Jesse Richards , Madisen Fae Dorand , Maria Paszkowiak , Sana Ahmed , Courtney McCorkle , Pranay Kathuria
{"title":"肥胖和终末期肾病患者的KIDINS220多态性发生率显著升高。","authors":"Jesse Richards , Madisen Fae Dorand , Maria Paszkowiak , Sana Ahmed , Courtney McCorkle , Pranay Kathuria","doi":"10.1016/j.obpill.2024.100155","DOIUrl":null,"url":null,"abstract":"<div><h3>Background</h3><div>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.</div></div><div><h3>Methods</h3><div>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<sup>2</sup> test of independence was utilized to compare genetic mutation rates in this cohort to all individuals tested nationally.</div></div><div><h3>Results</h3><div>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<sup>2</sup> = 27.8, <em>p</em> < 0.0001) compared to the national positivity rate of all individuals tested for genetic causes of obesity.</div></div><div><h3>Conclusions</h3><div>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.</div></div>","PeriodicalId":100977,"journal":{"name":"Obesity Pillars","volume":"13 ","pages":"Article 100155"},"PeriodicalIF":0.0000,"publicationDate":"2024-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11719405/pdf/","citationCount":"0","resultStr":"{\"title\":\"Significantly higher rates of KIDINS220 polymorphisms in patients with obesity and end-stage renal disease\",\"authors\":\"Jesse Richards , Madisen Fae Dorand , Maria Paszkowiak , Sana Ahmed , Courtney McCorkle , Pranay Kathuria\",\"doi\":\"10.1016/j.obpill.2024.100155\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><h3>Background</h3><div>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.</div></div><div><h3>Methods</h3><div>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<sup>2</sup> test of independence was utilized to compare genetic mutation rates in this cohort to all individuals tested nationally.</div></div><div><h3>Results</h3><div>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<sup>2</sup> = 27.8, <em>p</em> < 0.0001) compared to the national positivity rate of all individuals tested for genetic causes of obesity.</div></div><div><h3>Conclusions</h3><div>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.</div></div>\",\"PeriodicalId\":100977,\"journal\":{\"name\":\"Obesity Pillars\",\"volume\":\"13 \",\"pages\":\"Article 100155\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2024-12-05\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11719405/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Obesity Pillars\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S2667368124000573\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Obesity Pillars","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2667368124000573","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Significantly higher rates of KIDINS220 polymorphisms in patients with obesity and end-stage renal disease
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 χ2 test of independence was utilized to compare genetic mutation rates in this cohort to all individuals tested nationally.
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 %, χ2 = 27.8, p < 0.0001) compared to the national positivity rate of all individuals tested for genetic causes of obesity.
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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