What kind of kidney injury does Tislelizumab cause?

Acute Interstitial Nephritis — Immune-mediated inflammation of the renal interstitium — the signature kidney injury of checkpoint inhibitors. Other reported patterns: Prerenal / Hemodynamic AKI, Thrombotic Microangiopathy, Glomerular Injury / Proteinuria.

How should kidney function be monitored during Tislelizumab therapy?

Urinalysis for proteinuria, pyuria, and hematuria; Surveillance for concurrent immune-related adverse events (thyroid, hepatic, GI, skin); Electrolytes (including Mg, K) if other irAEs or losses present; Trend creatinine after any drug hold or steroid course to confirm recovery.

How can kidney injury from Tislelizumab be prevented?

Review and minimize concomitant nephritis-associated drugs (PPIs, NSAIDs) Maintain euvolemia; reassess RAAS inhibitors and diuretics Hold drug and evaluate before attributing AKI to a benign cause

Who is at higher risk of kidney injury from Tislelizumab?

Concurrent or prior immune-related adverse events (strongest associated risk); Pre-existing hypertension; Combination with other nephritis-associated drugs (PPIs, NSAIDs, antibiotics); RAAS inhibitor or diuretic use (predisposes to prerenal AKI); Pre-existing chronic kidney disease; Higher cumulative checkpoint-inhibitor exposure.

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Printable monograph

PD-1 immune checkpoint inhibitor

Tislelizumab

Tevimbra · PD-1 inhibitor

PD-1 immune checkpoint inhibitor · approved 2024 · 8 citations

Up to date· through 2026

Fairly sourced4/9 · 4 signals

Met: 8 citations
Not met: 12+ references
Not met: Accrued over 10+ years (span: 6y)
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.

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

Moderatecheckpoint-immunotherapy

Advanced or metastatic esophageal squamous cell carcinoma (second-line, monotherapy)Advanced or metastatic esophageal squamous cell carcinoma (first-line, with chemotherapy)Advanced/metastatic gastric or gastroesophageal junction adenocarcinoma (with chemotherapy, PD-L1+)

§01

Signature kidney injury

Signature lesion

Acute Interstitial Nephritis

Representative incidence2%

1–3% range across studies

Drug-specific renal data are sparse: the registrational ESCC trials (RATIONALE-302, RATIONALE-306) did not report nephritis as a notable adverse event, and no tislelizumab-specific biopsy series exists. Reasoning from the PD-1 class, immune-mediated acute interstitial nephritis (the class signature) is uncommon at roughly 1-3% of treated patients, while any-cause AKI in real-world ICI cohorts is far higher (16-17%) but mostly prerenal/non-immune rather than true ICI-nephritis.Source: No tislelizumab-specific renal incidence is published; the ~1-3% AIN estimate is extrapolated from PD-1-class cohorts. In a single-center ICI cohort, 16.5% developed AKI but only ~2% (6/309) had biopsy/clinically attributed interstitial nephritis (Meraz-Munoz et al., J Immunother Cancer 2020, PMID 32601079); in an anti-PD-1 melanoma cohort, 17% had AKI but only 3.3% had AIN, most AKI being prerenal (Stein et al., NDT 2021, PMID 32941608).

Onset & rechallenge

Time to injuryDelayed (>6 weeks / cumulative)

Weeks to several months, often 8–12+ weeks; can follow a single dose or even after stopping.

Distilled from: “Delayed: commonly weeks to several months after initiation (often 8-12+ weeks); can occur after multiple cycles or after a single dose, and rarely after drug discontinuation.”

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

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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 · Signaturequalitative — no citable incidence
Immune-mediated inflammation of the renal interstitium — the signature kidney injury of checkpoint inhibitors.
Prerenal / Hemodynamic AKISecondaryqualitative — no citable incidence
Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.
Thrombotic MicroangiopathyRarequalitative — no citable incidence
Endothelial injury with microvascular thrombi, hemolysis and thrombocytopenia — gemcitabine, mitomycin C, anti-VEGF.
Glomerular Injury / ProteinuriaRareno population incidence denominator
Case-level: ANCA-associated glomerulonephritis (GPA) reported PMID 40420929 (opens PubMed in a new tab)

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

2%incidence

SeverityModerate

ReversibilityPartially reversible

Evidence8 citations

Nephron map

Glomerulus

Vasculature / Endothelium

InterstitiumSupporting tissue around the tubules

Acute Interstitial Nephritis

Immune-mediated inflammation of the renal interstitium — the signature kidney injury of checkpoint inhibitors.

§03

Kidney injury

Mechanism of kidney injury

The dominant kidney lesion of PD-1 blockade is immune-mediated acute interstitial nephritis: loss of peripheral tolerance unmasks autoreactive T cells, producing a granulomatous or lymphocytic tubulointerstitial infiltrate, often with a delayed onset weeks to months into therapy and frequently concurrent with extrarenal immune-related adverse events. Less commonly, checkpoint blockade is associated with de novo or relapsing glomerular disease (minimal change, membranous, pauci-immune) and rare thrombotic microangiopathy. Much AKI in these patients is not drug-immune at all but prerenal/hemodynamic (volume depletion, concurrent nephrotoxins, RAAS inhibitors).

Clinical presentation

Typically a subacute, often asymptomatic rise in serum creatinine detected on routine labs, sometimes with sterile pyuria or subnephrotic proteinuria; eosinophiluria is insensitive. Overt oliguria is uncommon. AIN is frequently accompanied by other immune-related adverse events (rash, colitis, hepatitis, thyroiditis), which is an important diagnostic clue. Glomerular involvement may present with nephrotic-range proteinuria or hematuria.

Management

For immune-mediated AIN: hold tislelizumab, exclude prerenal and obstructive causes, and consider kidney biopsy when the diagnosis is unclear. Grade 2-3 nephritis is treated with corticosteroids (e.g., prednisone 0.5-1 mg/kg/day, higher for severe cases) with a slow taper; discontinue offending co-medications (PPIs/NSAIDs). Permanently discontinue for grade 3-4 or recurrent immune-mediated nephritis. Rechallenge after resolved low-grade AIN can be considered cautiously with monitoring. Prerenal AKI is managed with volume optimization and removal of contributing agents rather than steroids.Lesion-level management framework

Risk factors

Concurrent or prior immune-related adverse events (strongest associated risk)
Pre-existing hypertension
Combination with other nephritis-associated drugs (PPIs, NSAIDs, antibiotics)
RAAS inhibitor or diuretic use (predisposes to prerenal AKI)
Pre-existing chronic kidney disease
Higher cumulative checkpoint-inhibitor exposure

Prevention

Review and minimize concomitant nephritis-associated drugs (PPIs, NSAIDs)
Maintain euvolemia; reassess RAAS inhibitors and diuretics
Hold drug and evaluate before attributing AKI to a benign cause

Anticancer mechanism· how it treats cancer

Tislelizumab is a humanized IgG4-variant monoclonal antibody that binds programmed cell death protein 1 (PD-1) on T cells, blocking its engagement by PD-L1/PD-L2 and releasing the brake on cytotoxic T-cell responses against tumor cells. It is uniquely Fc-engineered to minimize binding to FcγRI on macrophages, reducing antibody-dependent phagocytosis of activated effector T cells. Approved in the US (Tevimbra) for esophageal squamous cell carcinoma and gastric/GEJ adenocarcinoma.

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Clinical depth

Renal dose adjustment

No starting-dose adjustment for renal impairment is recommended; tislelizumab is given as a fixed 200 mg IV every 3 weeks. As a ~150 kDa monoclonal antibody it is cleared by reticuloendothelial proteolysis, not the kidney, so mild-to-moderate renal impairment does not alter exposure. Data in severe impairment/dialysis are limited. Dose modification is event-driven (hold/discontinue for immune-mediated nephritis), not pharmacokinetic.

Dialyzability & ESKD dosing

Not dialyzable. Large IgG4 monoclonal antibodies are not removed by hemodialysis or peritoneal dialysis; timing relative to dialysis is irrelevant.

Differential diagnosis

Distinguish true immune-mediated AIN from the much more common prerenal/hemodynamic AKI (volume depletion, sepsis, contrast, cardiorenal). Other considerations: concurrent PPI/NSAID/antibiotic-induced AIN, tumor-related obstruction, hypercalcemia, and checkpoint-associated glomerulonephritis or thrombotic microangiopathy. Concurrent extrarenal immune-related adverse events and sterile pyuria favor AIN; bland sediment with a clear hemodynamic trigger favors prerenal. Kidney biopsy is the reference standard when management hinges on the distinction.

Monitoring

Urinalysis for proteinuria, pyuria, and hematuria
Surveillance for concurrent immune-related adverse events (thyroid, hepatic, GI, skin)
Electrolytes (including Mg, K) if other irAEs or losses present
Trend creatinine after any drug hold or steroid course to confirm recovery

Key trials & series

RATIONALE-302 (NCT03430843): phase 3, second-line tislelizumab vs chemotherapy in advanced/metastatic ESCC; OS benefit, fewer grade 3+ treatment-related AEs (18.8% vs 55.8%)
RATIONALE-306 (NCT03783442): phase 3, first-line tislelizumab + chemotherapy vs placebo + chemotherapy in advanced/metastatic ESCC; OS 17.2 vs 10.6 months

Clinical pearls

Tislelizumab is Fc-engineered to minimize FcγRI binding (less macrophage-mediated T-cell clearance) — a theoretical efficacy/safety tweak, but no evidence it reduces renal immune toxicity versus other PD-1 agents.
Most AKI on any PD-1 agent is NOT drug-immune nephritis — it is prerenal/hemodynamic; reserve steroids for genuine immune-mediated AIN.
AIN classically appears weeks-to-months in and travels with other immune-related adverse events; look for a rash/colitis/thyroiditis clue.
Co-prescribed PPIs and NSAIDs are frequent AIN cofactors — review and stop them when checkpoint nephritis is suspected.
Paradoxically, biopsy-confirmed checkpoint AIN may signal a favorable tumor response, but it still warrants drug hold and steroids.

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

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References

5 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

5 references · 2020–2023 · 4 since 2021

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 · ModerateRenal-Limited Thrombotic Microangiopathy Induced by Fruquintinib and Tislelizumab: A Case Report.Liu Q et al. · Nephrology (Carlton) 2025 · PMID 40528285Biopsy-confirmed renal-limited thrombotic microangiopathy with nephrotic-range proteinuria after fruquintinib plus tislelizumab, resolving on drug withdrawal.CaseC · LimitedImmune-related nephritis, ureteritis and cystitis secondary to immune checkpoint inhibitors: A case report and review of the literature.Zhang G et al. · Exp Ther Med 2026 · PMID 42338801Describes immune-related nephritis (an interstitial-nephritis-type renal irAE) with rising serum creatinine in a patient exposed to immune checkpoint inhibitors including tislelizumab, resolving with steroids.CaseC · LimitedCase report of acute hepatorenal failure induced by third-line treatment with tislelizumab in a patient with cholangiocarcinoma: was influenza virus the culprit?.Zhang X et al. · Front Immunol 2025 · PMID 41459532Reports fulminant acute kidney injury occurring within days of tislelizumab (plus anlotinib) therapy as part of fatal multiorgan immune-related toxicity.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 177 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· 2 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 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.
Prerenal / Hemodynamic AKINot queried in FAERS — No MedDRA term set is defined for this phenotype, so FAERS was never asked about it.
Thrombotic MicroangiopathyNo disproportionate reporting — This phenotype IS reportable and this agent has enough reports, yet the reporting is not disproportionate — the one genuinely informative negative of the four.
Glomerular Injury / ProteinuriaNo disproportionate reporting — This phenotype IS reportable and this agent has enough reports, yet the reporting is not disproportionate — the one genuinely informative negative of the four.

SIADH / Hyponatremia

ROR 10.6895% CI 5.01–22.74· 7 reports

Electrolyte Disturbance

ROR 4.4895% CI 2.10–9.54· 7 reports

FAERS outcomes & reporting trend· 18.1% of reports w/ death · 27.7% w/ hospitalization

18.1%

Reported with a death outcome

32 of 177 reports

27.7%

Reported with hospitalization

49 of 177 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 9 systems · 177 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 0.7895% CI 0.11–5.54· 1 AKI reports ·no disproportionate AKI reporting signal (CI spans 1).

Renal & urinary

Renal Impairment5

Blood & lymphatic

Anaemia21Thrombocytopenia19Myelosuppression4Neutrophil Count Decreased4Febrile Neutropenia3

Immune / infection

Pneumonia9Infusion Related Reaction6Infection3

Metabolic & electrolyte

Decreased Appetite7Hyponatraemia7

General / constitutional

Pyrexia8Fall3

Hepatobiliary

Alanine Aminotransferase Increased3Aspartate Aminotransferase Increased3

Endocrine

Hypothyroidism4

Gastrointestinal

Nausea4

Respiratory

Interstitial Lung Disease3

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 Tislelizumab sits in nephrotoxicity space — each dot is an anti-cancer agent, positioned so neighbors share a kidney-injury phenotype. Its 6 closest are filled and lead to a numbered marker, matching the numbered cards below.

Position is a 2-D projection (MDS) of each agent's injury signature, nephron target, severity, and class, so two dots can sit close on the page while differing on an axis the projection flattened — the numbered ranking is computed from the full metric, not from the distance you see. Open the full map.

Phenotype-similar agents· the numbered markers on the map above

Ivonescimab

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

Profile

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

GLOMHTNAIN

Moderate#1 · 83% phenotype match

Ipilimumab

Yervoy · CTLA-4 checkpoint inhibitor

Profile

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

AINCINGLOM

Severe#2 · 76% phenotype match

Avelumab

Bavencio · Anti-PD-L1 antibody

Profile

ICI-associated AIN.

AINGLOM

Moderate#3 · 73% phenotype match

Cemiplimab

Libtayo · Anti-PD-1 antibody

Profile

ICI-associated AIN.

AINGLOM

Moderate#4 · 73% phenotype match

Dostarlimab

Jemperli · Anti-PD-1 antibody

Profile

ICI-associated AIN.

AINGLOM

Moderate#5 · 73% phenotype match

Durvalumab

Imfinzi · Anti-PD-L1 antibody

Profile

ICI-associated AIN.

AINGLOM

Moderate#6 · 73% phenotype match

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

Gao, Yan — their work on Tislelizumab, on PubMed (opens in a new tab)2 papers · 5 citesPMID 40528285 (opens PubMed in a new tab)PMID 39588116 (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 11 clinical records among all 12 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.