ISSN No. 1606-7754                   Vol.13 No.2  August 2005

The role of calcium channel blockers in the treatment of diabetic nephropathy
Wael M Yousef1, Adel H Omar1, Mohamed D Morsy2, Moshira M. Abd El-Wahed3, Naglaa M Ghanayem4
Departments of Clinical Pharmacology1, Physiology2, Pathology3, Biochemistry4, Faculty of Medicine, Menoufiya University, Egypt

Abstract

Diabetic nephropathy (DNP) is a chronic renal disease (CRD) and a major cause of illness and premature death in people with diabetes mellitus (DM). It is the single most important cause of end-stage renal disease in the Western world and accounts for more than a quarter of all end-stage renal diseases. This article reviews the current development in DNP and the therapeutic challenge with particular reference to the role of calcium channel blockers. Moreover, renal ischaemia hastens the progression of DNP. Diltiazem and amlodipine have a tendency to reverse the changed parameters toward normal values but do not affect the biochemical parameters. Generally speaking, diltiazem is better than amlodipine in reversing biochemical and histopathological changes produced by DNP, and captopril reverses most of the changed parameters with the exception of the histopathological changes. These agents have nephroprotective properties and delay the progression of DNP.

Key words: Amlodipine, calcium channel blockers, diabetic nephropathy, diabetes mellitus, diltiazem, ischaemia

Diabetes Mellitus

Diabetes mellitus (DM) is a major health problem all over the world. It is defined as a group of syndromes characterized by hyperglycaemia, altered metabolism of lipids, carbohydrate and proteins, resulting from a defect in insulin secretion, insulin action or both. This chronic hyperglycaemic condition is associated with long term damage, dysfunction and failure of various organs especially eyes, kidney, nerves, heart and blood vessels.1

Complications of diabetes mellitus include acute complications that are generally a reflection of altered energy homeostasis either from hyperglycaemia (diabetic ketoacidosis and non-ketotic hyperosmolar syndrome) or hypoglycaemia and chronic complications consisting of retinopathy, nephropathy, neuropathy and angiopathy.2,3

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