Is kidney injury from Ziv-aflibercept reversible?

Reversible. Typical onset: Within weeks to a few months of therapy..

How should kidney function be monitored during Ziv-aflibercept therapy?

Blood pressure every 2 weeks or with each cycle; Urine dipstick and/or UPCR during therapy (in practice, before each dose); 24-h collection if dipstick >=2+ or UPCR >1; Serum creatinine; CBC/LDH/haptoglobin and smear if TMA suspected.

How can kidney injury from Ziv-aflibercept be prevented?

Aggressive blood pressure control before and during therapy

Who is at higher risk of kidney injury from Ziv-aflibercept?

Pre-existing hypertension; Diabetes or baseline proteinuria/CKD.

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Printable monograph

VEGF trap

Ziv-aflibercept

Zaltrap · Afli

VEGF trap · approved 2012 · 8 citations

Aging evidence· through 2022

Fairly sourced6/9 · 5 signals

Met: 8 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 14y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Not met: Current through 2022
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 soluble VEGF trap that, like bevacizumab, hits the glomerulus with hypertension, proteinuria and TMA.

ModerateVEGF trap (decoy receptor)

Metastatic colorectal cancer (with FOLFIRI)

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Signature kidney injury

Signature lesion

Hypertension

Representative incidence42.4%

Hypertension and proteinuria are common class effects; in the registrational VELOUR trial, grade 3-4 hypertension and proteinuria were more frequent with aflibercept plus FOLFIRI than with FOLFIRI alone. Nephrotic-range proteinuria and renal thrombotic microangiopathy are documented, including with the ophthalmic formulation, indicating a direct VEGF-trap mechanism. A meta-analysis of 15 trials (4,451 patients) put the summary all-grade hypertension incidence at 42.4%.Source: Qi et al., Clin Drug Investig 2014 (meta-analysis, all-grade hypertension 42.4%); Van Cutsem et al., VELOUR (J Clin Oncol 2012 / Target Oncol 2016)

Onset & rechallenge

Time to injurySubacute (~1–6 weeks)

Within weeks to a few months of therapy.

Distilled from: “Within weeks to a few months of therapy.”

Long-term outlook & thresholds

Renal recoveryUsually reversible

Hypertension, proteinuria and the renal-limited TMA typically improve after the drug is stopped; per label the drug is suspended for proteinuria >=2 g/24 h and resumed at lower dose once <2 g/24 h, and biopsy-proven aflibercept-associated TMA with nephrotic-range proteinuria has completely resolved months after discontinuation.PMID 36309669 (opens PubMed in a new tab)

Early-detection biomarkers

Urine protein-to-creatinine ratio / albuminuria (UPCR, dipstick) — glomerular endothelial and podocyte injury from VEGF-A/PlGF sequestration — the earliest and most sensitive renal signal, preceding any creatinine rise and driving label-mandated dose suspension. The dose-hold schedule is the ziv-aflibercept label's, not this paper's: dipstick and/or UPCR during therapy, a 24-h collection when the dipstick is >=2+ or the UPCR is above 1, and suspension at >=2 g/24 h. What the cited case adds is why the test is worth doing — a 55-year-old with 20-year type 2 diabetes on intravitreal aflibercept (2 mg every 4 weeks for diabetic macular edema) presented 14 months after the first injection with hypertension, leg edema and nephrotic-range proteinuria, and the nephrotic syndrome resolved six months after stopping the drug alone. Read it with its two limits: the biopsy showed diabetic nephropathy WITH a renal thrombotic microangiopathy the authors could only call probably drug-associated, and it is one patient at ocular dosing. It is evidence that proteinuria is the presenting sign of VEGF-trap glomerular injury even at ophthalmic exposure, not a validated oncology monitoring interval.PMID 36309669 (opens PubMed in a new tab)
Microangiopathic hemolysis panel — serum LDH, haptoglobin, platelet count, peripheral-smear schistocytes — renal-limited thrombotic microangiopathy, the lesion specifically associated with direct VEGF-A ligand traps (aflibercept/bevacizumab) rather than the MCD/FSGS pattern of receptor-blocking TKIs. Class-specific: VEGF trap / anti-VEGF antibody produces renal-specific TMA, so a falling platelet count with rising LDH, low haptoglobin and schistocytes signals evolving microangiopathy warranting drug discontinuation.PMID 30642877 (opens PubMed in a new tab)

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

Recovery across agents

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Renal toxicities, ranked

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

Hypertension#1 · Signature44.2%PMID 37657052 (opens PubMed in a new tab)
All-grade hypertension 44.2% (95% CI 39.7-48.7), grade III/IV 22.6%, in a meta-analysis of aflibercept plus chemotherapy for metastatic colorectal cancer (2,889 pts, 10 studies); RR 6.30 vs control.
Glomerular Injury / ProteinuriaSecondary31.3%PMID 37657052 (opens PubMed in a new tab)
All-grade proteinuria 31.3% (95% CI 19.3-43.3), grade III/IV 7.4% (VEGF-trap podocyte injury), from the same aflibercept mCRC meta-analysis.
Thrombotic MicroangiopathyRarequalitative — no citable incidence
Endothelial injury with microvascular thrombi, hemolysis and thrombocytopenia — gemcitabine, mitomycin C, anti-VEGF.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

42.4%incidence

SeverityModerate

ReversibilityReversible

Evidence8 citations

Nephron map

GlomerulusFiltration barrier (podocytes + endothelium)

Vasculature / EndotheliumGlomerular & peritubular capillaries

Hypertension

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.

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Kidney injury

Deep diveVEGF-inhibitor thrombotic microangiopathyStarve a tumor of its blood supply and you also cut the survival signal podocytes whisper to the glomerular endothelium next door — the capillary tuft answers with thrombi, protein spilling into the urine, and a blood pressure that will not come down.

Mechanism of kidney injury

Sequestration of circulating VEGF-A (and PlGF) removes the endothelial survival and permeability signaling that maintains fenestrated glomerular endothelium, causing endothelial injury, loss of fenestrae, podocyte stress and proteinuria, reduced nitric-oxide-dependent vasodilation (hypertension), and renal-limited thrombotic microangiopathy. Because aflibercept binds the ligand itself (like bevacizumab), it produces a TMA-predominant lesion rather than the MCD/FSGS pattern more typical of receptor-blocking TKIs.

Clinical presentation

Hypertension with new proteinuria, sometimes nephrotic-range with edema; biopsy shows TMA (glomerular endotheliosis, capillary-wall double contours, mesangiolysis, intracapillary foam cells) and foot-process effacement.

Management

Antihypertensive therapy (ACE inhibitor/ARB favored); per label, suspend for urine protein >=2 g/24 h and resume at a lower dose when <2 g/24 h, and discontinue for nephrotic syndrome or any TMA. Renal abnormalities typically improve after drug discontinuation.Lesion-level management framework

Risk factors

Pre-existing hypertension
Diabetes or baseline proteinuria/CKD

Prevention

Aggressive blood pressure control before and during therapy

Anticancer mechanism· how it treats cancer

Recombinant fusion protein combining the second Ig domain of VEGFR1 and the third Ig domain of VEGFR2 fused to the Fc of human IgG1, acting as a high-affinity soluble decoy that binds and sequesters VEGF-A, VEGF-B and placental growth factor (PlGF), blocking their interaction with native receptors and inhibiting angiogenesis. Used with FOLFIRI in metastatic colorectal cancer previously treated with an oxaliplatin regimen.

Note · Direct VEGF-A sequestration (like bevacizumab) predisposes to renal-limited TMA more than to glomerulopathy alone. The 'ziv-' prefix distinguishes the oncology formulation from intravitreal aflibercept, but the renal mechanism is identical.

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Clinical depth

Renal dose adjustment

No pharmacokinetic renal dose adjustment for a fusion-protein decoy; dose modification is driven by proteinuria thresholds and hypertension grade. Renal impairment does not alter clearance of the Fc-fusion molecule.

Dialyzability & ESKD dosing

Not dialyzable — a ~115 kDa Fc-fusion protein is not removed by hemodialysis or peritoneal dialysis; no dose change for dialysis patients.

Differential diagnosis

Ligand-trap (aflibercept/bevacizumab) renal injury skews toward TMA/endotheliosis on biopsy, contrasting with the MCD/FSGS pattern of VEGFR-TKIs; distinguish also from prerenal AKI and from chemotherapy (oxaliplatin/5-FU) effects within the FOLFIRI backbone.

Monitoring

Blood pressure every 2 weeks or with each cycle
Urine dipstick and/or UPCR during therapy (in practice, before each dose); 24-h collection if dipstick >=2+ or UPCR >1
Serum creatinine; CBC/LDH/haptoglobin and smear if TMA suspected

Key trials & series

VELOUR phase III trial of aflibercept + FOLFIRI in second-line metastatic colorectal cancer (carrying the hypertension/proteinuria signal)
Kikuchi et al. biopsy-proven aflibercept-associated renal TMA case (BMC Nephrol 2022)

Clinical pearls

As a VEGF ligand trap, aflibercept causes a TMA-type glomerular lesion, mirroring bevacizumab and the Eremina knockout model.
Even intravitreal aflibercept has caused renal TMA, underscoring how little systemic VEGF blockade the glomerulus tolerates.

Beyond the kidney — non-renal toxicities· 4 organ systems

Class-level context for the major non-renal toxicities of the VEGF trap 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

7 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

7 references · 2008–2022 · 2 since 2020

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.

CaseB · ModerateNephrotic Syndrome with Focal Segmental Glomerulosclerosis Induced by Intravitreal Injections of Vascular Endothelial Growth Factor Inhibitor.Kakeshita K et al. · Intern Med 2020 · PMID 32727981Biopsy-proven focal segmental glomerulosclerosis and nephrotic syndrome induced by aflibercept, improving after the drug was stopped.

FDA label — boxed warning & renal dosing· renal impairment

Quoted verbatim from this agent's current FDA label (Oct 2025) — not paraphrased or interpreted. Full label on DailyMed .

Renal impairment — from the label

No dosage modification is recommended for patients with renal impairment [see Clinical Pharmacology (12.3) ] .

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 32,367 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

Glomerular Injury / Proteinuriacorroborated · ROR 4.59 — on the terms that name the lesion (ROR 2.74)
Hypertensioncorroborated · ROR 1.29 — on the terms that name the lesion (ROR 1.72)
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 / Proteinuria

ROR 4.5995% CI 4.00–5.27· 204 reports

Hypertension

ROR 1.2995% CI 1.20–1.39· 765 reports

FAERS outcomes & reporting trend· 28.1% of reports w/ death · 14.1% w/ hospitalization

28.1%

Reported with a death outcome

9,088 of 32,367 reports

14.1%

Reported with hospitalization

4,568 of 32,367 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 4 systems · 32,367 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 0.5195% CI 0.42–0.61· 120 AKI reports ·AKI is reported less often than for other drugs (CI entirely below 1) — no disproportionate signal.

Eye

Visual Impairment2,119Blindness1,494Endophthalmitis1,420Visual Acuity Reduced1,295Eye Pain1,239

Vascular

Eye Haemorrhage820Retinal Haemorrhage605Hypertension527

Gastrointestinal

Diarrhoea641

Nervous system

Headache475

Guidelines & consensus· 17

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.

KDIGOManagement of Blood Pressure in Patients With Chronic Kidney Disease Not Receiving Dialysis: Synopsis of the 2021 KDIGO Clinical Practice GuidelineAnn Intern Med 2021 · PMID 34152826Recommends standardized office BP measurement and a target systolic BP <120 mm Hg for most CKD patients, with RAAS inhibitors first-line when albuminuria is present — the BP-management basis for anti-VEGF/TKI-induced hypertension and proteinuria.ESC2022 ESC Guidelines on cardio-oncology developed in collaboration with the European Hematology Association (EHA), the European Society for Therapeutic Radiology and Oncology (ESTRO) and the International Cardio-Oncology Society (IC-OS)Eur Heart J 2022 · PMID 36017568For VEGF/VEGFR inhibitors, perform baseline cardiovascular risk assessment, monitor blood pressure (weekly during the first cycle, then regularly) and treat to a target <140/90 mmHg with ACE inhibitors/ARBs and dihydropyridine calcium-channel blockers; manage VEGFi-associated hypertension and proteinuria with interruption/dose modification when severe.ESCEuropean Society of Cardiology quality indicators for the prevention and management of cancer therapy-related cardiovascular toxicity in cancer treatmentEur Heart J Qual Care Clin Outcomes 2022 · PMID 36316010Adherence quality indicators require documented baseline cardiovascular risk assessment and structured monitoring of cardiovascular complications (including hypertension) during cancer therapy such as VEGF-pathway inhibitors.UK Consensus PanelUsing bevacizumab to treat metastatic cancer: UK consensus guidelinesBr J Hosp Med (Lond) 2010 · PMID 21135762Assess and monitor blood pressure and proteinuria during bevacizumab therapy; treat emergent hypertension to standard targets and interrupt/discontinue the drug for uncontrolled hypertension, nephrotic-range proteinuria or other severe vascular toxicity.

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 Ziv-aflibercept 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

Bevacizumab

Avastin · Anti-VEGF antibody

Profile

Proteinuria, hypertension, glomerular TMA.

GLOMHTNTMA

Moderate#1 · 100% phenotype match

Ramucirumab

Cyramza · Anti-VEGFR2 antibody

Profile

Hypertension and proteinuria, class effect.

HTNGLOMTMA

Moderate#2 · 100% phenotype match

VEGFR TKIs (sunitinib · sorafenib · pazopanib · axitinib)

VEGFR TKI

Profile

Hypertension as an on-target marker; proteinuria.

HTNGLOMTMA

Moderate#3 · 100% phenotype match

Pazopanib

Votrient · VEGFR TKI

Profile

VEGFR-TKI; hypertension, proteinuria, TMA.

GLOMHTNTMA

Moderate#4 · 98% phenotype match

Axitinib

Inlyta · VEGFR TKI

Profile

Potent VEGFR-TKI; hypertension and proteinuria dominate.

HTNGLOMTMA

Moderate#5 · 98% phenotype match

Nintedanib

Ofev · VEGFR/FGFR/PDGFR TKI

Profile

Proteinuria and rare TMA.

HTNTMAGLOM

Mild#6 · 95% phenotype match

Compare Ziv-aflibercept 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 Anti-angiogenic (VEGF)

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.