What kind of kidney injury does Penpulimab cause?

Acute Interstitial Nephritis — Immune-mediated inflammation of the renal interstitium — the signature kidney injury of checkpoint inhibitors. Other reported patterns: Acute Tubular Necrosis, Electrolyte Disturbance, Glomerular Injury / Proteinuria.

How should kidney function be monitored during Penpulimab therapy?

Urinalysis with microscopy (sterile pyuria, white-cell casts, proteinuria); Spot urine protein-to-creatinine ratio if proteinuria develops; Serum electrolytes including sodium, potassium, magnesium (combination chemotherapy); Surveillance for extrarenal immune-related adverse events (thyroid, liver, GI, skin); Blood pressure and CBC/peripheral smear if TMA is suspected with the platinum/gemcitabine backbone.

How can kidney injury from Penpulimab be prevented?

Review and minimize concomitant nephritis-associated drugs (PPIs, NSAIDs) Maintain euvolemia and adequate hydration, especially around platinum/gemcitabine cycles

Who is at higher risk of kidney injury from Penpulimab?

Concurrent use of other AIN-associated drugs (proton-pump inhibitors, NSAIDs, antibiotics); Combination with nephrotoxic chemotherapy (cisplatin/carboplatin plus gemcitabine) in the registrational regimen; Prior or concurrent extrarenal immune-related adverse events; Lower baseline eGFR / pre-existing chronic kidney disease; Combination immunotherapy (e.g., dual checkpoint or PD-1 plus TIM-3 blockade under study); Volume depletion and intercurrent illness.

Back to explorer

Printable monograph

PD-1 immune checkpoint inhibitor

Penpulimab

Penpulimab (AK105) · PD-1 inhibitor

PD-1 immune checkpoint inhibitor · approved 2025 · 5 citations

Up to date· through 2026

Thinly sourced3/9 · 3 signals

Not met: 5 citations
Not met: 12+ references
Not met: Accrued over 10+ years (span: 4y)
Met: Beyond single case reports
Not met: Peer-reviewed sources
Met: Landmark reference
Met: Current through 2026
Not met: Real-world FAERS signal

Describes how this page is sourced, not how dangerous the drug is. Thinly sourced means fewer of the sourcing signals are met — not that the agent is kidney-safe. A rule-based summary, not a formal certainty appraisal.

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

ModeratePD-1/PD-L1 checkpoint-inhibitor era (FDA approval 2025; China approval 2021 for Hodgkin lymphoma)

Recurrent or metastatic nasopharyngeal carcinoma (first-line, in combination with cisplatin/carboplatin plus gemcitabine)Recurrent or metastatic nasopharyngeal carcinoma (later-line monotherapy after platinum-based chemotherapy)Relapsed/refractory classic Hodgkin lymphoma (approved in China)

§01

Signature kidney injury

Signature lesion

Acute Interstitial Nephritis

Representative incidence3%

2–5% range across studies

Penpulimab-specific renal data are limited. In the pivotal first-line phase 3 trial (penpulimab plus chemotherapy), grade >=3 immune-related adverse events occurred in only 4.1% of patients, and renal events were not separately prominent; the most common toxicities were hematologic. By class, immune checkpoint inhibitor-associated AKI (predominantly acute tubulointerstitial nephritis) occurs in roughly 2-5% of patients on PD-1 monotherapy, with higher rates when combined with nephrotoxic chemotherapy. Platinum (cisplatin) and gemcitabine in the registrational backbone independently contribute ATN and (rarely) thrombotic microangiopathy risk, so observed kidney injury in this regimen is often multifactorial.Source: Class incidence of ICI-associated AKI/AIN ~2-5% (Zhou P et al., Front Immunol 2024, PMID 38464524; Miao J et al., Front Nephrol 2022, PMID 37674988). Penpulimab grade >=3 irAEs 4.1% in the first-line phase 3 trial (Huang S et al., Signal Transduct Target Ther 2026, PMID 41946687).

Onset & rechallenge

Time to injuryDelayed (>6 weeks / cumulative)

ICI-AIN commonly weeks to several months (median ~3–4 months); combination-chemo ATN occurs earlier, peri-infusion.

Distilled from: “Variable and often delayed: ICI-associated AIN commonly emerges weeks to several months after initiation (median around 3-4 months), and can appear after multiple cycles or even after discontinuation. Chemotherapy-related ATN in the combination regimen tends to occur earlier, peri-infusion.”

RechallengeCase-by-case

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

Long-term outlook & thresholds

Renal recoveryOften partial recovery

Class-level checkpoint-inhibitor AKI recovery: in a 138-patient multicenter ICI-AKI cohort, complete, partial, and no recovery of kidney function occurred in roughly 40%, 45%, and 15% of patients respectively. Two covariates carried a better renal prognosis — treatment with steroids, and the PRESENCE of a concomitant tubulointerstitial-nephritis-causing medication (69% of patients were on one). The second is an observational association, not an intervention: the cohort analysed no effect of stopping that drug, and the likeliest reading is that a competing culprit makes the ICI a less certain cause. Rechallenge is feasible in selected patients but recurrent AKI occurs in about a quarter.PMID 31896554 (opens PubMed in a new tab)

CKD trajectory.: Roughly 15% of patients have no renal recovery, leaving residual chronic kidney disease, and recovery is often incomplete (partial recovery in ~45%) — a class-level pattern across checkpoint inhibitors. A separate single-center cohort of 1,037 ICI-treated patients sharpens the comparison: complete kidney recovery was less common after ICI-attributed AKI than after AKI from other causes (54% versus 79%, p=0.01), and ICI-AKI reached higher AKI stages.PMID 37499561 (opens PubMed in a new tab)
Dialysis / RRT.: Severe checkpoint-inhibitor AKI can require dialysis, though most ICI-attributed AKI is not dialysis-requiring.

Long-term outcome and threshold data distilled from the agent's cited literature — educational, not a substitute for the primary sources.

Recovery across agents

§02

Renal toxicities, ranked

This agent's kidney lesions ordered by prominence — the #1 signature lesion first, then secondary and rare patterns. Cited incidence is shown where a citable figure exists; otherwise the tier stands qualitatively.

Acute Interstitial Nephritis#1 · Signatureno population incidence denominator
Acute tubulointerstitial nephritis is the signature ICI renal lesion — dominant in 93% of the 60 biopsied patients in a 138-patient multicenter ICI-AKI cohort (a biopsy-lesion proportion, not a treated-population incidence). PMID 31896554 (opens PubMed in a new tab)
Electrolyte DisturbanceSecondaryqualitative — no citable incidence
Renal electrolyte derangement — magnesium/potassium/calcium wasting (cisplatin, anti-EGFR antibodies) or retention (FGFR-inhibitor hyperphosphatemia, tumor-lysis hyperkalemia/hyperphosphatemia).
Acute Tubular NecrosisRareno population incidence denominator
Minority histologic pattern — tubulointerstitial nephritis dominates 93% of ICI-AKI biopsies, with ATN and other lesions making up the remainder. PMID 31896554 (opens PubMed in a new tab)
Glomerular Injury / ProteinuriaRareno population incidence denominator
Case-level; glomerular lesions (2 membranous nephropathy, 2 minimal change disease) among 12 biopsy/nephrologist-attributed ICI nephrotoxicity cases. PMID 32601079 (opens PubMed in a new tab)

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

3%incidence

SeverityModerate

ReversibilityPartially reversible

Evidence5 citations

Nephron map

Glomerulus

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.

§03

Kidney injury

Mechanism of kidney injury

The dominant kidney lesion is immune-mediated acute tubulointerstitial nephritis: PD-1 blockade lowers peripheral tolerance, allowing reactivation of autoreactive/drug-primed T cells that infiltrate the renal interstitium, with a predominantly CD4+ and CD8+ T-cell infiltrate and occasional granulomas. Loss of PD-1/PD-L1 tolerance to commonly co-administered tubulointerstitial-acting drugs (PPIs, NSAIDs, antibiotics) is a frequent trigger. Less commonly, immune dysregulation produces glomerular lesions (minimal change, podocytopathy, pauci-immune/ANCA-type glomerulonephritis) or electrolyte disturbances. Penpulimab's FcgammaR-silent design is hypothesized to reduce immune-related toxicity overall, but does not eliminate the interstitial-nephritis mechanism. In the platinum/gemcitabine combination, direct tubular toxicity (ATN) and rare TMA are chemotherapy-driven rather than checkpoint-driven.

Clinical presentation

Typically a subacute, asymptomatic rise in serum creatinine detected on routine labs, often without oliguria. Sterile pyuria, white-cell casts, mild sub-nephrotic proteinuria, and occasionally eosinophilia/eosinophiluria may be present but are insensitive. Fever and rash are inconsistent. Extrarenal immune-related adverse events (thyroiditis, hepatitis, colitis, dermatitis) may coexist and raise suspicion. Heavy proteinuria or nephrotic syndrome suggests a coexisting glomerular irAE. Hyponatremia or electrolyte wasting can occur but is less characteristic than with platinum or anti-EGFR agents.

Management

Grade the AKI and exclude pre-renal and obstructive causes. For suspected immune-related AIN: hold penpulimab, discontinue contributing AIN-associated drugs, and start corticosteroids (typically prednisone ~0.5-1 mg/kg/day, up to 1-2 mg/kg/day for higher-grade injury) with a taper over weeks once renal function improves. Kidney biopsy confirms AIN and excludes ATN/glomerular lesions when the diagnosis is uncertain or steroids fail. Most patients recover at least partially. Permanent discontinuation is warranted for grade 3-4 or recurrent nephritis; rechallenge after lower-grade, fully recovered AIN may be considered cautiously with monitoring. For chemotherapy-driven ATN/TMA in the combination regimen, manage supportively and adjust the platinum/gemcitabine component.Lesion-level management framework

Risk factors

Concurrent use of other AIN-associated drugs (proton-pump inhibitors, NSAIDs, antibiotics)
Combination with nephrotoxic chemotherapy (cisplatin/carboplatin plus gemcitabine) in the registrational regimen
Prior or concurrent extrarenal immune-related adverse events
Lower baseline eGFR / pre-existing chronic kidney disease
Combination immunotherapy (e.g., dual checkpoint or PD-1 plus TIM-3 blockade under study)
Volume depletion and intercurrent illness

Prevention

Review and minimize concomitant nephritis-associated drugs (PPIs, NSAIDs)
Maintain euvolemia and adequate hydration, especially around platinum/gemcitabine cycles

Anticancer mechanism· how it treats cancer

Penpulimab is a humanized IgG1 monoclonal antibody that binds programmed cell death protein 1 (PD-1) on T cells and blocks engagement with its ligands PD-L1/PD-L2, releasing the inhibitory checkpoint and restoring cytotoxic T-cell anti-tumor activity. It is deliberately engineered to abolish Fc-gamma-receptor (FcgammaR) binding, which is intended to prevent FcgammaR-mediated activation-induced T-cell apoptosis and reduce pro-inflammatory cytokine release while preserving receptor blockade.

§04

Clinical depth

Renal dose adjustment

No pharmacokinetic dose adjustment for renal impairment: penpulimab is a ~150 kDa IgG1 monoclonal antibody eliminated by reticuloendothelial catabolism, not by glomerular filtration or tubular secretion. Dosing is fixed (200 mg IV every 2 or 3 weeks depending on regimen). Modifications are driven by immune-related toxicity grade (hold/discontinue and add steroids) rather than by eGFR. The cisplatin component of the combination regimen does require renal dosing/eligibility consideration, and carboplatin substitution is used for patients unable to tolerate cisplatin.

Dialyzability & ESKD dosing

Not dialyzable. As a large IgG monoclonal antibody, penpulimab is not removed by hemodialysis or peritoneal dialysis; timing relative to dialysis sessions is irrelevant. No data establish its use in dialysis-dependent patients, but pharmacokinetics are not expected to be altered by renal replacement therapy.

Differential diagnosis

Distinguish immune-related AIN from: (1) cisplatin/gemcitabine-induced ATN (earlier, peri-infusion, often with classic muddy-brown casts); (2) pre-renal azotemia from poor intake, vomiting, or diarrhea; (3) gemcitabine- or platinum-associated thrombotic microangiopathy (hemolysis, thrombocytopenia, schistocytes, hypertension); (4) contrast-associated AKI from staging imaging; (5) obstructive uropathy from tumor; (6) a glomerular irAE (heavy proteinuria, hematuria). Coexisting extrarenal irAEs and sterile pyuria favor checkpoint-related AIN; kidney biopsy is the definitive arbiter.

Monitoring

Urinalysis with microscopy (sterile pyuria, white-cell casts, proteinuria)
Spot urine protein-to-creatinine ratio if proteinuria develops
Serum electrolytes including sodium, potassium, magnesium (combination chemotherapy)
Surveillance for extrarenal immune-related adverse events (thyroid, liver, GI, skin)
Blood pressure and CBC/peripheral smear if TMA is suspected with the platinum/gemcitabine backbone

Key trials & series

AK105-304 / NCT04974398: randomized double-blind phase 3 of penpulimab plus cisplatin-or-carboplatin/gemcitabine vs placebo plus chemotherapy, first-line R/M NPC (n=291); median PFS 9.63 vs 7.00 months, HR 0.45; grade >=3 irAEs 4.1% (PMID 41946687)
Single-arm phase 2 of penpulimab monotherapy in heavily pretreated metastatic NPC (n=130); ORR 28.0%, grade >=3 irAEs 7.6% (PMID 38890298)
Phase 2 exploratory study of penpulimab/gemcitabine with or without anlotinib in metastatic NPC (PMID 42093316)

Clinical pearls

Kidney injury from penpulimab is class-typical immune AIN, not a direct tubular toxin — treat suspected cases with drug hold plus corticosteroids, not just hydration.
An unexplained creatinine rise in a patient on a checkpoint inhibitor is AIN until proven otherwise; do not anchor on pre-renal causes.
In the registrational regimen the kidney sees three potential hits at once — penpulimab (AIN), cisplatin (ATN), and gemcitabine (rare TMA) — so always parse the timing and urine sediment.
Penpulimab's Fc-silent IgG1 design is intended to lower immune-related toxicity (grade >=3 irAEs were only ~4% in the phase 3 trial), but interstitial nephritis can still occur.
Penpulimab is not renally cleared and is not dialyzable — no eGFR-based dose change is needed; toxicity management is steroid- and grade-driven.
Co-prescribed PPIs and NSAIDs are common AIN co-triggers under PD-1 blockade — deprescribe them when feasible.

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 immune checkpoint inhibitor class.

Endocrine

Thyroiditis, hypophysitis, diabetes

Thyroiditis, hypophysitis, type-1 diabetes

Gastrointestinal

Diarrhea, colitis, mucositis, perforation

Immune colitis

Hepatic / Liver

Transaminitis, hepatitis, VOD/SOS

Immune hepatitis

Pulmonary

Pneumonitis, ILD, effusions, hypertension

Pneumonitis

Dermatologic

Rash, HFS, SJS/TEN, vitiligo

Rash, vitiligo, rarely SJS/TEN

§05

References

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

Evidence accrual

5 references · 2022–2026 · 4 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 70 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.

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· 4 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

Glomerular Injury / Proteinuriacorroborated · ROR 55.37 — but the naming terms alone are not disproportionate, so this rests on terms merely consistent with the lesion
Electrolyte Disturbancecorroborated · ROR 6.59 — but the naming terms alone are not disproportionate, so this rests on terms merely consistent with the lesion
Acute Interstitial NephritisNot measurable in reporting — Reporters cannot reliably name this lesion, so its absence from FAERS is expected and is not evidence against the documented injury.
Acute Tubular NecrosisNot measurable in reporting — Reporters cannot reliably name this lesion, so its absence from FAERS is expected and is not evidence against the documented injury.

Glomerular Injury / Proteinuria

ROR 55.3795% CI 22.29–137.50· 5 reports

Hemorrhagic Cystitis

ROR 8.8795% CI 2.17–36.20· 2 reports

Electrolyte Disturbance

ROR 6.5995% CI 2.40–18.08· 4 reports

Hypertension

ROR 3.2495% CI 1.18–8.88· 4 reports

FAERS outcomes & reporting trend· 10% of reports w/ death · 40% w/ hospitalization

10%

Reported with a death outcome

7 of 70 reports

40%

Reported with hospitalization

28 of 70 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 12 systems · 70 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.

Renal & urinary

Proteinuria5Adrenal Insufficiency3

Blood & lymphatic

Myelosuppression13Anaemia12Leukopenia9Thrombocytopenia9Neutropenia6

Gastrointestinal

Diarrhoea9Nausea7Vomiting7

Hepatobiliary

Alanine Aminotransferase Increased6Aspartate Aminotransferase Increased6Hepatic Function Abnormal5Blood Bilirubin Increased4

Skin

Rash9Palmar-Plantar Erythrodysaesthesia Syndrome5Pruritus4

General / constitutional

Fatigue6Pyrexia5

Endocrine

Hypothyroidism10

Respiratory

Pneumonitis6Oxygen Saturation Decreased4

Immune / infection

Anaphylactic Shock8

Metabolic & electrolyte

Decreased Appetite5

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 Penpulimab 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 · 100% phenotype match

Cosibelimab

Unloxcyt · PD-L1 immune checkpoint inhibitor

Profile

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

AINGLOMLYTE

Moderate#2 · 76% 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#3 · 76% phenotype match

Nivolumab

Opdivo · PD-1 checkpoint inhibitor

Profile

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

AINCINGLOM

Moderate#4 · 72% phenotype match

Checkpoint inhibitors (pembrolizumab · nivolumab · ipilimumab)

Immune checkpoint inhibitor

Profile

Acute interstitial nephritis with long latency.

AINGLOMLYTE

Moderate#5 · 67% phenotype match

Pembrolizumab

Keytruda · PD-1 checkpoint inhibitor

Profile

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

AINCINGLOM

Moderate#6 · 66% phenotype match

Compare Penpulimab 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.