Is kidney injury from Ramucirumab reversible?

Reversible. Typical onset: Within the first one to two cycles (weeks)..

How should kidney function be monitored during Ramucirumab therapy?

Blood pressure every 2 weeks or with each infusion; Urine protein (dipstick/UPCR) before dosing; quantify with 24-h collection if >=2+; Serum creatinine periodically; CBC/LDH if TMA suspected.

How can kidney injury from Ramucirumab be prevented?

Optimize blood pressure control before and during therapy

Who is at higher risk of kidney injury from Ramucirumab?

Pre-existing hypertension; Pre-existing chronic kidney disease or proteinuria; Diabetes.

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Printable monograph

Anti-VEGFR2 antibody

Ramucirumab

Cyramza · Ramu

Anti-VEGFR2 antibody · approved 2014 · 11 citations

Up to date· through 2025

Deeply sourced7/9 · 6 signals

Met: 11 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 17y)
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.

A VEGFR2-blocking antibody that strips the glomerular endothelium of VEGF, driving hypertension and proteinuria.

ModerateAnti-VEGFR2 monoclonal antibody

Gastric / gastroesophageal junction adenocarcinomaMetastatic colorectal cancerNon-small-cell lung cancerHepatocellular carcinoma

§01

Signature kidney injury

Signature lesion

Hypertension

Representative incidence22%

Hypertension and proteinuria are common class effects; nephrotic syndrome is a less frequent but reported event, sometimes after only 1-2 doses and typically accompanied by hypertension.Source: Muro et al., J Gastroenterol Hepatol 2016 (RAINBOW East Asian subgroup, all-grade hypertension 22%); Fujii et al., Medicine (Baltimore) 2019

Onset & rechallenge

Time to injurySubacute (~1–6 weeks)

Within the first one to two cycles (weeks).

Distilled from: “Within the first one to two cycles (weeks).”

Long-term outlook & thresholds

Renal recoveryUsually reversible

Proteinuria and hypertension generally improve after dose interruption or withdrawal; a renal-limited thrombotic microangiopathy, when it occurs, warrants permanent discontinuation rather than resolving on rechallenge.PMID 31277139 (opens PubMed in a new tab)

Early-detection biomarkers

Urine protein-to-creatinine ratio (proteinuria) — Glomerular endothelial/podocyte VEGF-axis disruption (endotheliosis, slit-diaphragm injury). The cited source is a CLASS review of VEGF-pathway inhibitors that predates ramucirumab's 2014 approval, so it carries no ramucirumab-specific rule: what it states is that blood pressure and proteinuria (by dipstick) be assessed in every patient before starting anti-VEGF therapy and monitored throughout, that severe proteinuria or impaired renal function warrants nephrology referral, and that progression may require tapering or withdrawal. It gives no numeric dipstick trigger, no 24-h quantification rule and no interruption threshold — for those, read the agent's own label rather than this row.PMID 23537524 (opens PubMed in a new tab)
Serum LDH with peripheral schistocytes and haptoglobin — Renal-limited thrombotic microangiopathy (microangiopathic hemolysis). Rising LDH, falling haptoglobin, schistocytes and thrombocytopenia flag anti-VEGF TMA; monitoring calls for CBC/LDH if TMA is suspected, and confirmed TMA mandates permanent 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

§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.

Hypertension#1 · Signature20%PMID 25697774 (opens PubMed in a new tab)
All-grade hypertension ~20.0% (high-grade ~8.6%) in meta-analysis of 11 studies, n=3,851; RR 2.77 vs control
Glomerular Injury / ProteinuriaSecondaryno population incidence denominator
Proteinuria significantly increased vs control (all-grade RR 3.31, high-grade RR 5.28); grade >=3 proteinuria ~0.6% non-East-Asian and higher (~3.9%) in East Asian patients PMID 26302785 (opens PubMed in a new tab)
Thrombotic MicroangiopathyRareno population incidence denominator
Renal-limited thrombotic microangiopathy with podocytopathy / nephrotic syndrome reported only at the case level PMID 39289295 (opens PubMed in a new tab)

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

22%incidence

SeverityModerate

ReversibilityReversible

Evidence11 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.

§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.

Mechanism of kidney injury

Blockade of VEGFR2 on glomerular endothelium and podocyte-derived VEGF signaling disrupts the constitutive paracrine podocyte-to-endothelium VEGF axis required to maintain fenestrated glomerular endothelium and the slit diaphragm. The result is endothelial swelling (endotheliosis), loss of fenestrae, reduced nitric-oxide-mediated vasodilation (hypertension), proteinuria, and — in severe cases — a renal-limited thrombotic microangiopathy with fibrin thrombi. The mechanism parallels the podocyte-specific VEGF-knockout phenotype demonstrated experimentally.

Clinical presentation

New or worsening hypertension and proteinuria; nephrotic-range proteinuria with edema and sometimes a creatinine rise. Biopsy, when performed, shows glomerular endotheliosis/TMA (double contours, mesangiolysis) with variable foot-process effacement.

Management

Control hypertension (ACE inhibitor/ARB preferred to also reduce proteinuria); per label, interrupt for urine protein >=2 g/24 h and reduce the dose on resumption, and permanently discontinue for urine protein >3 g/24 h, nephrotic syndrome, or any TMA. Proteinuria and hypertension generally improve after dose interruption or withdrawal.Lesion-level management framework

Risk factors

Pre-existing hypertension
Pre-existing chronic kidney disease or proteinuria
Diabetes

Prevention

Optimize blood pressure control before and during therapy

Anticancer mechanism· how it treats cancer

Fully human IgG1 monoclonal antibody that binds the extracellular domain of VEGF receptor 2 (VEGFR2/KDR), blocking ligand binding by VEGF-A, VEGF-C and VEGF-D and inhibiting receptor activation, downstream signaling and tumor angiogenesis. Used in gastric/GEJ, colorectal, hepatocellular and non-small-cell lung cancers.

Note · Renal effects are a shared VEGF-pathway class effect; reversibility with early discontinuation is well described, but TMA can occur and warrants permanent discontinuation.

§04

Clinical depth

Renal dose adjustment

No pharmacokinetic renal dose adjustment is required for a monoclonal antibody, but dosing is modified by toxicity: interrupt/reduce for grade 3 hypertension until controlled and for proteinuria thresholds above. Renal impairment does not alter antibody clearance.

Dialyzability & ESKD dosing

Not dialyzable — a ~147 kDa IgG1 monoclonal antibody is not removed by hemodialysis or peritoneal dialysis; no dose change is needed for dialysis patients.

Differential diagnosis

Anti-VEGF glomerular injury (hypertension + proteinuria + endotheliosis/TMA on biopsy) versus prerenal AKI, versus minimal change/FSGS seen more with VEGFR-TKIs, versus a paraneoplastic membranous nephropathy. The temporal link to dosing and accompanying hypertension favor the drug; biopsy confirms TMA.

Monitoring

Blood pressure every 2 weeks or with each infusion
Urine protein (dipstick/UPCR) before dosing; quantify with 24-h collection if >=2+
Serum creatinine periodically; CBC/LDH if TMA suspected

Key trials & series

REGARD (gastric, Lancet 2014) and RAINBOW (gastric + paclitaxel, Lancet Oncol 2014) — registrational trials reporting hypertension/proteinuria
RAINBOW East Asian subgroup (Muro, J Gastroenterol Hepatol 2016) — all-grade hypertension 22%, proteinuria 27%
Fujii et al. single-center nephrotic-syndrome case series (Medicine 2019)

Clinical pearls

Anti-VEGF antibodies favor a TMA/endotheliosis pattern, whereas oral VEGFR-TKIs more often cause MCD/FSGS — the biopsy pattern hints at the culprit class.
Use an ACE inhibitor or ARB to treat both the hypertension and the proteinuria.
Permanently stop for nephrotic syndrome or TMA; lesser proteinuria can be managed by interruption and dose reduction.

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

Class-level context for the major non-renal toxicities of the Anti-VEGFR2 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

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 · 2008–2020 · 4 since 2018

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· 4

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 30634936Case report of biopsy-proven renal-limited thrombotic microangiopathy attributed to ramucirumab after switching from bevacizumab.CaseB · ModerateA case of ramucirumab-induced renal failure with nephrotic-range proteinuria and its pathological findings.Nakano Y et al. · BMJ Case Rep 2021 · PMID 33653851Case report of ramucirumab-induced renal failure with nephrotic-range proteinuria, including renal biopsy pathology showing glomerular endothelial injury.CaseB · ModerateClinicopathological Study on Endothelial Injury in Severe Glomerular Microangiopathy Induced by Ramucirumab.Sakai M et al. · Intern Med 2025 · PMID 40603057Ramucirumab (anti-VEGFR2) caused nephrotic-range proteinuria with biopsy-proven hyaline occlusive glomerular microangiopathy, podocyte hyperplasia, and an unusual fibrocellular crescent; CD34 immunostaining documented severe kidney-specific endothelial injury.CaseB · ModerateGlomerular Microangiopathy with Cellular Crescent-like Formation and Endotheliopathy Due to Ramucirumab Treatment for Metastatic Sigmoid Colon Cancer.Yoshimura Y et al. · Intern Med 2022 · PMID 35569979Case report of ramucirumab-induced glomerular microangiopathy with cellular crescent-like formation and endotheliopathy on renal biopsy.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 6,218 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· 5 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 26.72 — on the terms that name the lesion (ROR 26.47)
Thrombotic Microangiopathycorroborated · ROR 9.23
Hypertensioncorroborated · ROR 2.13 — on the terms that name the lesion (ROR 3.04)

Glomerular Injury / Proteinuria

ROR 26.7295% CI 23.35–30.57· 221 reports

Thrombotic Microangiopathy

ROR 9.2395% CI 6.81–12.50· 42 reports

Hypertension

ROR 2.1395% CI 1.87–2.42· 238 reports

SIADH / Hyponatremia

ROR 1.9895% CI 1.48–2.63· 47 reports

Electrolyte Disturbance

ROR 1.5495% CI 1.25–1.91· 87 reports

FAERS outcomes & reporting trend· 26.6% of reports w/ death · 38.1% w/ hospitalization

26.6%

Reported with a death outcome

1,653 of 6,218 reports

38.1%

Reported with hospitalization

2,369 of 6,218 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 9 systems · 6,218 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 1.2995% CI 0.99–1.67· 58 AKI reports ·no disproportionate AKI reporting signal (CI spans 1).

Renal & urinary

Proteinuria140

Blood & lymphatic

Neutropenia263Febrile Neutropenia262Neutrophil Count Decreased179Anaemia159Platelet Count Decreased116

Gastrointestinal

Diarrhoea228Nausea206Vomiting136Abdominal Pain127

Respiratory

Interstitial Lung Disease299Dyspnoea133Pneumonitis99

General / constitutional

Fatigue200Pyrexia190Malaise127

Vascular

Hypertension192Epistaxis101

Metabolic & electrolyte

Decreased Appetite231

Nervous system

Neuropathy Peripheral173

Immune / infection

Pneumonia161

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 Ramucirumab 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

Bevacizumab

Avastin · Anti-VEGF antibody

Profile

Proteinuria, hypertension, glomerular TMA.

GLOMHTNTMA

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 Ramucirumab 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 Ramucirumab’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 Ramucirumab; 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 68 clinical records among all 83 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.