What kind of kidney injury does Ivonescimab cause?

Glomerular Injury / Proteinuria — Damage to the filtration barrier — podocyte injury, FSGS and protein leak from VEGF and mTOR blockade. Other reported patterns: Hypertension, Acute Interstitial Nephritis, Thrombotic Microangiopathy, Prerenal / Hemodynamic AKI.

How should kidney function be monitored during Ivonescimab therapy?

Urinalysis and urine protein-to-creatinine ratio (UPCR) at baseline and before each cycle; Blood pressure at every visit and home monitoring; CBC and peripheral smear / LDH if TMA suspected; Clinical surveillance for extrarenal immune-related adverse events.

How can kidney injury from Ivonescimab be prevented?

Optimize blood-pressure control before and during therapy Hold or dose-modify for >=2+ proteinuria or nephrotic-range proteinuria per VEGF-class precedent Maintain euvolemia and minimize concurrent nephrotoxins, especially with platinum doublets

Who is at higher risk of kidney injury from Ivonescimab?

Pre-existing hypertension or chronic kidney disease; Baseline proteinuria; Prior or concurrent anti-VEGF therapy (bevacizumab, VEGF-TKIs); Nephrotoxin co-exposure (platinum chemotherapy, NSAIDs, contrast); Prior immune-related adverse events on checkpoint inhibitors; Diabetic or hypertensive nephropathy reducing renal reserve.

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Printable monograph

PD-1 x VEGF bispecific antibody

Ivonescimab

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

PD-1 x VEGF bispecific antibody · approved 2024 · 5 citations

Up to date· through 2025

Fairly sourced4/9 · 4 signals

Not met: 5 citations
Not met: 12+ references
Not met: Accrued over 10+ years (span: 1y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Met: Current through 2025
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.

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

Moderate2020s targeted/immuno-angiogenic era

EGFR-mutated locally advanced/metastatic non-squamous NSCLC progressing after EGFR-TKI therapy (with pemetrexed + carboplatin; China approval May 2024)First-line PD-L1-positive advanced NSCLC (HARMONi-2, investigational/regional)First-line advanced squamous NSCLC with chemotherapy (HARMONi-6, investigational)

§01

Signature kidney injury

Signature lesion

Glomerular Injury / Proteinuria

Representative grade ≥3 incidence3.1%

Renal-specific data are immature for this newly approved agent; no dedicated nephrotoxicity series exists. In registrational trials, grade >=3 VEGF-related adverse events (a class category encompassing proteinuria, hypertension, and hemorrhage) occurred in roughly 3% of patients (HARMONi-A: 5/161, 3.1%) — against 4/161 (2.5%) in the chemotherapy-alone arm of the same trial, a one-patient difference that is not separable from background. Grade >=3 immune-related adverse events (the checkpoint-inhibitor category that includes AIN) occurred in ~6-9% across trials, though kidney-specific irAE rates were not separately tabulated. Clinically significant AKI was uncommon.Source: HARMONi-A (JAMA 2024, PMID 38820549): grade >=3 VEGF-related AEs 3.1% (5/161); grade >=3 irAEs 6.2%. HARMONi-2 (Lancet 2025, PMID 40057343): grade >=3 irAEs 7%.

Onset & rechallenge

Time to injuryVariable / unpredictable

VEGF-pathway proteinuria/hypertension within the first weeks-to-cycles; checkpoint-inhibitor AIN usually delayed, often 8–16 weeks.

Distilled from: “VEGF-pathway proteinuria/hypertension typically within the first weeks-to-cycles; checkpoint-inhibitor AIN usually delayed, often 8-16 weeks (range days to >1 year).”

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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.

Glomerular Injury / Proteinuria#1 · Signaturequalitative — no citable incidence
Damage to the filtration barrier — podocyte injury, FSGS and protein leak from VEGF and mTOR blockade.
HypertensionSecondaryqualitative — no citable incidence
Raised blood pressure — archetypally on-target loss of endothelial nitric oxide from VEGF-pathway blockade, studied as a pharmacodynamic marker of drug exposure. Other agents raise it too: vascular effects of BCR-ABL, BTK and RET inhibitors and of copanlisib; abiraterone's mineralocorticoid excess; androgen suppression or blockade.
Acute Interstitial NephritisSecondaryqualitative — no citable incidence
Immune-mediated inflammation of the renal interstitium — the signature kidney injury of checkpoint inhibitors.
Thrombotic MicroangiopathySecondaryqualitative — no citable incidence
Endothelial injury with microvascular thrombi, hemolysis and thrombocytopenia — gemcitabine, mitomycin C, anti-VEGF.
Prerenal / Hemodynamic AKISecondaryqualitative — no citable incidence
Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

3.1%grade ≥3 incidence

SeverityModerate

ReversibilityVariable

Evidence5 citations

Nephron map

GlomerulusFiltration barrier (podocytes + endothelium)

Vasculature / Endothelium

Interstitium

Glomerular Injury / Proteinuria

Damage to the filtration barrier — podocyte injury, FSGS and protein leak from VEGF and mTOR blockade.

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Kidney injury

Mechanism of kidney injury

Two convergent mechanisms. (1) VEGF-A sequestration removes podocyte-derived VEGF support of the glomerular filtration barrier, causing podocyte/endothelial dysfunction that manifests as proteinuria, VEGF-pathway hypertension (reduced nitric-oxide bioavailability, rarefaction), and rarely thrombotic microangiopathy - the same biology seen with bevacizumab and VEGF-TKIs. (2) PD-1/PD-L1 blockade can break renal immune tolerance and precipitate acute (granulomatous) interstitial nephritis, the canonical checkpoint-inhibitor kidney lesion. Direct tubular toxicity is not expected; pre-renal/hemodynamic contributions are minor.

Clinical presentation

Most commonly asymptomatic new or worsening proteinuria and rising blood pressure during therapy (VEGF effect). AIN presents as subacute creatinine rise weeks-to-months in, often with bland or sterile-pyuric sediment, sometimes eosinophilia; concurrent extrarenal irAEs are a clue. Nephrotic-range proteinuria, microangiopathic hemolysis (schistocytes, thrombocytopenia) suggest VEGF-mediated TMA and warrant drug hold.

Management

VEGF-related proteinuria/hypertension: standard anti-VEGF algorithm - antihypertensives (ACEi/ARB preferred for proteinuria), dose interruption for nephrotic-range proteinuria or uncontrolled hypertension, discontinue for nephrotic syndrome or TMA. Suspected checkpoint-inhibitor AIN: hold the drug, exclude alternative causes, and treat with corticosteroids (e.g., prednisone ~0.5-1 mg/kg/day with taper) per immune-related AE guidelines; kidney biopsy when diagnosis is uncertain or response is inadequate. Nephrology co-management for persistent AKI, heavy proteinuria, or TMA.Lesion-level management framework

Risk factors

Pre-existing hypertension or chronic kidney disease
Baseline proteinuria
Prior or concurrent anti-VEGF therapy (bevacizumab, VEGF-TKIs)
Nephrotoxin co-exposure (platinum chemotherapy, NSAIDs, contrast)
Prior immune-related adverse events on checkpoint inhibitors
Diabetic or hypertensive nephropathy reducing renal reserve

Prevention

Optimize blood-pressure control before and during therapy
Hold or dose-modify for >=2+ proteinuria or nephrotic-range proteinuria per VEGF-class precedent
Maintain euvolemia and minimize concurrent nephrotoxins, especially with platinum doublets

Anticancer mechanism· how it treats cancer

Tetravalent humanized bispecific IgG that simultaneously blocks PD-1/PD-L1 (relieving T-cell immunosuppression) and sequesters VEGF-A (blocking VEGFR2-driven tumor angiogenesis). Co-targeting produces cooperative avidity-driven binding enriched in the VEGF-rich tumor microenvironment.

Note · This profile is grounded in the ivonescimab registrational program. Renal toxicity is inferred from trial-reported VEGF-related and immune-related adverse-event categories plus VEGF-inhibitor/checkpoint-inhibitor class biology.

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Clinical depth

Renal dose adjustment

Dosed by weight (20 mg/kg IV every 3 weeks) as a monoclonal antibody; no pharmacokinetic renal dose adjustment is defined, and antibodies are not cleared by the kidney. Management is by holding/modifying for renal toxicity (proteinuria, hypertension, AIN) rather than by GFR-based dose reduction. No data in dialysis or severe CKD; use with nephrology input.

Dialyzability & ESKD dosing

Not dialyzable. As a ~150+ kDa IgG bispecific antibody, it is not removed by hemodialysis or peritoneal dialysis; timing of dosing around dialysis is irrelevant.

Differential diagnosis

Distinguish VEGF-pathway injury (proteinuria + hypertension, podocyte/endothelial) from checkpoint-inhibitor AIN (subacute creatinine rise, sterile pyuria, steroid-responsive) - the management diverges (drug hold/antihypertensives vs steroids). Also consider concurrent platinum (cisplatin/carboplatin) ATN, contrast-associated AKI, pre-renal azotemia from poor intake, and tumor-related obstruction. Microangiopathic hemolysis points to VEGF-mediated TMA rather than AIN.

Monitoring

Urinalysis and urine protein-to-creatinine ratio (UPCR) at baseline and before each cycle
Blood pressure at every visit and home monitoring
CBC and peripheral smear / LDH if TMA suspected
Clinical surveillance for extrarenal immune-related adverse events

Key trials & series

HARMONi-A (NCT05184712): ivonescimab + chemotherapy vs chemotherapy in EGFR-mutant TKI-relapsed NSCLC; basis of first approval (PMID 38820549)
HARMONi-2 (NCT05499390): ivonescimab vs pembrolizumab in PD-L1+ first-line NSCLC, PFS 11.1 vs 5.8 months (PMID 40057343)
HARMONi-6 (NCT05840016): ivonescimab + chemo vs tislelizumab + chemo in first-line squamous NSCLC (PMID 41125109)
Phase 1a/1b dose-finding and first-in-human safety (PMID 38642937, 37879536)

Clinical pearls

One molecule, two distinct renal mechanisms - read the urine: proteinuria + hypertension = VEGF arm; rising creatinine with sterile pyuria = checkpoint AIN arm. They are managed differently.
No GFR-based dose adjustment and not dialyzable - it is an IgG antibody, so renal handling does not drive dosing.
ACEi/ARB are first-line for VEGF-pathway proteinuria and hypertension; reserve corticosteroids for biopsy-supported or strongly suspected immune AIN.

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· 4 organ systems

Class-level context for the major non-renal toxicities of the PD-1 x VEGF bispecific antibody class.

Vascular

Hypertension, VTE/ATE, bleeding, aneurysm

Hypertension, arterial/venous thrombosis, bleeding, impaired wound healing

Cardiac

Cardiomyopathy, QT, ischemia, myocarditis

LV dysfunction; QT (some TKIs)

Gastrointestinal

Diarrhea, colitis, mucositis, perforation

Diarrhea, perforation/fistula

Dermatologic

Rash, HFS, SJS/TEN, vitiligo

Hand-foot skin reaction

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References

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

Evidence accrual

5 references · 2024–2025 · 5 since 2023

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.

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 Ivonescimab 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

Tislelizumab

Tevimbra · PD-1 immune checkpoint inhibitor

Profile

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

AINPRETMA

Moderate#1 · 83% phenotype match

Trametinib

Mekinist · MEK inhibitor

Profile

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

PREAINGLOM

Moderate#2 · 78% phenotype match

Ipilimumab

Yervoy · CTLA-4 checkpoint inhibitor

Profile

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

AINCINGLOM

Severe#3 · 77% phenotype match

Sunitinib

Sutent · VEGFR TKI

Profile

VEGFR-TKI; hypertension and proteinuria, TMA reported.

HTNGLOMTMA

Moderate#4 · 70% phenotype match

Ibrutinib

Imbruvica · BTK inhibitor

Profile

Tumor lysis, hypertension and AKI.

HTNPREGLOM

Moderate#5 · 70% phenotype match

Axitinib

Inlyta · VEGFR TKI

Profile

Potent VEGFR-TKI; hypertension and proteinuria dominate.

HTNGLOMTMA

Moderate#6 · 61% phenotype match

Compare Ivonescimab 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.