Uric acid and risk of diabetic kidney disease
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REVIEW
Uric acid and risk of diabetic kidney disease Michael Mauer1 · Alessandro Doria2 Received: 30 April 2020 / Accepted: 2 July 2020 © Italian Society of Nephrology 2020
Abstract Diabetic kidney disease (DKD) is the leading cause of end-stage kidney disease (ESKD) in the Western world. Better control of glycemia and blood pressure, including renin-angiotensin system blockade (RASB), appear to have slowed DKD progression rate but have been unable to substantially decrease the annual incidence of new cases of DKD related ESKD. Thus, new treatment targets are needed. Higher levels of serum uric acid (SUA) have been associated with increased risk and progression of DKD in persons with types 1 (T1D) and 2 (T2D) diabetes and of chronic kidney disease (CKD) in general. This review presents the epidemiological, clinical, and clinical trial evidence regarding the hypothesis that SUA reduction could slow progression of DKD and/or CKD in general. Keywords Diabetes · Kidney disease · Uric acid
Introduction Despite improvements in glycemia [1] and blood pressure control and the use of renin angiotensin system blocking (RASB) drugs [2] the number of persons in the US who develop diabetes-related end-stage kidney disease (ESKD) each year continues to rise [3], in parallel with the worldwide epidemic of diabetes [4]. In fact, we have yet to experience the full impact of the recent marked increases in the number of people with obesity and diabetes, who may take decades to reach ESKD [4]. Importantly, the benefits of RASB on progression of glomerular filtration rate loss (GFR) loss in patients with diabetic kidney disease (DKD) has only been seen in patients with estimated GFRs 4.2 mg/dL) vs. only 10% in the lower three quartiles (p = 0.006). These findings were independent of baseline body mass index (BMI), HbA1c, albumin excretion rate, serum creatinine, serum cholesterol, and mean arterial blood pressure (BP). Adjusted for these variables, the HR was 2.93 [1.25–6.86] per 1.7 mg/ dL (100 µmol/L) increase in SUA; P 0.013) [5]. However, baseline SUA did not predict the risk of microalbuminuria or GFR loss. In another study of normoalbuminuric T1D patients, conducted in the US, Jalal et al. [6] asked whether baseline SUA
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Journal of Nephrology
was a risk factor for micro- or macroalbuminuria over the subsequent 6-years; SUA at baseline was higher in the 25 subjects progressing to micro- or macroalbuminuria vs. the 299 remaining normoalbuminuric (p = 0.02). After adjustments for age, sex, T1D duration, treatment with renin-angiotensin system blockers (RASB), BMI, BP, HbA1c, serum creatinine, cystatin C, and lipid levels, higher baseline SUA increased the odds of new onset of increased albuminuria by 1.8 fold (p = 0.005) [6]. Consistent with these findings, a cross-sectional study of 20,464 adult patients with T1D from Italy, 11,162 of whom had SUA measurements, found that each 1 mg/dL increase of SUA was associated with an increased prevalence of DKD (OR = 1.56; 95% CI 1.49–1.63; P 6.0 mg/dL), iGFR
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