How should kidney function be monitored during Toripalimab therapy?

Urinalysis with protein and microscopy (sterile pyuria, proteinuria); Serum electrolytes including magnesium and potassium (cisplatin co-therapy); Surveillance for concurrent extrarenal irAEs; Spot urine protein-to-creatinine ratio if proteinuria emerges.

How can kidney injury from Toripalimab be prevented?

Review and deprescribe unnecessary PPIs/NSAIDs that can prime AIN Maintain euvolemia and apply standard cisplatin nephroprotection (hydration, magnesium repletion)

Who is at higher risk of kidney injury from Toripalimab?

Concurrent platinum (cisplatin) chemotherapy — used in the nasopharyngeal carcinoma regimen; Concomitant AIN-associated drugs (proton pump inhibitors, NSAIDs, antibiotics); Prior or concurrent extrarenal immune-related adverse events; Pre-existing chronic kidney disease or reduced baseline GFR; Volume depletion / nephrotoxin exposure from cisplatin.

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Printable monograph

PD-1 immune checkpoint inhibitor

Toripalimab

Loqtorzi · PD-1 inhibitor

PD-1 immune checkpoint inhibitor · approved 2023 · 7 citations

Recent· through 2024

Fairly sourced4/9 · 4 signals

Met: 7 citations
Not met: 12+ references
Not met: Accrued over 10+ years (span: 7y)
Met: Beyond single case reports
Not met: Peer-reviewed sources
Met: Landmark reference
Met: Current through 2024
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.

First FDA-approved drug for nasopharyngeal carcinoma; renal risk is class-typical immune-mediated interstitial nephritis.

ModeratePD-1 checkpoint inhibitor era; first FDA approval (Oct 2023) for nasopharyngeal carcinoma.

Recurrent or metastatic nasopharyngeal carcinoma (first-line, with gemcitabine and cisplatin)Recurrent, unresectable, or metastatic nasopharyngeal carcinoma (monotherapy, after platinum-based chemotherapy)

§01

Signature kidney injury

Signature lesion

Acute Interstitial Nephritis

Representative incidence3%

3–5% range across studies

Drug-specific renal data are limited; reasoning from the PD-1 class is required. Across PD-1/PD-L1 agents, clinically significant immune-related AKI (predominantly AIN) occurs in roughly 1-5% of patients, with attributable PD-L1-related AKI under 1% in one large cohort but pooled estimates as high as ~3-5% with platinum co-therapy. In the JUPITER-02 registrational trial, immune-related adverse events were more frequent with toripalimab (54.1% vs 21.7%) and grade ≥3 irAEs occurred in 9.6%, but kidney-specific irAEs were not individually quantified.Source: Class estimate from PD-L1/ICI cohorts (Seethapathy 2020, PMID 33102962; Wanchoo 2017 review, PMID 28076863; ASON position statement, PMID 39455026); trial-level irAE data from JUPITER-02 (PMID 38015220). Toripalimab-specific renal incidence not separately reported.

Onset & rechallenge

Time to injuryDelayed (>6 weeks / cumulative)

Characteristically 3–10 months after initiation, later than CTLA-4 agents.

Distilled from: “Delayed; PD-1-related AIN characteristically appears 3-10 months after initiation (later than CTLA-4 agents), though it can occur at any point during or after treatment.”

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 · Signaturequalitative — no citable incidence
Immune-mediated inflammation of the renal interstitium — the signature kidney injury of checkpoint inhibitors.
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 / ProteinuriaRarequalitative — no citable incidence
Damage to the filtration barrier — podocyte injury, FSGS and protein leak from VEGF and mTOR blockade.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

3%incidence

SeverityModerate

ReversibilityPartially reversible

Evidence7 citations

Nephron map

Glomerulus

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

Class-mechanistic: PD-1 blockade abrogates peripheral immune tolerance, permitting activated T-cell infiltration of the renal interstitium and a delayed-type hypersensitivity-like acute (tubulo)interstitial nephritis. Loss of PD-1 signaling may also unmask reactivity to tubular or drug-hapten antigens, which is why concurrent AIN-associated drugs (PPIs, NSAIDs, antibiotics) and platinum co-therapy amplify risk. Less commonly, checkpoint activation drives immune-complex or podocyte-pattern glomerular disease and electrolyte handling disturbances.

Clinical presentation

Typically a subacute, often asymptomatic rise in serum creatinine weeks to months into therapy. Sterile pyuria, low-grade subnephrotic proteinuria, and occasionally eosinophilia or other concurrent irAEs (rash, colitis, thyroiditis, hepatitis) may be present. Frank nephrotic syndrome or active urinary sediment should prompt consideration of a superimposed glomerular lesion. Definitive diagnosis is by kidney biopsy showing interstitial inflammation.

Management

Hold toripalimab for significant AKI and exclude prerenal, obstructive, and platinum-related ATN causes. Per American Society of Onco-nephrology guidance, suspected ICI-AIN is treated by withholding the checkpoint inhibitor, discontinuing concurrent AIN-culprit drugs, and initiating corticosteroids (e.g., prednisone ~0.5-1 mg/kg/day with taper) for grade ≥2 injury; kidney biopsy is favored when feasible to confirm AIN and guide steroid duration. Many patients recover at least partial renal function. Rechallenge can be considered after recovery for lower-grade events with close monitoring, but carries recurrence risk and should be individualized.Lesion-level management framework

Risk factors

Concurrent platinum (cisplatin) chemotherapy — used in the nasopharyngeal carcinoma regimen
Concomitant AIN-associated drugs (proton pump inhibitors, NSAIDs, antibiotics)
Prior or concurrent extrarenal immune-related adverse events
Pre-existing chronic kidney disease or reduced baseline GFR
Volume depletion / nephrotoxin exposure from cisplatin

Prevention

Review and deprescribe unnecessary PPIs/NSAIDs that can prime AIN
Maintain euvolemia and apply standard cisplatin nephroprotection (hydration, magnesium repletion)

Anticancer mechanism· how it treats cancer

Humanized IgG4 monoclonal antibody that binds the PD-1 receptor on T cells and blocks engagement by its ligands PD-L1/PD-L2, releasing the inhibitory checkpoint and restoring antitumor T-cell activity. In recurrent/metastatic nasopharyngeal carcinoma it is combined with gemcitabine-cisplatin chemotherapy.

§04

Clinical depth

Renal dose adjustment

No starting dose adjustment for renal impairment is specified; toripalimab is a monoclonal antibody cleared by reticuloendothelial proteolysis, not renal excretion. Pharmacologic dose modification for kidney function is not required; instead, management is by holding/discontinuing for immune-related toxicity per severity grade. Mild-to-moderate renal impairment is not expected to alter exposure.

Dialyzability & ESKD dosing

Not dialyzable. As a ~150 kDa IgG4 monoclonal antibody it is not removed by hemodialysis or peritoneal dialysis; no supplemental dosing is needed in dialysis patients.

Differential diagnosis

Distinguish immune-related AIN from cisplatin-induced acute tubular necrosis (concurrent in the NPC regimen), prerenal azotemia from chemotherapy-related GI losses, contrast or other nephrotoxin exposure, and obstructive uropathy from pelvic/nasopharyngeal disease. A superimposed checkpoint-related glomerular lesion (e.g., podocytopathy, immune-complex GN) should be considered when nephrotic-range proteinuria or hematuria is present. Kidney biopsy is the reference standard separating AIN from ATN.

Monitoring

Urinalysis with protein and microscopy (sterile pyuria, proteinuria)
Serum electrolytes including magnesium and potassium (cisplatin co-therapy)
Surveillance for concurrent extrarenal irAEs
Spot urine protein-to-creatinine ratio if proteinuria emerges

Key trials & series

JUPITER-02 (NCT03581786): phase 3 toripalimab + gemcitabine-cisplatin vs placebo in recurrent/metastatic NPC — improved PFS and OS; basis for FDA approval
POLARIS-02: phase 2 toripalimab monotherapy in previously treated recurrent/metastatic NPC supporting the monotherapy indication

Clinical pearls

First-ever FDA-approved therapy for nasopharyngeal carcinoma (Oct 2023); a PD-1 inhibitor, so default kidney signature is immune-related AIN.
Toripalimab-specific renal toxicity is not separately quantified in trials — incidence is inferred from the PD-1/PD-L1 class and is likely low (~1-5%).
Concurrent cisplatin in the NPC regimen is itself nephrotoxic (ATN) and a recognized amplifier of ICI-AIN; separating the two often requires biopsy.
Onset is characteristically late (months), so an unexplained creatinine creep well into therapy should raise suspicion.
Being a monoclonal antibody, it needs no renal dose adjustment and is not dialyzable; the lever is immunosuppression and drug hold, not dose reduction.

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

6 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

6 references · 2017–2024 · 3 since 2022

Primary (non–case-report) references per year — a proxy for how actively the agent's renal literature is accruing. Recent years are highlighted. Reflects curation depth, not a systematic bibliometric count.

Case reports — ranked by strength· 1

Single-patient and small-series reports, graded by evidentiary strength — A Strong (biopsy-proven plus a series and/or positive rechallenge), B Moderate, and C Limited (a single clinically-diagnosed case). Strongest first. Grades are inferred automatically from each report's abstract and journal — a heuristic ranking aid, not a formal quality appraisal.

CaseC · LimitedFatal cytokine-release syndrome in a patient receiving toripalimab: a case report.Zhou Y et al. · Immunotherapy 2023 · PMID 37139989Patient with hypopharyngeal carcinoma developed acute kidney injury (alongside myelosuppression and DIC) as part of fatal toripalimab-induced cytokine-release syndrome.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 15 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.
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 outcomes & reporting trend· 8 of 15 reports w/ death · 6 w/ hospitalization

15 reports is below the 50 this atlas requires before quoting a percentage, so the counts are shown instead of shares.

8 of 15

Reported with a death outcome

too few reports to express as a share

6 of 15

Reported with hospitalization

too few reports to express as a share

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 9 systems · 15 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 9.7695% CI 1.28–74.25· 1 AKI reports ·the CI clears 1, but on fewer than 50 reports for this agent in total — too thin a base to call a signal, and the atlas does not count it as one.

Renal & urinary

Acute Kidney Injury1

Gastrointestinal

Abdominal Pain1Constipation1

Vascular

Blood Pressure Decreased1Hypertension1

General / constitutional

Fatigue1Weight Decreased1

Immune / infection

Hypersensitivity1Sepsis1

Blood & lymphatic

Neutropenia1Neutrophil Count Decreased1

Hepatobiliary

Hepatitis1

Musculoskeletal

Musculoskeletal Pain1

Skin

Rash1

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 Toripalimab 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

Cosibelimab

Unloxcyt · PD-L1 immune checkpoint inhibitor

Profile

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

AINGLOMLYTE

Moderate#1 · 100% phenotype match

Checkpoint inhibitors (pembrolizumab · nivolumab · ipilimumab)

Immune checkpoint inhibitor

Profile

Acute interstitial nephritis with long latency.

AINGLOMLYTE

Moderate#2 · 85% phenotype match

Avelumab

Bavencio · Anti-PD-L1 antibody

Profile

ICI-associated AIN.

AINGLOM

Moderate#3 · 81% phenotype match

Cemiplimab

Libtayo · Anti-PD-1 antibody

Profile

ICI-associated AIN.

AINGLOM

Moderate#4 · 81% phenotype match

Dostarlimab

Jemperli · Anti-PD-1 antibody

Profile

ICI-associated AIN.

AINGLOM

Moderate#5 · 81% phenotype match

Durvalumab

Imfinzi · Anti-PD-L1 antibody

Profile

ICI-associated AIN.

AINGLOM

Moderate#6 · 81% phenotype match

Compare Toripalimab 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 Toripalimab’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 Toripalimab; the PMIDs beside each name are up to three of their most recent papers on it, not the full count.

Li, Yu-Feng — their work on Toripalimab, on PubMed (opens in a new tab)2 papers · 38 citesPMID 37935113 (opens PubMed in a new tab)PMID 37139989 (opens PubMed in a new tab)

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 10 clinical records among all 13 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.