, secondary to the predominant interstitial nephritis. PMID 32601079 (opens PubMed in a new tab)
Thrombotic MicroangiopathyRareno population incidence denominator
Thrombotic microangiopathy is a rare, case-level ICI kidney lesion (2 of 12 biopsied in one ICI-AKI cohort). PMID 32601079 (opens PubMed in a new tab)
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.
Hemorrhagic CystitisRarequalitative — no citable incidence
Case-level immune-related (irAE) cystitis - immune-mediated, not acrolein toxicity.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

3.6%incidence

SeverityModerate

ReversibilityPartially reversible

Evidence15 citations

Nephron map

Glomerulus

Vasculature / Endothelium

Distal Tubule / Collecting Duct

InterstitiumSupporting tissue around the tubules

Bladder / Urothelium

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.

Mechanism of kidney injury

ICI-AKI is thought to be an off-target, T-cell-mediated immune reaction within the kidney rather than direct tubular toxicity. Loss of PD-1-mediated peripheral tolerance is thought to permit reactivation of drug-specific effector T cells (for example, against PPIs, NSAIDs, or antibiotics acting as haptens), producing acute interstitial nephritis with a lymphohistiocytic interstitial infiltrate. Less commonly, the same dysregulated immunity is reported to drive podocytopathy (minimal change disease), other glomerular lesions, thrombotic microangiopathy, or tubular dysfunction manifesting as distal renal tubular acidosis with hypokalemic non-anion-gap metabolic acidosis.

Clinical presentation

Typically a subacute, asymptomatic rise in serum creatinine detected on routine labs. Urinalysis is often bland or shows modest sterile pyuria and subnephrotic proteinuria; eosinophiluria is neither sensitive nor specific. Concurrent extrarenal immune-related adverse events (rash, colitis, thyroiditis, hepatitis) are common clues. Glomerular variants (minimal change disease) can present with abrupt edema, weight gain, and nephrotic-range proteinuria. Renal tubular acidosis variants present with hypokalemia and a non-anion-gap metabolic acidosis.

Management

Hold pembrolizumab and evaluate for and remove competing AIN culprits (PPIs, NSAIDs). Kidney biopsy is often used to confirm the lesion and exclude alternative causes. Corticosteroids are the mainstay for moderate-to-severe ICPi-AKI; in the largest cohort, corticosteroid treatment — and earlier initiation (within 3 days) — was associated with higher odds of renal recovery. About two-thirds of patients recover kidney function. Rechallenge can be considered after recovery but carries a recurrent-AKI risk (~16% in cohort data); decisions should weigh oncologic need against renal risk. Electrolyte/RTA variants require alkali and potassium repletion alongside steroids.Lesion-level management framework

Risk factors

Concurrent proton pump inhibitor use
Lower baseline eGFR / pre-existing CKD
Other (extrarenal) immune-related adverse events
Concomitant NSAIDs or antibiotics (potential hapten triggers)
Combination checkpoint blockade (e.g., added CTLA-4 inhibitor)

Prevention

Review and discontinue non-essential PPIs and other AIN-associated drugs before/during therapy

Anticancer mechanism· how it treats cancer

Humanized IgG4 monoclonal antibody against PD-1 that blocks the PD-1/PD-L1 inhibitory axis, releasing the brakes on T cells and restoring antitumor immunity. The same loss of peripheral tolerance that drives efficacy also underlies its immune-related adverse events, including the kidney.

Note · Most quantitative incidence and outcome data come from pooled ICI cohorts (PD-1/PD-L1/CTLA-4), not pembrolizumab-only series; the qualitative lesion spectrum (AIN-dominant, with glomerular and tubular variants) is well supported for pembrolizumab specifically via biopsy-proven case reports.

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Clinical depth

Renal dose adjustment

No pharmacokinetic renal dose adjustment is required — pembrolizumab is a monoclonal antibody cleared by catabolism, not renal excretion, so none is needed across the spectrum of renal impairment. Management is immunologic (hold drug, grade the irAE, treat) rather than dose-based: per standard irAE grading, grade 2 nephritis prompts holding the drug and corticosteroids, and grade 3-4 prompts permanent discontinuation.

Dialyzability & ESKD dosing

Not dialyzable — as a ~149 kDa IgG4 monoclonal antibody it is not removed by hemodialysis. Patients on dialysis can receive pembrolizumab without dose change; dialysis does not mitigate the immune-mediated nephritis.

Differential diagnosis

Distinguish ICI-attributable AIN from prerenal azotemia, contrast- or chemotherapy-associated ATN, obstruction, and AIN from concurrent drugs (PPIs, NSAIDs, antibiotics) — these often coexist. Bland urinalysis with a slow creatinine rise and concurrent extrarenal irAEs favors ICI-AIN; abrupt nephrotic syndrome suggests a glomerular (minimal-change) variant; non-anion-gap hypokalemic acidosis suggests distal RTA. Kidney biopsy is frequently needed because clinical features are nonspecific. Pseudo-AKI (a creatinine rise from another mechanism, not true injury) should be considered before attributing every rise to the drug.

Monitoring

Serum electrolytes and bicarbonate (for RTA/hypokalemia)
Urinalysis with protein quantification when AKI or edema develops
Surveillance for concurrent extrarenal immune-related adverse events

Key trials & series

KEYNOTE-021 (NSCLC; AKI reported as a treatment-related adverse event in the pembrolizumab-chemotherapy arm)
Gupta et al. 30-site international ICPi-AKI cohort (J Immunother Cancer 2021)
Meraz-Munoz/Kitchlu single-center ICPi-AKI cohort (J Immunother Cancer 2020)

Clinical pearls

AIN is by far the most common ICI kidney lesion — >80% of biopsies in the largest cohort.
PPI co-exposure is a recurring, modifiable risk factor; deprescribe when possible.
Onset is famously delayed and variable — weeks to many months — so keep ICI-AIN on the differential long after starting therapy.
Earlier steroids (within ~3 days of AKI) were associated with better renal recovery.
Rechallenge is feasible but recurrent AKI occurs in roughly 1 in 6.
Watch for the rarer faces: minimal change disease with nephrotic syndrome, and distal RTA with hypokalemic non-gap acidosis.
Immune-related cystitis — occasionally frankly hemorrhagic — is a rare pembrolizumab irAE that responds to corticosteroids; biopsy in one reported case showed CD8+ lymphocytic urothelial infiltration.

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

12 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

12 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 · ModerateC3 Glomerulonephritis Associated With Anti-complement Factor B Antibodies Following Anti-cancer Treatment With Pembrolizumab.Stroppou P et al. · Kidney Med 2026 · PMID 42004655A 78-year-old man on two years of pembrolizumab for metastatic bladder cancer developed stage 3 AKI with biopsy-proven crescentic C3 glomerulonephritis and acquired anti-complement-factor-B autoantibodies, attributed to PD-1-inhibitor loss of tolerance.CaseB · ModerateAnti-GBM glomerulonephritis in a patient with lung adenocarcinoma following pembrolizumab therapy.Abouelyazid R et al. · BMJ Case Rep 2026 · PMID 41887681A man in his 60s on pembrolizumab for lung adenocarcinoma presented with acute renal failure requiring renal replacement therapy and biopsy-confirmed anti-GBM glomerulonephritis linked to checkpoint-inhibitor breakdown of self-tolerance.CaseB · ModeratePembrolizumab-Induced Tubulointerstitial Nephritis in Early-Stage Triple-Negative Breast Cancer: A Case Report.Ferreira C et al. · Cureus 2025 · PMID 41510480A woman in her 50s developed AKI after three cycles of pembrolizumab for early-stage triple-negative breast cancer, with kidney biopsy showing acute tubulointerstitial nephritis that responded to drug withdrawal and corticosteroids.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 104,614 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· 9 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 11.65
Glomerular Injury / Proteinuriacorroborated · ROR 8.47 — on the terms that name the lesion (ROR 3.26)
Electrolyte Disturbancecorroborated · ROR 2.12 — on the terms that name the lesion (ROR 2.97)
Thrombotic Microangiopathycorroborated · ROR 2.04
Hemorrhagic Cystitiscorroborated · ROR 1.14 — on the terms that name the lesion (ROR 1.65)
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 11.6595% CI 10.93–12.41· 1,024 reports

Glomerular Injury / Proteinuria

ROR 8.4795% CI 7.99–8.98· 1,174 reports

Acute Tubular Necrosis

ROR 6.9395% CI 6.20–7.73· 329 reports

SIADH / Hyponatremia

ROR 2.5895% CI 2.42–2.74· 1,022 reports

Hypertension

ROR 2.4495% CI 2.37–2.51· 4,539 reports

Electrolyte Disturbance

ROR 2.1295% CI 2.03–2.22· 1,992 reports

Thrombotic Microangiopathy

ROR 2.0495% CI 1.75–2.39· 157 reports

Fanconi Syndrome

ROR 1.4995% CI 1.08–2.05· 38 reports

Hemorrhagic Cystitis

ROR 1.1495% CI 1.03–1.26· 394 reports

FAERS outcomes & reporting trend· 17.9% of reports w/ death · 42% w/ hospitalization

17.9%

Reported with a death outcome

18,745 of 104,614 reports

42%

Reported with hospitalization

43,931 of 104,614 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 12 systems · 104,614 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. Showing the top 10 of 12 classified systems; 2 lower-ranked systems are not drawn. As of 2026-10-01.

Disproportionality (acute kidney injury):ROR 3.3195% CI 3.18–3.45· 2,447 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 Injury2,447

General / constitutional

Fatigue5,113Pyrexia3,870Asthenia2,774Malaise2,383Weight Decreased1,818

Gastrointestinal

Diarrhoea5,719Nausea3,563Vomiting2,206Colitis1,959

Respiratory

Interstitial Lung Disease2,532Dyspnoea2,351Pneumonitis2,221

Blood & lymphatic

Anaemia2,417Neutropenia2,336

Skin

Rash3,719

Metabolic & electrolyte

Decreased Appetite3,305

Vascular

Hypertension3,232

Endocrine

Hypothyroidism2,918

Immune / infection

Pneumonia2,223

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 Pembrolizumab 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

Nivolumab

Opdivo · PD-1 checkpoint inhibitor

Profile

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

AINCINGLOM

Moderate#1 · 70% 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#2 · 68% phenotype match

Cosibelimab

Unloxcyt · PD-L1 immune checkpoint inhibitor

Profile

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

AINGLOMLYTE

Moderate#3 · 67% phenotype match

Sugemalimab

Cejemly · PD-L1 immune checkpoint inhibitor

Profile

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

AINATNLYTE

Moderate#4 · 66% phenotype match

Penpulimab

Penpulimab (AK105) · PD-1 immune checkpoint inhibitor

Profile

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

AINATNLYTE

Moderate#5 · 66% 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#6 · 64% phenotype match

Compare Pembrolizumab 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 Pembrolizumab’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 Pembrolizumab; 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 153 clinical records among all 178 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.