Key Laboratory of Hormones and Development (Ministry of Health), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Metabolic Diseases Hospital & Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin, China.
J Diabetes Investig. 2019 Jan;10(1):118-123. doi: 10.1111/jdi.12850. Epub 2018 May 4.
AIMS/INTRODUCTION: Hyperuricemia (HUA) occurs because of decreased excretion of uric acid, increased synthesis of uric acid or a combination of both mechanisms. The proportions of these three types of HUA in type 2 diabetes patients are not known. In the mean time, we assume that different types of HUA might manifest with different renal damage, even in patients with normal renal filtration function.
We included 435 inpatients with type 2 diabetes at the Metabolic Disease Hospital of Tianjin Medical University from 2015 to 2016. Based on the clearance of uric acid, 90 patients with HUA were divided into three types: synthesis-increased HUA, excretion-decreased HUA and mixed type of HUA.
Patients with the mixed type of HUA had the severest kidney injury manifested by a high level of 24 h urinary microalbumin, urinary immunoglobulin G, transferrin, α-galactosidase and β2-microglobulin compared with the normal uric acid group. Urinary immunoglobulin G, transferrin and α-galactosidase were also increased in patients with synthesis-increased HUA compared with the normal uric acid group. Patients with excretion-decreased HUA did not have an increased level of renal impairment markers; however, these patients had an increased body mass index, which might cause dysfunction of kidney excretion.
Excretion-decreased HUA is a more common type of HUA in type 2 diabetes patients that might be caused by dysfunction of tubular excretion instead of structural damage. The mixed type of HUA patients had the severest kidney glomerular and tubular damage compared with the normal uric acid group. Clinically, different types of hyperuricemia should be given individualized treatment according to their own characteristics.
目的/引言:高尿酸血症(HUA)是由于尿酸排泄减少、尿酸合成增加或这两种机制的结合而发生的。在 2 型糖尿病患者中,这三种 HUA 类型的比例尚不清楚。同时,我们假设不同类型的 HUA 可能表现出不同的肾损伤,即使在肾功能正常的患者中也是如此。
我们纳入了 2015 年至 2016 年在天津医科大学代谢病医院住院的 435 例 2 型糖尿病患者。根据尿酸清除率,将 90 例 HUA 患者分为三种类型:合成型 HUA、排泄型 HUA 和混合型 HUA。
与正常尿酸组相比,混合型 HUA 患者的肾脏损伤最严重,表现为 24 小时尿微量白蛋白、尿免疫球蛋白 G、转铁蛋白、α-半乳糖苷酶和β2-微球蛋白水平升高。与正常尿酸组相比,合成型 HUA 患者的尿免疫球蛋白 G、转铁蛋白和α-半乳糖苷酶也升高。排泄型 HUA 患者的肾功能损害标志物水平没有升高;然而,这些患者的体重指数增加,这可能导致肾脏排泄功能障碍。
排泄型 HUA 是 2 型糖尿病患者中更为常见的 HUA 类型,可能是由于肾小管排泄功能障碍而不是结构损伤所致。与正常尿酸组相比,混合型 HUA 患者的肾小球和肾小管损伤最严重。临床上,应根据不同类型高尿酸血症的特点,给予个体化治疗。