[ Diabetes Solutions ]

High Serum Uric Acid as a Novel Risk Factor for Type 2 Diabetes

Left untreated, gout can lead to permanent bone, joint and tissue damage, as well as other health problems such as kidney stones. Associate Professor, Department of Biochemistry, 2. We analyzed data from the Atherosclerosis Risk in Communities (ARIC) Study and quantified the independent association between uric acid level and incident diabetes via Cox proportional hazards models. Material and Method: This was a case control study. Our data suggest that serum uric acid concentrations have a limited influence on CVD complicating type 2 diabetes. Patients with type 2 diabetes and UASF had lower 24-h urine pH than NV. This review focuses on the evidence that supports serum UA levels as a biomarker of renal and cardiovascular risk and as a potential additional therapeutic target in diabetes.

Randomized controlled trials on drugs that lower uric acid need to be conducted to evaluate the causal relationship between serum uric acid and development and progression of diabetic kidney disease; in addition, large scale long-term treatment trials need to be performed, as they are still lacking. Elevated SUA levels within the normal range (men >6.3 mg/dL, women >5.1) at the onset of overt nephropathy resulted in an increased risk for declining renal function in type 2 diabetes patients. 5.7 ± 1.4 mg/dl, P = 0.007). By multivariate analyses, in men, abnormal sUA was negatively associated with diabetes (odds ratio [OR] 0.451 [95% CI 0.349–0.583], P < 0.001), but anti-HCV was not an independent factor. In women, positive anti-HCV was positively associated with diabetes (1.634 [1.068–2.498], P = 0.02), but sUA was not an independent factor. The results after excluding 56 cases using diuretics were similar. (1). Another striking association we observed is the relationship between diabetes and lower sUA levels in men with a lack of association between diabetes and abnormal sUA levels in women. When waste materials in urine do not dissolve completely, microscopic particles begin to form and, over time, grow into stones. The principle of Mendelian randomization is that if a biomarker (such as serum uric acid level) is causally related to the pathogenesis of disease (such as T2DM), genetic variation resulting in changes in the biomarker should have the same effect on disease risk as that predicted by the biomarker levels (14, 15). Although the important study conducted by Dehghan et al. (1) meets with agreed applause, we suggest that further studies are necessary to elucidate the role of sUA levels on the development of diabetes and the pathogenetic mechanism for the sex-based disparity, taking chronic HCV infection into consideration.

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