代谢综合征、2型糖尿病和慢性肾病患者的交感神经系统活动再溶酶和α淀粉酶的作用

H. Le, He Gp, A. Ca, ánchez Dcv, García Ag
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引用次数: 0

摘要

目的:评价代谢综合征(MS)、2型糖尿病(T2DM)和终末期肾病(ESRD)患者血清肾再化酶和唾液α淀粉酶浓度及其与血浆儿茶酚胺水平的关系。方法:采用横断面研究方法,纳入163例患者;MS 43例,t2dm 93例,ESRD 13例,健康者14例(对照组)。所有患者均归属于墨西哥米却肯州莫雷利亚市的UMAA/UMF第75号。测定血清葡萄糖、肌酐、胆固醇、甘油三酯、高密度脂蛋白、肾化酶,测定血浆多巴胺(DA)、肾上腺素(E)、去甲肾上腺素(NE)。采集唾液样品进行淀粉酶测定。结果:T2DM和ESRD患者血浆DA、E、NE浓度较高(p<0.0001)。ESRD患者的Renalase较MS和T2DM患者低(p<0.0001)。与对照组相比,MS、T2DM和ESRD患者α -淀粉酶浓度较高(p<0.0001)。儿茶酚胺与α淀粉酶和糖尿病进化呈正相关。结论:MS、T2DM和ESRD患者存在交感神经亢进。Renalase可作为肾功能的生物标志物,而唾液α淀粉酶可作为交感神经亢进的生物标志物。需要进一步的研究来评估SNS在CKD发展中的病理生理机制。
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Sympathetic Nervous System Activity in Patients with Metabolic Syndrome, Type 2 Diabetes Mellitus and Chronic Kidney Disease. Role of Renalase and Alpha Amylase
Aim: To evaluate serum renalase and salivary alpha amylase concentrations and their relationship with plasma catecholamine levels in patients with Metabolic Syndrome (MS), Type 2 Diabetes Mellitus (T2DM), and End-Stage Renal Disease (ESRD). Method: In cross-sectional study 163 patients were enrolled; 43 patients with MS, 93 withT2DM, 13 with ESRD, and 14 healthy subjects (control group). All patients had their ascription to the UMAA/UMF No. 75, in Morelia, Michoacan, Mexico. Glucose, creatinine, cholesterol, triglycerides, HDL, and renalase were measurement in serum, and Dopamine (DA), Epinephrine (E) and Norepinephrine (NE) in plasma. An aliquot of saliva was collected for alpha amylase determination. Results: High plasma concentrations of DA, E and NE (p<0.0001) was founded in T2DM and ESRD patients. Renalase was lower in ESRD compared to MS and T2DM patients (p<0.0001). High concentrations of alpha amylase were found in MS, T2DM, and ESRD patients in comparison with control group (p<0.0001). Catecholamines correlated positively with alpha amylase and diabetes evolution. Conclusion: Sympathetic hyperactivity in MS, T2DM and ESRD patients was founded. Renalase could be proposed as biomarker of renal function and salivary alpha amylase as sympathetic hyperactivity. Additional studies are required to evaluate the pathophysiological mechanisms involved of SNS in CKD development.
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