Is kidney injury from Nintedanib reversible?

Reversible. Typical onset: Over months of therapy in reported cases..

How should kidney function be monitored during Nintedanib therapy?

Blood pressure and urine protein periodically; Serum creatinine; CBC/LDH and smear if TMA suspected; Liver enzymes (the more common dose-limiting toxicity).

How can kidney injury from Nintedanib be prevented?

Dose reduction for emerging renal or other toxicity

Who is at higher risk of kidney injury from Nintedanib?

Higher dose / cumulative exposure; Pre-existing hypertension or CKD.

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Printable monograph

VEGFR/FGFR/PDGFR TKI

Nintedanib

Ofev · Ninte

VEGFR/FGFR/PDGFR TKI · approved 2014 · 9 citations

Up to date· through 2026

Deeply sourced7/9 · 6 signals

Met: 9 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 13y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Met: Current through 2026
Not met: Real-world FAERS signal

Describes how this page is sourced, not how dangerous the drug is. Thinly sourced means fewer of the sourcing signals are met — not that the agent is kidney-safe. A rule-based summary, not a formal certainty appraisal.

An antifibrotic VEGFR/FGFR/PDGFR TKI that can rarely cross into the kidney as proteinuria or thrombotic microangiopathy.

MildVEGFR/FGFR/PDGFR inhibitor

Non-small-cell lung cancer (adenocarcinoma, with docetaxel)Idiopathic pulmonary fibrosis (non-oncologic)

§01

Signature kidney injury

Signature lesion

Hypertension

Renal effects are uncommon; proteinuria and rare biopsy-proven renal thrombotic microangiopathy have been reported, consistent with VEGF-pathway inhibition. Renal incidence is not well quantified (case-level), and much of the published renal experience comes from pulmonary-fibrosis rather than oncology cohorts.Source: Fujita et al., Case Rep Nephrol Dial 2021 (TMA case)

Onset & rechallenge

Time to injuryDelayed (>6 weeks / cumulative)

Reported over months of therapy.

Distilled from: “Over months of therapy in reported cases.”

§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 · Signaturequalitative — 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.
Glomerular Injury / ProteinuriaSecondaryno population incidence denominator
VEGF-pathway proteinuria / glomerular microangiopathy; documented at case level, population incidence unknown PMID 32279192 (opens PubMed in a new tab)
Thrombotic MicroangiopathyRareno population incidence denominator
renal thrombotic microangiopathy in isolated case reports PMID 31699213 (opens PubMed in a new tab)

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

Incidence not quantified

SeverityMild

ReversibilityReversible

Evidence9 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

Mechanism of kidney injury

VEGFR inhibition reduces glomerular endothelial VEGF signaling, which can injure the fenestrated endothelium and filtration barrier, producing proteinuria/hypertension and, in rare reported cases, a dose-dependent and reversible renal thrombotic microangiopathy with microaneurysms, glomerular basement-membrane double contours and intracapillary foam cells. The added FGFR/PDGFR activity does not clearly amplify the renal lesion.

Clinical presentation

Proteinuria and reduced kidney function, sometimes with hypertension; biopsy in reported TMA cases shows microaneurysms filled with pale material, segmental GBM double contours and intracapillary foam cells. Diarrhea and hepatotoxicity are the more common general toxicities.

Management

Dose-reduce or discontinue for proteinuria/renal dysfunction; reported renal TMA improved after discontinuation (and partially with dose reduction). Control blood pressure (ACE inhibitor/ARB) and provide supportive care.Lesion-level management framework

§ Receptor target map

Which kinases Nintedanib blocks — and where the blockade reaches the kidney

6targeted

VEGFR2 is the target with documented renal consequences across every VEGFR TKI; multi-kinase breadth beyond it (PDGFR-β, FGFR, and off-target receptor kinases) adds further renal and hypertensive liability. Select a lit receptor for its renal consequence.

VEGFR family

PDGFR

Other receptor kinases

KITRETMETEGFRFLT3AXLCSF1RTIE2RAF-1/BRAF

VEGFR2 · renal target

Glomerular endothelial VEGFR2: loss of podocyte-derived paracrine VEGF signaling → fenestrae loss, nephrin downregulation, nitric-oxide depletion → hypertension, proteinuria, and thrombotic microangiopathy.

renal consequence (4)targetednot a target

Risk factors

Higher dose / cumulative exposure
Pre-existing hypertension or CKD

Prevention

Dose reduction for emerging renal or other toxicity

Anticancer mechanism· how it treats cancer

Oral intracellular inhibitor of VEGFR1-3, FGFR1-3 and PDGFR-alpha/beta (plus Src-family kinases). In oncology it is combined with docetaxel for non-small-cell lung adenocarcinoma; it is also widely used as an antifibrotic in idiopathic pulmonary fibrosis and other progressive fibrosing interstitial lung diseases.

Note · Renal toxicity is rare and case-level; the TMA signal reflects its VEGFR-inhibitor activity.

§04

Clinical depth

Renal dose adjustment

No dose adjustment for mild-to-moderate renal impairment; <1% is excreted renally and nintedanib is predominantly cleared by hydrolytic ester cleavage and biliary/fecal excretion. It has not been studied in severe renal impairment (CrCl < 30 mL/min). Dose reduction is driven by hepatotoxicity (transaminitis) more than by renal function.

Dialyzability & ESKD dosing

Highly protein-bound (~98%) with biliary/fecal elimination, so it is not meaningfully dialyzable; no supplemental dosing for HD. ESKD data are essentially absent.

Differential diagnosis

Nintedanib-associated renal TMA/proteinuria (biopsy microaneurysms, double contours) versus other anti-VEGF-pathway TMA, versus baseline hypertensive/diabetic nephropathy, and — in lung-cancer patients — versus concurrent cisplatin/other nephrotoxins or paraneoplastic glomerulopathy.

Monitoring

Blood pressure and urine protein periodically
Serum creatinine; CBC/LDH and smear if TMA suspected
Liver enzymes (the more common dose-limiting toxicity)

Key trials & series

LUME-Lung 1 phase III trial (docetaxel +/- nintedanib in previously treated NSCLC) — registrational oncology trial
INPULSIS trials (IPF) — large antifibrotic safety database from which much renal experience derives

Clinical pearls

Nintedanib is mostly an antifibrotic in practice, so its renal literature comes largely from IPF, not oncology — treat the renal evidence as thin and class-based.
Its dominant dose-limiting toxicity is hepatotoxicity, not nephrotoxicity; renal TMA is rare and reversible.
Negligible renal excretion means no renal dose adjustment, but it is also non-dialyzable.

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

Class-level context for the major non-renal toxicities of the VEGFR/FGFR/PDGFR TKI 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

5 primary references — trials, cohorts, mechanism, and reviews. Single-patient case reports are listed separately below, graded by strength. Citation metadata via PubMed / NLM.

Evidence accrual

5 references · 2013–2021 · 2 since 2019

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.

CaseA · StrongSlipping Through the Chasm of Multicenter Hand-offs-Rare Incidence of Nintedanib Induced Renal Failure: Case Report.Abid MM et al. · J Community Hosp Intern Med Perspect 2026 · PMID 41809227Nintedanib-induced dialysis-requiring AKI with biopsy-proven minimal change disease plus focal glomerulosclerosis; inadvertent rechallenge reproduced worse injury on repeat biopsy, giving strong positive-rechallenge causality.CaseB · ModerateNintedanib-induced glomerular microangiopathy: a case report.Hasegawa M et al. · CEN Case Rep 2020 · PMID 32279192A 68-year-old man developed proteinuria and leg edema after starting nintedanib, with kidney biopsy showing endothelial and mesangial injury (glomerular microangiopathy) that improved after withdrawal, consistent with VEGF-inhibitor renal endothelial toxicity.CaseB · ModerateRenal thrombotic microangiopathy during nintedanib treatment for idiopathic pulmonary fibrosis .Inoue D et al. · Clin Nephrol 2020 · PMID 31699213A 45-year-old man developed isolated proteinuria with biopsy-confirmed renal thrombotic microangiopathy attributed to nintedanib, resolving after drug cessation following lung transplant.CaseB · ModerateMicroscopic polyangiitis with histopathologic evolution in serial renal biopsies during treatment of idiopathic pulmonary fibrosis.Yamaguchi Y et al. · CEN Case Rep 2025 · PMID 40802046IPF patient on nintedanib developed MPO-ANCA microscopic polyangiitis; serial biopsies showed evolution from tubulointerstitial nephritis to pauci-immune crescentic glomerulonephritis. Dedicated nephrology case-report venue.

FDA label — boxed warning & renal dosing· renal impairment

Quoted verbatim from this agent's current FDA label (Aug 2026) — not paraphrased or interpreted. Full label on DailyMed .

Renal impairment — from the label

Based on a single-dose study, less than 1% of the total dose of nintedanib is excreted via the kidney [see Clinical Pharmacology ( 12.3 )]. Adjustment of the starting dose in patients with mild to moderate renal impairment is not required. The safety, efficacy, and pharmacokinetics of nintedanib have not been studied in patients with severe renal impairment (less than 30 mL/min CrCl) and end-stage renal disease. 8.8 Smokers Smoking was associated with decreased exposure to nintedanib capsules [see Clinical Pharmacology ( 12.3 )], which may alter the efficacy profile of nintedanib capsules. Encourage patients to stop smoking prior to treatment with nintedanib capsules and to avoid smoking when using nintedanib capsules.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 31,339 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· 4 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

Hypertensioncorroborated · ROR 1.88 — on the terms that name the lesion (ROR 1.92)
Glomerular Injury / Proteinuriacorroborated · ROR 1.66 — on the terms that name the lesion (ROR 2.44)
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.

Hypertension

ROR 1.8895% CI 1.77–2.00· 1,067 reports

Glomerular Injury / Proteinuria

ROR 1.6695% CI 1.32–2.09· 72 reports

Hemorrhagic Cystitis

ROR 1.6295% CI 1.39–1.88· 167 reports

Crystal / Obstructive Nephropathy

ROR 1.4795% CI 1.23–1.75· 122 reports

FAERS outcomes & reporting trend· 19.8% of reports w/ death · 33.7% w/ hospitalization

19.8%

Reported with a death outcome

6,218 of 31,339 reports

33.7%

Reported with hospitalization

10,549 of 31,339 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 7 systems · 31,339 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 0.8295% CI 0.71–0.95· 187 AKI reports ·AKI is reported less often than for other drugs (CI entirely below 1) — no disproportionate signal.

Gastrointestinal

Diarrhoea10,159Nausea4,716Vomiting2,769Constipation2,027Abdominal Pain Upper1,884

Respiratory

Dyspnoea4,046Cough3,269Idiopathic Pulmonary Fibrosis2,117Productive Cough1,267Oxygen Saturation Decreased1,131

General / constitutional

Weight Decreased3,048Fatigue2,969Asthenia1,722Malaise1,123Fall848

Nervous system

Headache2,034Dizziness1,565

Metabolic & electrolyte

Decreased Appetite3,098

Immune / infection

Pneumonia1,488Covid-19747

Vascular

Epistaxis754

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 Nintedanib 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 · 95% phenotype match

Bevacizumab

Avastin · Anti-VEGF antibody

Profile

Proteinuria, hypertension, glomerular TMA.

GLOMHTNTMA

Moderate#2 · 95% phenotype match

Ramucirumab

Cyramza · Anti-VEGFR2 antibody

Profile

Hypertension and proteinuria, class effect.

HTNGLOMTMA

Moderate#3 · 95% phenotype match

VEGFR TKIs (sunitinib · sorafenib · pazopanib · axitinib)

VEGFR TKI

Profile

Hypertension as an on-target marker; proteinuria.

HTNGLOMTMA

Moderate#4 · 95% phenotype match

Pazopanib

Votrient · VEGFR TKI

Profile

VEGFR-TKI; hypertension, proteinuria, TMA.

GLOMHTNTMA

Moderate#5 · 93% phenotype match

Axitinib

Inlyta · VEGFR TKI

Profile

Potent VEGFR-TKI; hypertension and proteinuria dominate.

HTNGLOMTMA

Moderate#6 · 92% phenotype match

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

Johnson, Tim — their work on Nintedanib, on PubMed (opens in a new tab)2 papers · 53 citesPMID 34857869 (opens PubMed in a new tab)PMID 31048591 (opens PubMed in a new tab)

Ranked by a 50/50 blend of publication volume and a position-weighted, capped Relative Citation Ratio (NIH iCite) on this agent’s renal literature; the citation count shown is the raw total, not the ranking score — counted over the 20 clinical records among all 23 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.