---
title: "Nintedanib-Linked Glomerular Endothelial Injury and Secondary Collapsing FSGS: SGLT2 Inhibitor as"
id: "pubmed-42674550"
canonical_url: "https://medichelpline.com/clinical-feed/pubmed-42674550"
content_type: "clinical_feed_article"
specialty: "Pharmacology"
source_name: "PubMed / NCBI"
source_url: "https://pubmed.ncbi.nlm.nih.gov/42674550/"
doi: "10.1111/nep.70274"
published_at: "2026-09-01T00:00:00.000Z"
evidence_level: "Case Reports"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Nintedanib-Linked Glomerular Endothelial Injury and Secondary Collapsing FSGS: SGLT2 Inhibitor as
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/pubmed-42674550
- **Specialty:** [Pharmacology](https://medichelpline.com/clinical-feed/pharmacology.md)
- **Primary Source:** PubMed / NCBI
- **Source URL:** [Original Journal Publication](https://pubmed.ncbi.nlm.nih.gov/42674550/)
- **DOI:** [10.1111/nep.70274](https://doi.org/10.1111%2Fnep.70274)
- **Published At:** 2026-09-01T00:00:00.000Z
- **Evidence Rating:** Case Reports
## Executive GIST (TL;DR)
- A 69-year-old man with idiopathic pulmonary fibrosis (IPF), hypertension, diabetes, and preexisting chronic kidney disease developed persistent nephrotic syndrome and renal dysfunction 16 months after starting **nintedanib**, a small-molecule tyrosine kinase inhibitor (TKI). - Kidney biopsy showed **glomerular endothelial injury** with microangiopathic features, secondary collapsing focal segmental glomerulosclerosis (**collapsing FSGS**), and background diabetic kidney disease. - Reported nephrotoxic presentations of nintedanib include nephrotic syndrome, acute kidney injury, thrombotic microangiopathy (TMA), and anti-glomerular basement membrane nephritis; optimal management remains undefined. - After discontinuing nintedanib and intensifying renin–angiotensin system blockade plus mineralocorticoid receptor antagonism, nephrotic-range proteinuria persisted. - Initiation of the **SGLT2 inhibitor** dapagliflozin was temporally associated with a gradual, sustained reduction in proteinuria and attainment of partial remission while preserving estimated glomerular filtration rate (eGFR). - Authors note this is the first reported case of nintedanib-associated glomerular endothelial injury with secondary collapsing FSGS in which SGLT2 inhibition was temporally linked to sustained proteinuria reduction under supportive therapy. - The case highlights that TKIs can cause both endothelial and podocyte injury and that therapeutic options beyond drug withdrawal are limited; **SGLT2 inhibition** is proposed as a potential adjunctive strategy needing systematic evaluation. - Background references include prior reports of nintedanib-associated renal TMA and other glomerular lesions; detailed case data (exact lab values, timelines beyond 16 months, and quantitative outcomes) were not reported in the abstract.
## Clinical Analysis & Structured Key Points
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Affiliations Expand ### Affiliations * 1 Department of Hypertension and Nephrology, NTT Medical Center Tokyo, Tokyo, Japan. * 2 Department of Pathology, Tokyo Women's Medical University, Tokyo, Japan. * 3 Department of Diagnostic Pathology, NTT Medical Center Tokyo, Tokyo, Japan. * PMID: **42674550** * DOI: [ 10.1111/nep.70274 ](https://doi.org/10.1111/nep.70274) Item in Clipboard Case Reports # Nintedanib-Associated Glomerular Endothelial Injury With Secondary Collapsing Focal Segmental Glomerulosclerosis: Potential Role of Sodium-Glucose Cotransporter 2 Inhibition Yoshitaka Furuto et al. Nephrology (Carlton). 2026 Sep. Show details Display options Display options Format Abstract PubMed PMID Nephrology (Carlton) Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Nephrology+%28Carlton%29%22%5Bjour%5D&sort=date&sort_order=desc) * [ Search in NLM Catalog ](https://www.ncbi.nlm.nih.gov/nlmcatalog?term=%22Nephrology+%28Carlton%29%22%5BTitle+Abbreviation%5D) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42674550/) . 2026 Sep;31(9):e70274. doi: 10.1111/nep.70274. ### Authors [Yoshitaka Furuto](https://pubmed.ncbi.nlm.nih.gov/?term=Furuto+Y&cauthor_id=42674550)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42674550/#short-view-affiliation-1 "Department of Hypertension and Nephrology, NTT Medical Center Tokyo, Tokyo, Japan."), [Hirotsugu Hashimoto](https://pubmed.ncbi.nlm.nih.gov/?term=Hashimoto+H&cauthor_id=42674550)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42674550/#short-view-affiliation-2 "Department of Pathology, Tokyo Women's Medical University, Tokyo, Japan."), [Daiki Yoshino](https://pubmed.ncbi.nlm.nih.gov/?term=Yoshino+D&cauthor_id=42674550)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42674550/#short-view-affiliation-1 "Department of Hypertension and Nephrology, NTT Medical Center Tokyo, Tokyo, Japan."), [Sayako Ikeda](https://pubmed.ncbi.nlm.nih.gov/?term=Ikeda+S&cauthor_id=42674550)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42674550/#short-view-affiliation-1 "Department of Hypertension and Nephrology, NTT Medical Center Tokyo, Tokyo, Japan."), [Akio Namikawa](https://pubmed.ncbi.nlm.nih.gov/?term=Namikawa+A&cauthor_id=42674550)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42674550/#short-view-affiliation-1 "Department of Hypertension and Nephrology, NTT Medical Center Tokyo, Tokyo, Japan."), [Dai Sato](https://pubmed.ncbi.nlm.nih.gov/?term=Sato+D&cauthor_id=42674550)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42674550/#short-view-affiliation-1 "Department of Hypertension and Nephrology, NTT Medical Center Tokyo, Tokyo, Japan."), [Hiroko Takahashi](https://pubmed.ncbi.nlm.nih.gov/?term=Takahashi+H&cauthor_id=42674550)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42674550/#short-view-affiliation-1 "Department of Hypertension and Nephrology, NTT Medical Center Tokyo, Tokyo, Japan."), [Teppei Morikawa](https://pubmed.ncbi.nlm.nih.gov/?term=Morikawa+T&cauthor_id=42674550)[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42674550/#short-view-affiliation-3 "Department of Diagnostic Pathology, NTT Medical Center Tokyo, Tokyo, Japan."), [Yuko Shibuya](https://pubmed.ncbi.nlm.nih.gov/?term=Shibuya+Y&cauthor_id=42674550)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42674550/#short-view-affiliation-1 "Department of Hypertension and Nephrology, NTT Medical Center Tokyo, Tokyo, Japan.") ### Affiliations * 1 Department of Hypertension and Nephrology, NTT Medical Center Tokyo, Tokyo, Japan. * 2 Department of Pathology, Tokyo Women's Medical University, Tokyo, Japan. * 3 Department of Diagnostic Pathology, NTT Medical Center Tokyo, Tokyo, Japan. * PMID: **42674550** * DOI: [ 10.1111/nep.70274 ](https://doi.org/10.1111/nep.70274) Item in Clipboard Cite Display options Display options Format Abstract PubMed PMID ## Abstract Nintedanib (NIB), a small-molecule tyrosine kinase inhibitor (TKI), is approved for idiopathic pulmonary fibrosis (IPF) and systemic sclerosis-associated interstitial lung disease. Although nephrotoxicity is uncommon, cases of nephrotic syndrome (NS), acute kidney injury (AKI) and glomerular lesions including thrombotic microangiopathy (TMA) and anti-glomerular basement membrane (GBM) nephritis have been reported. However, the optimal management of NIB-associated glomerular disease remains undefined. We report a 69-year-old man with IPF, hypertension, diabetes and underlying chronic kidney disease who developed persistent NS and renal dysfunction 16 months after initiation of NIB. Kidney biopsy demonstrated glomerular endothelial injury with microangiopathic features, accompanied by secondary collapsing focal segmental glomerulosclerosis (FSGS) and background diabetic kidney disease. Despite discontinuation of NIB and intensification of renin-angiotensin system inhibition and mineralocorticoid receptor blockade, nephrotic-range proteinuria persisted. Subsequent initiation of the sodium-glucose cotransporter 2 inhibitor (SGLT2i) dapagliflozin was temporally associated with a gradual and sustained reduction in proteinuria, with partial remission achieved while preserving the estimated glomerular filtration rate. To our knowledge, this is the first report of NIB-associated glomerular endothelial injury with secondary collapsing FSGS in which SGLT2i initiation was temporally associated with sustained proteinuria reduction under concomitant supportive therapy. TKIs may induce both endothelial and podocyte injury and therapeutic options beyond drug withdrawal remain limited. In this context, SGLT2 inhibition may represent a potential adjunctive therapeutic strategy in selected cases with underlying chronic kidney disease and warrants further systematic evaluation. **Keywords:** collapsing focal segmental glomerulosclerosis; diabetic kidney disease; nintedanib; sodium–glucose cotransporter 2 inhibitor; thrombotic microangiopathy. © 2026 Asian Pacific Society of Nephrology. [PubMed Disclaimer](https://pubmed.ncbi.nlm.nih.gov/disclaimer/) ## References 1. 1. L. Richeldi, R. M. Du Bois, G. Raghu, et al., “Efficacy and Safety of Nintedanib in Idiopathic Pulmonary Fibrosis,” New England Journal of Medicine 370 (2014): 2071–2082. 2. 1. D. Inoue, H. Nishi, K. Honda, et al., “Renal Thrombotic Microangiopathy During Nintedanib Treatment for Idiopathic Pulmonary Fibrosis,” Clinical Nephrology 93 (2020): 47–50. 3. 1. T. Fujita, H. Nakagawa, T. Yokota, et al., “Nintedanib‐Induced Renal Thrombotic Microangiopathy,” Case Reports in Nephrology and Dialysis 11 (2021): 227–232. 4. 1. M. Hasegawa, A. Uehara, T. Suzuki, et al., “Nintedanib‐Induced Glomerular Microangiopathy: A Case Report,” CEN Case Reports 9 (2020): 295–300. 5. 1. I. Ismail, S. Nigam, A. Parnham, and V. Srinivasa, “Anti‐Glomerular Basement Membrane Glomerulonephritis Following Nintedanib for Idiopathic Pulmonary Fibrosis: A Case Report,” Journal of Medical Case Reports 11 (2017): 214. 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