Lipids, protein intake, and diabetic nephropathy

Progressive impairment of kidney function is one of the major problems in diabetic patients. Control of glycaemia and blood pressure is the main strategy for preventing or slowing impairment in renal function in this condition. However, contributing factors such as hyperlipidaemia and high protein intake have now been identified, and their control can be regarded as a complementary measure. The role of lipid abnormalities and hypercholesterolaemia in the pathogenesis of glomerular injury has been demonstrated in animal models, and a link between hypercholesterolaemia and diabetic nephropathy has been established in humans. To date, few intervention studies in diabetic 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 not be the cause of renal injury, it represents an aggravating factor. High serum cholesterol seems to have a similar action on glomerular mesangial cells and endothelial cells. This appears to be analogous to the process of atherosclerosis, as mesangial cells possess binding sites for LDL and oxidised LDL, help recruit macrophages and secrete proliferative factors. Protein intake is another factor that can influence renal deterioration. Two meta-analyses have confirmed the beneficial effect of a low-protein diet in diabetic nephropathy, showing no adverse effects on the glycaemic control. Protein intake even seems to enhance the sensitivity of tissues and liver to insulin. Thus, there appear to be no contraindications to such diets in well-controlled diabetic patients. In short, although glycaemic and blood pressure control are still the main lines of treatment for diabetic patients, lowering blood cholesterol and restricting protein intake represent complementary measures that can help slow renal impairment.