CHOLESTEROL-LOWERING THERAPY MAY RETARD THE PROGRESSION OF DIABETIC NEPHROPATHY

There is experimental evidence to suggest that hypercholesterolaemia m ay play a pathogenetic role in progressive glomerular injury. We inves tigated the effect of cholesterol-lowering therapy on the progression of diabetic nephropathy in 34 patients with non-insulin-dependent diab etes mellitus. Patients were randomly assigned in a single-blind fashi on to treatment with either lovastatin, an HMG CoA reductase inhibitor (n = 16; mean dose 30.0 +/- 12.6 mg/day) or placebo (n = 18) for 2 ye ars. Renal function was assessed by serially measuring the serum creat inine, glomerular filtration rate (using Cr-51-EDTA), and 24-h urinary protein excretion. Lovastatin treatment was associated with significa nt reductions in total cholesterol (p < 0.001), LDL-cholesterol (p < 0 .001) and apo B (p < 0.01), the reductions at 24 months being 26, 30 a nd 18%, respectively. Beneficial effects on serum triglyceride, HDL-ch olesterol and apo Al levels were also observed. Lp(a) showed no signif icant change in both groups. Glomerular filtration rate deteriorated s ignificantly in the placebo group after 24 months (p < 0.025) but show ed no significant change in the lovastatin-treated patients. The incre ase in serum creatinine was statistically significant (p < 0.02) in pl acebo-treated patients at 12 and 24 months, and in the lovastatin grou p after 24 months. Twenty-four hour urinary protein excretion increase d in both groups (p < 0.05). Lovastatin treatment was not associated w ith significant elevations in liver or muscle enzymes. We conclude tha t effective normalisation of hypercholesterolaemia may retard the prog ression of diabetic nephropathy.