A correlative study of copper, ceruloplasmin, iron, total iron binding capacity and total antioxidant capacity in diabetic nephropathy

Abstract

Introduction and Aim:   Diabetic nephropathy is the common cause of final stage of kidney disease. Studies on trace elements and oxidant-antioxidant status in diabetes mellitus are required for establishing the mechanisms involved in pathogenesis of diabetic complications, and also to establish biomarkers of diabetic nephropathy in addition to the conventional markers. The present study aimed to assess and correlate the blood levels of copper, iron, ceruloplasmin, total iron binding capacity (TIBC) and total antioxidant capacity (TAC) in diabetic nephropathy patients in comparison to diabetic individuals without complications and normal healthy controls.   Materials and Methods: The study subjects were, diabetic patients with nephropathy (group 1), diabetic patients without complications (group 2), and healthy controls (group 3). In the serum samples of all study subjects levels of copper, iron, ceruloplasmin, TIBC and TAC were estimated by standard spectrophotometric methods.   Results: Levels of copper, ceruloplasmin, iron and TIBC in serum were significantly higher and TAC was lower in diabetic patients when compared to controls, and more pronounced changes were seen in diabetic nephropathy patients when compared to diabetic patients with no complications. There was significant positive correlation among glycated hemoglobin, copper, iron and microalbumin in diabetic patients with or without nephropathy. Serum Total antioxidant capacity showed significant negative correlation with HbA1c, microalbuminuria, copper, and iron in diabetic patients with and without nephropathy.   Conclusion: Serum levels of trace elements could serve as diagnostic and prognostic biomarkers of diabetic nephropathy complimentary to microalbuminuria and glycated haemoglobin. Monitoring the trace elements and oxidative stress biomarkers in diabetic patients could be beneficial to prevent oxidative stress and pathogenesis of diabetic complications.