Renal impairment markers in type 2 diabetes patients with different types of hyperuricemia

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Abstract

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. Materials and Methods: 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. Results: 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. Conclusions: 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.

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APA

Gao, Z., Zuo, M., Han, F., Yuan, X., Sun, M., Li, X., … Yang, J. (2019). Renal impairment markers in type 2 diabetes patients with different types of hyperuricemia. Journal of Diabetes Investigation, 10(1), 118–123. https://doi.org/10.1111/jdi.12850

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