Abstract
Background: Diabetic nephropathy (DN) is one of the major complications of diabetes. Hyperglycemia, inflammation and oxidative stress as well as advanced glycation end products (AGEs) are reported as the risk factors for DN. Sevelamer has shown promising results in reducing inflammation and even HbA1c levels in DN. Objectives: We aim to evaluate the therapeutic effects of sevelamer on blood sugar, HbA1c level, lipid profile, and high sensitivity CRP (hs-CRP) in patients with diabetic nephropathy. Patients and Methods: In this clinical trial, 18 patients (13 female with mean age of 61.22±9.32 years) with stages 2-4 of diabetic nephropathy were recruited. Patients were administered with 800 mg of sevelamer twice a day for three months. Blood sugar, HbA1C, hs-CRP, lipid profile and other laboratory findings were measured before and 1, 2 and three months after initiation of the treatment. Results: There was significant decline in HbA1c (p=0.001), postprandial blood sugar (p=0.02) and phosphorus (p<0.001) at the end of the study period. Sevelamer had no effect on fasting blood sugar, lipid profile, blood urea nitrogen, creatinine, Na, K and hs-CRP. Conclusion: Our results indicated that along with its phosphorus reducing effects, sevelamer plays an important role in decreasing postprandial blood sugar and HbA1c level. Sevelamer had no effects on lipid profile and hs-CRP.
Highlights
Diabetic nephropathy (DN) is one of the major complications of diabetes
Our results indicated that along with its phosphorus reducing effects, sevelamer plays an important role in decreasing postprandial blood sugar and hemoglobin A1C (HbA1c) level
Sevelamer had no effects on lipid profile and high sensitivity C-reactive protein (hs-CRP)
Summary
Hyperglycemia, inflammation and oxidative stress as well as advanced glycation end products (AGEs) are reported as the risk factors for DN. Diabetic nephropathy (DN) is one of the major microvascular complications of diabetes and has become the leading cause of end-stage renal disease (ESRD) [1,2]. Hyperglycemia, inflammation and oxidative stress are reported as the risk factors for the induction and progression of DN [3,4]. Along with these factors, advanced glycation end products (AGEs) are another factor which cause the increase of inflammatory markers and oxidative stresses which can result in the progress of chronic kidney disease (CKD) [5].
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