Lipids, protein intake, and diabetic nephropathy

Progressive impairment of kidney function is one of the major problems in d iabetic patients. Control of glycaemia and blood presl sure is the main str ategy for preventing or slowing impairment in renal function in this condit ion. However, contributing factors such as hyperlipidaemia and high protein intake have now been identified, and their control can be regarded as a co mplementary measure. The role of lipid abnormalities and hypercholesterolae mia in the pathogenesis of glomerular injury has been demonstrated in anima l models, and a link between hypercholesterolaemia and diabetic nephropathy has been established in humans. To date, few intervention studies in diabe tic patients have shown a slower decline in renal function. Nonetheless, in every study in which follow-up was long enough, cholesterol lowering had a beneficial effect on renal function. Although hypercholesterolaemia may no t be the cause of renal injury, it represents an aggravating factor. High s erum cholesterol seems to have a similar action on glomerular mesangial cel ls and endothelial cells. This appears to he analogous to the process of at herosclerosis, as mesangial cells possess binding sites for LDL and oxidise d LDL help recruit macrophages and secrete proliferative factors. Protein i ntake is another factor that can influence renal deterioration. Two meta-an alyses have confirmed the beneficial effect of a low-protein diet in diabet ic nephropathy, showing no adverse effects on the glycaemic central. Protei n intake even seems to enhance the sensitivity of tissues and liver to insu lin. Thus, there appear to be no contraindications to such diets in well-co ntrolled diabetic patients. In short, although glycaemic and blood pressure control are still the main lines of treatment for diabetic patients, lower ing blood cholesterol and restricting protein intake represent complementar y measures that can help slow renal impairment.