Evidence map›Paper›PMID 34414215›Full record

ArticleCase reports in nephrology and dialysis

Nintedanib-Induced Renal Thrombotic Microangiopathy.

Takeshi Fujita, Hideyuki Nakagawa, Takashi Yokota, Jun Umetani, Daiki Nagawa, Masamichi Nakata, Ikuyo Narita-Kinjo, Reiichi Murakami, Michiko Shimada, Norio Nakamura and 1 more

Open access · goldAbstract readCase Reports
In one paragraph

Article in Case reports in nephrology and dialysis. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.8field-weighted citation impact, top 27% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
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  4. Article
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  8. Article
  9. Article
  10. Thrombotic microangiopathy associated with lenvatinib therapy.Endocrine oncology (Bristol, England) · 2023
    Article
  11. Renal Fibrosis in Lupus Nephritis.International journal of molecular sciences · 2022
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 1 country.

Takeshi FujitaNephrology, Hirosaki University Graduate School of Medicine, Hirosaki, Aomori, Japan.
Hideyuki NakagawaRespiratory Medicine, Hirosaki National Hospital, Hirosaki, Aomori, Japan.
Takashi YokotaCardiology, Hirosaki University Graduate School of Medicine, Hirosaki, Aomori, Japan.
Jun UmetaniNephrology, Hirosaki University Graduate School of Medicine, Hirosaki, Aomori, Japan.
Daiki NagawaNephrology, Hirosaki University Graduate School of Medicine, Hirosaki, Aomori, Japan.
Masamichi NakataNephrology, Hirosaki University Graduate School of Medicine, Hirosaki, Aomori, Japan.
Ikuyo Narita-KinjoNephrology, Hirosaki University Graduate School of Medicine, Hirosaki, Aomori, Japan.
Reiichi MurakamiNephrology, Hirosaki University Graduate School of Medicine, Hirosaki, Aomori, Japan.
Michiko ShimadaNephrology, Hirosaki University Graduate School of Medicine, Hirosaki, Aomori, Japan.
Norio NakamuraNephrology, Hirosaki University Graduate School of Medicine, Hirosaki, Aomori, Japan.
Hirofumi TomitaNephrology, Hirosaki University Graduate School of Medicine, Hirosaki, Aomori, Japan.
Hirosaki University · JPHirosaki National Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nintedanib is a unique tyrosine kinase inhibitor used to suppress fibrosis in patients with idiopathic pulmonary fibrosis (IPF). Nintedanib has been shown to suppress multiple processes of fibrosis, thereby reducing the rate of lung function decline in patients with IPF. Since vascular endothelial growth factor is one of this agent's targets, nephrotoxicity, including renal thrombotic microangiopathy (TMA), is a possible major adverse effect. However, only 2 previous cases of nintedanib-induced renal TMA have been published. Our patient was an 83-year-old man with IPF. As adverse effects including liver enzyme level elevation, diarrhoea, anorexia, and nephrotoxicity developed, the nintedanib dosage was reduced after 9 months. The digestive symptoms resolved promptly, but the proteinuria and reduced kidney function remained. Although the kidney injury had improved to some extent, we performed a percutaneous renal biopsy. The biopsy revealed typical TMA findings such as microaneurysms filled with pale material, segmental double contours of glomerular basement membranes, and intracapillary foam cells. After discontinuation of nintedanib, the patient's nephrotoxicity improved. Nintedanib-induced renal TMA is reversible and is possibly dose-dependent. Here, we report the clinical course of our case and review the characteristics of nintedanib-induced renal TMA.

Indexed as

Drug-induced kidney injuryIdiopathic pulmonary fibrosisNephrotic syndromeNintedanibProteinuriaThrombotic microangiopathyTyrosine kinase inhibitor

Identifiers

PMID34414215
PMCPMC8339448
OpenAlexW3183478304

What Socratic holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.