ArticleObesity pillars2025
Significantly higher rates of KIDINS220 polymorphisms in patients with obesity and end-stage renal disease.
Article in Obesity pillars, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Kinase D-interacting substrate of 220 kDa ("KIDINS220") is an integral plasma membrane protein essential to signaling throughout the body; abnormalities are linked to a variety of disorders, including obesity, but have never been directly linked to chronic- or end-stage renal disease. Methods: Retrospective chart review identified patients with severe obesity who presented for pre-kidney transplant weight management. 20 individuals met criteria for testing for genetic causes of obesity. A χ Results: This case series presents a cohort of patients with severe obesity and end-stage renal disease who were subsequently found to have a significantly higher rate of KIDINS220 mutations (20 %, χ Conclusions: Mutations within KIDINS220 may play a modulatory role in the progression of chronic kidney disease in patients with obesity, as evidenced by this small retrospective study. The relationship between KIDINS200, kidney disease, and obesity is complex and requires further study, but may represent a potential therapeutic target in the future.
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