{"title":"IL1RN VNTR多态性与镰状细胞性贫血患者肾脏损害","authors":"B. Lakkakula, S. Pattnaik","doi":"10.34172/npj.2022.10437","DOIUrl":null,"url":null,"abstract":"Introduction: Sickle cell anemia (SCA) is a chronic illness associated with acute and chronic hemolytic anemia, recurrent vaso-occlusion episodes, intense pain, progressive multiple organ damage, and early mortality. Inflammation plays a significant role in the pathophysiology of SCA. Elevated levels of pro-inflammatory cytokines are involved in worsening the degree of kidney damage in SCA patients. Objectives: The present study aimed to assess whether IL1RN VNTR polymorphism is associated with kidney damage in patients with SCA. Patients and Methods: We have investigated 190 SCA patients (104 with Normal kidney function and 86 with kidney damage). Creatinine-based estimated glomerular filtration rate (eGFR) was calculated to assess kidney function. Interleukin-1 receptor antagonist gene (IL1RN) variable number tandem repeats (VNTR) genotypes were analyzed using PCR-electrophoresis. The association between IL1RN-VNTR and kidney damage was evaluated by using χ2 test. Odds ratios (OR) and 95% CI were calculated. The relationship between kidney damage and fetal hemoglobin (HbF) and their interaction with IL1RN-VNTR genotypes, was investigated using a Mantel-Haenszel (M-H) stratified analysis. Results: There were no significant differences in genotype frequencies between SCA patients with or without kidney damage (P=0.107). Furthermore, no significant interactions between IL1RN VNTR and HbF on determining kidney damage were found. Conclusion: These results conflict with the biological plausibility that interleukin levels modulate SCA pathophysiology and may deserve further exploration.","PeriodicalId":16388,"journal":{"name":"Journal of Nephropharmacology","volume":" ","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2021-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"IL1RN VNTR Polymorphism and kidney damage in sickle cell anemia patients\",\"authors\":\"B. Lakkakula, S. Pattnaik\",\"doi\":\"10.34172/npj.2022.10437\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Introduction: Sickle cell anemia (SCA) is a chronic illness associated with acute and chronic hemolytic anemia, recurrent vaso-occlusion episodes, intense pain, progressive multiple organ damage, and early mortality. Inflammation plays a significant role in the pathophysiology of SCA. Elevated levels of pro-inflammatory cytokines are involved in worsening the degree of kidney damage in SCA patients. Objectives: The present study aimed to assess whether IL1RN VNTR polymorphism is associated with kidney damage in patients with SCA. Patients and Methods: We have investigated 190 SCA patients (104 with Normal kidney function and 86 with kidney damage). Creatinine-based estimated glomerular filtration rate (eGFR) was calculated to assess kidney function. Interleukin-1 receptor antagonist gene (IL1RN) variable number tandem repeats (VNTR) genotypes were analyzed using PCR-electrophoresis. The association between IL1RN-VNTR and kidney damage was evaluated by using χ2 test. Odds ratios (OR) and 95% CI were calculated. The relationship between kidney damage and fetal hemoglobin (HbF) and their interaction with IL1RN-VNTR genotypes, was investigated using a Mantel-Haenszel (M-H) stratified analysis. Results: There were no significant differences in genotype frequencies between SCA patients with or without kidney damage (P=0.107). Furthermore, no significant interactions between IL1RN VNTR and HbF on determining kidney damage were found. Conclusion: These results conflict with the biological plausibility that interleukin levels modulate SCA pathophysiology and may deserve further exploration.\",\"PeriodicalId\":16388,\"journal\":{\"name\":\"Journal of Nephropharmacology\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2021-10-30\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Nephropharmacology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.34172/npj.2022.10437\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"Medicine\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Nephropharmacology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.34172/npj.2022.10437","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"Medicine","Score":null,"Total":0}
IL1RN VNTR Polymorphism and kidney damage in sickle cell anemia patients
Introduction: Sickle cell anemia (SCA) is a chronic illness associated with acute and chronic hemolytic anemia, recurrent vaso-occlusion episodes, intense pain, progressive multiple organ damage, and early mortality. Inflammation plays a significant role in the pathophysiology of SCA. Elevated levels of pro-inflammatory cytokines are involved in worsening the degree of kidney damage in SCA patients. Objectives: The present study aimed to assess whether IL1RN VNTR polymorphism is associated with kidney damage in patients with SCA. Patients and Methods: We have investigated 190 SCA patients (104 with Normal kidney function and 86 with kidney damage). Creatinine-based estimated glomerular filtration rate (eGFR) was calculated to assess kidney function. Interleukin-1 receptor antagonist gene (IL1RN) variable number tandem repeats (VNTR) genotypes were analyzed using PCR-electrophoresis. The association between IL1RN-VNTR and kidney damage was evaluated by using χ2 test. Odds ratios (OR) and 95% CI were calculated. The relationship between kidney damage and fetal hemoglobin (HbF) and their interaction with IL1RN-VNTR genotypes, was investigated using a Mantel-Haenszel (M-H) stratified analysis. Results: There were no significant differences in genotype frequencies between SCA patients with or without kidney damage (P=0.107). Furthermore, no significant interactions between IL1RN VNTR and HbF on determining kidney damage were found. Conclusion: These results conflict with the biological plausibility that interleukin levels modulate SCA pathophysiology and may deserve further exploration.