POS-407 Bariatric surgery repairs renal tubular uric acid transport in MS patients through circulating exosomes

Abstract

Metabolic surgery is increasingly becoming recognized as a more effective treatment for patients with metabolic syndrome as compared to lifestyle modification and medical management alone. Kidney plays a crucial role in maintaining the homeostasis of uric acid. The aim of the study was to imply that Whether circulating exosomes are involved in the change of renal uric acid transporter after weight loss surgery in patients with metabolic syndrome. We analyzed the basic data and blood and urine biochemical indicators of 30 normal people and 30 patients with metabolic syndrome preoperative and postoperative. The plasma exosomes of this cohort was extracted, and the human renal tubular epithelial cells were co-cultured with EVs. We determined the expressions of uric acid transporters URAT1, GLUT9 and ABCG2 on renal tubular epithelial cells by q-PCR and Western Blot. Compared with normal cohort, patients with metabolic syndrome have higher blood pressure, higher BMI, higher blood sugar, higher blood lipids and uric acid levels (P<0.001), but these biochemical indexes can return to near normal levels after bariatric surgery. The BMI of patients with metabolic syndrome was positively correlated with blood uric acid (R2 =0.14, P<0.001), then there was no significant correlation between BMI and 24-hour uric acid. The human renal tubular epithelial cells were co-cultured with EVs. The expression of URAT1, GLUT9 and ABCG2 on the cells was detected by q-PCR and Western Blot. Compared with the renal tubular epithelial cells stimulated by circulating EV after operation,the expression of URAT1 and GLUT9 on renal tubular epithelial cells stimulated by circulating EV from the preoperative increased (P<0.05), and the expression of ABCG2 decreased (P<0.05). Our results confirm that patients undergoing bariatric surgery changes in the composition of circulating extracellular vesicle , which can regulate renal tubular uric acid transporter, thereby affect renal uric acid metabolism.