Abstract

Background: Diabetic nephropathy is a microvascular complication associated with diabetes that causes the kidneys to slowly deteriorate, leading to end-stage renal disease. Nephropathy associated with diabetes has been attributed to oxidative stress. Chronic zinc deficiency generally results in an increased sensitivity to the effects of oxidative stress. Zinc deficiency is often seen in diabetic patients. This alteration in zinc status appears to be involved in the development of microvascular complications of diabetes. Aim: The objective of this study will be to explore the relationship between zinc status and the progression of nephropathy in type 2 diabetes. Method: The study involved 80 normotensive diabetic patients with positive microalbuminuria and 60 healthy non-diabetic subjects of corresponding age. For all subjects, a serum zinc assay was performed on the ICE 3300 atomic absorption spectrometer from Thermo Fisher, a serum creatinine assay on Cobas 501 from Roche Diagnostic with evaluation of GFR, as well as a microalbuminuria assay. on the DCA Vantage from Siemens. Results: Serum zinc levels were low (p <0.001) in diabetic patients compared to non-diabetic control subjects. Elevated levels of microalbuminuria (p <0.001) were observed in diabetic patients with low serum zinc levels compared to those with normal serum zinc levels. Serum zinc level in diabetic patients was inversely correlated with serum creatinine (r = −0.51, p <0.001), microalbuminuria (r = −0.587, p <0.001) and positively with GFR (r = 0.24, p <0.01). Discussion: The results of our study support the observation that diabetes affects zinc status with a significant decrease in serum zinc levels at the onset of diabetic complications. During progression to the stages of diabetic nephropathy, morphological and structural changes occur in the glomerular and basal membrane of the kidneys, hyperfiltration, thickening of the glomerular basement membrane. All of these changes will cause albumin with trace metals to leak into the urine. Therefore, the hypozincemia seen in diabetics can be attributed to hyperzincuria. The results of this study are consistent with results reported by others.

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