Is kidney injury from Bevacizumab reversible?

Reversible. Typical onset: Weeks to months; dose-dependent..

How should kidney function be monitored during Bevacizumab therapy?

Quantify proteinuria with urine dipstick before each cycle; if >=2+, confirm with a urine protein-to-creatinine ratio (UPCR) or 24-hour collection and hold dosing for proteinuria >=2 g/24 h.; Measure blood pressure before every infusion and intermittently at home; treat new or worsening hypertension promptly (ACE inhibitor/ARB preferred given concurrent proteinuria).; Track serum creatinine/eGFR each cycle, but recognize that early VEGF-inhibitor injury is often proteinuric with preserved GFR rather than a creatinine rise.; Evaluate for TMA (schistocytes on smear, falling platelets, rising LDH, low haptoglobin, worsening anemia) when proteinuria escalates abruptly or hypertension becomes refractory.; Consider nephrology referral and kidney biopsy for nephrotic-range proteinuria, AKI, or suspected TMA to guide whether to permanently discontinue..

How can kidney injury from Bevacizumab be prevented?

Proactive hypertension treatment

Who is at higher risk of kidney injury from Bevacizumab?

Higher dose; Pre-existing hypertension / CKD; Renal cell carcinoma.

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Printable monograph

Anti-VEGF antibody

Bevacizumab

Avastin · Bev

Anti-VEGF antibody · approved 2004 · 9 citations · FAERS AKI reporting ROR 1.23 (95% CI 1.16–1.30, 1,143 AKI reports)

Dated evidence· through 2019

Deeply sourced7/9 · 6 signals

Met: 9 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 11y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Not met: Current through 2019
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.

The proof that podocytes need VEGF — block it and the filter leaks.

ModerateAnti-VEGF monoclonal antibody

ColorectalLungRenalOvarianGlioblastoma

§01

Signature kidney injury

Signature lesion

Glomerular Injury / Proteinuria

Representative incidence18%

11.7–26.6% 95% CI

In a 72-trial meta-analysis (21,902 bevacizumab cases vs 20,608 controls), all-grade proteinuria was 18% (95% CI 11.7–26.6%) and high-grade 2.4% (1.8–3.2%); all-grade hypertension was 25.3% (21.5–29.5%). Relative to controls the risk ratios were 3.37 for all-grade and 5.49 for high-grade proteinuria. A separate 16-trial meta-analysis put high-grade proteinuria at 2.2% and nephrotic syndrome at RR 7.78, with renal cell carcinoma carrying the highest cumulative incidence (10.2%).Source: Zhao et al., Oncotarget 2017 (PMID 28881662); Wu et al., JASN 2010 (PMID 20538785)

Onset & rechallenge

Time to injurySubacute (~1–6 weeks)

Develops over weeks to months and is dose-dependent.

Distilled from: “Weeks to months; dose-dependent.”

Long-term outlook & thresholds

Renal recoveryUsually reversible

Proteinuria and hypertension are usually reversible once bevacizumab is held or stopped; thrombotic microangiopathy and nephrotic-range proteinuria can persist and warrant permanent discontinuation.PMID 27154025 (opens PubMed in a new tab)

Early-detection biomarkers

Urinary albumin-to-creatinine ratio (UACR) — Glomerular filtration-barrier injury (podocyte/endothelial dysfunction from VEGF-A withdrawal). In bevacizumab-treated cancer patients, albuminuria (UACR) marks ongoing glomerular injury and correlates tightly with the cumulative bevacizumab dose (r=0.77, p<0.001), whereas urinary podocyte-marker (nephrin/podocin mRNA) podocyturia did not correlate — favoring albuminuria over podocyturia for monitoring the preeclampsia-like renal toxicity. Typically rises before any creatinine change.PMID 29960864 (opens PubMed in a new tab)
Urine protein-to-creatinine ratio (UPCR) — Quantitative glomerular proteinuria — the graded, dose-limiting anti-VEGF renal signal. UPCR is the standard way anti-VEGF proteinuria is graded, but the cited study argues against reflexive per-cycle testing: across 89 gynecologic-oncology patients (mean 13 bevacizumab cycles) any-grade proteinuria reached 35%, yet 70% was grade 1 and only 2% grade 3, and no patient or disease factor was significantly associated with developing it. Its authors concluded that monitoring UPCR with every cycle may be unnecessary given the low grade-3 prevalence, and that UPCR may not adequately assess bevacizumab proteinuria toxicity — so treat a rising UPCR as a reason to look, not a threshold that has been validated against outcomes.PMID 26447100 (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

§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.

Glomerular Injury / Proteinuria#1 · Signature2.2%PMID 20538785 (opens PubMed in a new tab)
High-grade (grade 3-4) proteinuria 2.2% (95% CI 1.2-4.3) in a 12,268-patient meta-analysis; all-grade proteinuria far more common and dose-dependent, highest in renal-cell carcinoma (cumulative incidence 10.2%). VEGF blockade injures podocytes.
HypertensionSecondary23.6%PMID 20186127 (opens PubMed in a new tab)
All-grade hypertension 23.6% (95% CI 20.5-27.1), high-grade 7.9% (95% CI 6.1-10.2) across 12,656 patients; RR 5.28 for high-grade vs control.
Thrombotic MicroangiopathyRareno population incidence denominator
Case-level: renal thrombotic microangiopathy described in a 6-patient series with corroborating podocyte-VEGF-knockout mouse model; no cohort incidence rate established. PMID 18337603 (opens PubMed in a new tab)

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

18%incidence

SeverityModerate

ReversibilityReversible

Evidence9 citations

Nephron map

GlomerulusFiltration barrier (podocytes + endothelium)

Vasculature / Endothelium

Glomerular Injury / Proteinuria

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

§03

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.Appears in 2 documented synergy combinations

Mechanism of kidney injury

Podocytes secrete the VEGF that maintains glomerular endothelial fenestrae. Blocking it causes glomerular endotheliosis, podocyte injury, proteinuria and TMA — proven in podocyte-specific VEGF-knockout mice. Reduced endothelial nitric oxide drives the hypertension.

Clinical presentation

New or worsening hypertension, proteinuria (dipstick to nephrotic range), occasionally microangiopathic hemolysis and a rising creatinine.

Management

Antihypertensives (ACEi/ARB preferred — they also lower proteinuria), hold for nephrotic-range proteinuria or severe hypertension, discontinue for TMA.Lesion-level management framework

Risk factors

Higher dose
Pre-existing hypertension / CKD
Renal cell carcinoma

Prevention

Proactive hypertension treatment

Anticancer mechanism· how it treats cancer

Monoclonal antibody that binds and neutralizes circulating VEGF-A, starving tumor angiogenesis. Colorectal, lung, renal, ovarian and glioblastoma.

§04

Clinical depth

Renal dose adjustment

No renal dose adjustment is defined by the FDA label, as bevacizumab is a monoclonal antibody cleared by proteolytic catabolism rather than renal excretion, and pharmacokinetics are not meaningfully altered in renal impairment. Management is toxicity-driven, not level-driven: per label, interrupt for moderate-to-severe proteinuria pending resolution to <2 g/24 h, and discontinue permanently for nephrotic syndrome, biopsy-proven thrombotic microangiopathy, or hypertensive crisis.

Dialyzability & ESKD dosing

As a ~149 kDa IgG1 monoclonal antibody, bevacizumab is not removed by conventional or high-flux hemodialysis; HD does not mitigate its renal vascular toxicity. There are no special dosing recommendations for patients on dialysis, and clinical experience in ESKD/HD is limited to small reports.

Differential diagnosis

Distinguish drug-induced injury from pre-existing diabetic/hypertensive nephropathy and from cancer-associated (paraneoplastic) membranous nephropathy by the temporal link to bevacizumab and the characteristic VEGF-inhibitor signature: new proteinuria plus hypertension, with biopsy showing glomerular endotheliosis/TMA (endothelial swelling, loss of fenestrae, double contours) rather than immune-complex deposits. Unlike classic complement-mediated or shiga-toxin TMA, this is a localized, often renal-limited TMA driven by podocyte VEGF withdrawal that typically improves on drug cessation.

Monitoring

Quantify proteinuria with urine dipstick before each cycle; if >=2+, confirm with a urine protein-to-creatinine ratio (UPCR) or 24-hour collection and hold dosing for proteinuria >=2 g/24 h.
Measure blood pressure before every infusion and intermittently at home; treat new or worsening hypertension promptly (ACE inhibitor/ARB preferred given concurrent proteinuria).
Track serum creatinine/eGFR each cycle, but recognize that early VEGF-inhibitor injury is often proteinuric with preserved GFR rather than a creatinine rise.
Evaluate for TMA (schistocytes on smear, falling platelets, rising LDH, low haptoglobin, worsening anemia) when proteinuria escalates abruptly or hypertension becomes refractory.
Consider nephrology referral and kidney biopsy for nephrotic-range proteinuria, AKI, or suspected TMA to guide whether to permanently discontinue.

Key trials & series

Eremina et al. NEJM 2008 — mechanistic case series plus podocyte-specific Vegfa-knockout mouse model establishing that VEGF blockade causes a glomerular thrombotic microangiopathy with proteinuria, the foundational lesion for this class.
AVF2107g (Hurwitz, NEJM 2004) — pivotal metastatic colorectal cancer trial adding bevacizumab to IFL, which documented increased grade 3+ hypertension and proteinuria as on-target class toxicities.
AVOREN (Escudier, Lancet 2007) — bevacizumab plus interferon in metastatic RCC, reporting higher rates of proteinuria and hypertension than interferon alone.
Wu et al. Am J Kidney Dis 2010 — meta-analysis of randomized trials quantifying a significantly increased relative risk of proteinuria and high-grade proteinuria with bevacizumab across tumor types.

Clinical pearls

The injury is mechanism-based and on-target: bevacizumab sequesters circulating VEGF-A that podocytes secrete to maintain glomerular endothelial fenestrae, producing endotheliosis and a renal-limited TMA.
Proteinuria and hypertension are the dominant, dose- and exposure-related signals; severe proteinuria or refractory hypertension should prompt suspicion of underlying TMA.
Most proteinuria and hypertension are reversible after holding or stopping the drug, but TMA and nephrotic syndrome can persist and warrant permanent discontinuation.
ACE inhibitors/ARBs are the antihypertensives of choice because they simultaneously address the renin-angiotensin-driven hypertension and reduce proteinuria.
This is a class effect shared with other anti-VEGF/VEGFR agents (e.g., ramucirumab, aflibercept, VEGFR-TKIs), so prior anti-angiogenic exposure raises baseline risk.

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

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

§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 · 2008–2019 · 3 since 2017

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 after switching from bevacizumab to ramucirumab: a case report.Yamada R et al. · BMC Nephrol 2019 · PMID 30634936Biopsy-proven renal-limited thrombotic microangiopathy with nephrotic-range proteinuria developing after multiple courses of bevacizumab (then ramucirumab), illustrating VEGF-inhibitor glomerular injury.CaseC · LimitedBevacizumab-induced thrombotic microangiopathy and nephrotic syndrome.Shimamura Y et al. · Clin Exp Nephrol 2019 · PMID 29882112Case of bevacizumab-induced glomerular thrombotic microangiopathy presenting as nephrotic syndrome, the drug's signature proteinuric glomerular injury.CaseC · LimitedA severe case of bevacizumab-induced thrombotic microangiopathy.Bektas M et al. · J Oncol Pharm Pract 2019 · PMID 30253727Dose-dependent bevacizumab-induced thrombotic microangiopathy with thrombocytopenia and renal involvement, a glomerular toxicity of anti-VEGF therapy.

Conference abstracts & journal reports· 1 non-PubMed

Non-PubMed sources — conference abstracts (e.g. ASN Kidney Week, badged Abstract) and case reports from non-indexed field journals (e.g. Journal of Onco-Nephrology, badged Journal). Included for completeness; weigh below peer-reviewed PubMed citations.

AbstractBevacizumab-Associated Thrombotic Microangiopathy Treated with EculizumabASN Kidney Week 2019 2019 · Abstract TH-PO152Biopsy-proven chronic renal TMA from the anti-VEGF antibody bevacizumab, recurring on rechallenge, with hemolysis and hypertension and partial renal recovery on eculizumab — illustrating complement involvement in VEGF-blockade TMA.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 128,714 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· 8 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 23.28 — on the terms that name the lesion (ROR 7.34)
Thrombotic Microangiopathycorroborated · ROR 6.79
Hypertensioncorroborated · ROR 3.59 — on the terms that name the lesion (ROR 4.95)

Glomerular Injury / Proteinuria

ROR 23.2895% CI 22.47–24.12· 3,567 reports

Thrombotic Microangiopathy

ROR 6.7995% CI 6.26–7.36· 620 reports

Hypertension

ROR 3.5995% CI 3.51–3.67· 7,992 reports

Electrolyte Disturbance

ROR 2.4595% CI 2.36–2.54· 2,813 reports

SIADH / Hyponatremia

ROR 2.3695% CI 2.22–2.50· 1,149 reports

Hemorrhagic Cystitis

ROR 1.7095% CI 1.58–1.83· 720 reports

Crystal / Obstructive Nephropathy

ROR 1.3495% CI 1.22–1.47· 457 reports

Acute Interstitial Nephritis

ROR 1.2195% CI 1.02–1.43· 139 reports

FAERS outcomes & reporting trend· 22.2% of reports w/ death · 31.6% w/ hospitalization

22.2%

Reported with a death outcome

28,567 of 128,714 reports

31.6%

Reported with hospitalization

40,636 of 128,714 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 9 systems · 128,714 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 1.2395% CI 1.16–1.30· 1,143 AKI reports ·AKI is reported disproportionately more often than for other drugs (CI entirely above 1) — a hypothesis-generating signal, not proof of causation.

Renal & urinary

Proteinuria3,141

Gastrointestinal

Diarrhoea7,478Nausea6,674Vomiting5,061Abdominal Pain2,946Constipation2,397

General / constitutional

Fatigue6,642Pyrexia4,144Asthenia3,697Pain2,374

Blood & lymphatic

Anaemia4,471Neutropenia4,104Thrombocytopenia3,442Platelet Count Decreased2,402

Vascular

Hypertension6,109Epistaxis2,200

Nervous system

Neuropathy Peripheral3,039Headache2,430

Metabolic & electrolyte

Decreased Appetite3,533

Respiratory

Dyspnoea3,496

Skin

Rash2,398

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 Bevacizumab 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

Ziv-aflibercept

Zaltrap · VEGF trap

Profile

Hypertension and proteinuria like bevacizumab.

HTNGLOMTMA

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 Bevacizumab 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.

Who studies this

The leading contributors to Bevacizumab’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 Bevacizumab; the PMIDs beside each name are up to three of their most recent papers on it, not the full count.

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 239 clinical records among the 300 most-relevant of 793 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.