A Comparison of Progression in Diabetic and Non-Diabetic Renal Disease: Similarity of Progression Promoters

Abstract

The prevention of progressive renal function loss remains the major challenge for nephrologists today. Traditionally the progressive nature of renal function loss was attributed to the underlying disease, with a major role for hypertension [1]. The hypothesis, however, that common mechanisms account for the progressive renal function loss in many different renal conditions regardless the nature of initial renal damage [2], was fuelled by several observations. These include the linear renal function deterioration that occurs in many patients regardless their initial renal disease [3], as well as the similarity in histopathological abnormalities in end-stage kidneys with different underlying diseases. Systemic [4] and glomerular [5] hypertension, proteinuria [6] and lipid abnormalities [7] are assumed to be common mediators in the pathogenesis of focal segmental glomerulosclerosis, the alleged final common pathway of progressive renal disease [8]. Here we will briefly review current knowledge on progressive renal function loss in human diabetic and non-diabetic renal disease and on the response to intervention treatment. As to diabetic patients we will, for the sake of brevity, mainly focus on patients with type I (insulin-dependent) diabetes. We will specifically address the question whether current clinical evidence supports the hypothesis that common mechanisms underlie progressive renal function loss in diabetic and non-diabetic renal disease; this will help to devise future prevention strategies.