Managing diabetic nephropathy

Abstract

The earliest sign of DN is the development of microalbuminuria which is associated with a significant risk of both progressive renal failure and premature death from cardiovascular disease. Optimal glycaemic and BP control, including the use of RAAS blocking drugs, can prevent, slow and even reverse the processes causing DN.

Figures

Fig 1.

Simplified scheme for pathogenesis of diabetic nephropathy. AGEs = advanced glycation end products; PDGF = platelet-derived growth factor; PKC = protein kinase C; RAAS = renin–angiotensin–aldosterone system; TGF = transforming growth factor; VEGF = vascular endothelial growth factor

Fig 2.

Glomerular haemodynamic changes in diabetic nephropathy: (a) normal glomerular capillary pressure and glomerular filtration; (b) glomerular capillary hypertension, glomerular hypertrophy and hyperfiltration associated with angiotensin II-mediated efferent arteriolar vasoconstriction; (c) development of microalbuminuria associated with thickened but ‘leaky’ glomerular basement membrane. Ang = angiotensin; BP = blood pressure; GFR = glomerular filtration rate.

Fig 3.

Annual transition rates through stages of nephropathy to death from any cause, as described in the UK Prospective Diabetes Study. RRT = renal replacement therapy. Adapted from Ref 6 with permission from Macmillan Publishers Ltd: Kidney International © 2003