ABSTRACT
Allan Flyvbjerg, Dinah Khatir and Ruth Rasch Medical Department M (Diabetes and Endocrinology), Medical Research Laboratories, Institute of Experimental Clinical Research, Aarhus University Hospital, Aarhus, Denmark and Department of Cell Biology, Institute of Anatomy, Aarhus University, Aarhus, Denmark
INTRODUCTION
The development of diabetic nephropathy in Type 1 and Type 2 diabetes mellitus is still a significant clinical problem associated with increased morbidity and mortality [1-4]. The well known early changes of the diabetic kidney disease are renal enlargement and hyperfiltration. Later on in the incipient stage an increase in urinary albumin excretion (UAE) is followed by increased basement membrane thickness (BMT), mesangial proliferation and glomerular sclerosis that may lead to overt diabetic nephropathy and progressive renal insufficiency [1-4]. Interestingly, the renal functional and structural changes in animal models of Type 1 and Type 2 diabetes have fundamental similarities to those occurring in diabetic patients and accordingly spontaneously developing or chemically-induced (i.e. streptozotocin (STZ)) diabetic rodents have been used to elucidate the pathogenesis of diabetic kidney disease. These diabetic animal models develop renal enlargement, glomerular hypertrophy and renal hyperfiltration within weeks after diabetes debut and increased UAE, increased glomerular BMT and mesangial expansion within months [5,6]. Due to their growth promoting and proliferative effects, several growth factors have attracted attention in various aspects of diabetes research including conceivable effects on functional and structural changes in the development of diabetic kidney disease [6]. The present review will present
data on a definite role of the growth hormone (GH) and vascular endothelial growth factor (VEGF) in the pathogenesis of the renal changes in experimental diabetes.
