Glomerular Hyperfunction

From the onset of IDDM, kidney function is characterised by elevation of glomerular filtration rate (GFR) and renal plasma flow (RPF) [for reviews see 1,2]. Using precise measurements e.g. renal clearance of inulin or iothalamate, it has been found, that mean GFR in groups of short-term IDDM patients is increased by 15-25% - to approximately 135-140 ml/min/1.73m2 during 'usual metabolic control' [3-7]. Before start of insulin treatment, but in the absence of ketoacidosis, glomerular hyperfiltration is even more pronounced, often showing elevations of approximately 40% [8,9]. RPF is elevated synchronously

Mogensen CE (ed.) THE KIDNEY AND HYPERTENSION IN DIABETES MELLITUS. Copyright© 2004 by Martin Dunitz, a member of the Taylor & Francis Group, plc. All rights reserved.

with the increase in GFR, but less pronounced [3,5]. Estimation of RPF from renal clearance of hippuran appears to be a reliable measure also in the diabetic state [10].

During the first one or two decades of diabetes glomerular hyperfunction remains a characteristic feature of kidney function. In cross-sectional studies patients with microalbuminuria - typically developed after 10 to 15 years of diabetes - show more pronounced hyperfiltration than normoalbuminuric patients [7,11]. However, no prospective studies have described the individual course in GFR during transmission from normo- to microalbuminuria. With further increase in albumin excretion and development of nephropathy, GFR and RPF start to decline, whereas in patients with persistent normoalbuminuria a moderate degree of glomerular hyperfunction persists [12].

Early renal changes in experimental diabetes in some degree parallel the characteristic glomerular hyperfunction in early stages of human diabetes. As described elsewhere in this book, besides hyperperfusion, increased intraglomerular hydraulic pressure is an important factor in hyperfiltration in diabetic animals. In humans the larger increase in GFR than RPF (increased filtration fraction) suggests similar intraglomerular hypertension. However, elevation of the ultrafiltration coefficient due to increased filtration surface may also represent a mechanism for the increased filtration fraction [13].

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