PubMed · 5498747
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J Richter, L Kny, K Gerecke. 1970. [Vasoactive agents. 48].. https://pubmed.ncbi.nlm.nih.gov/5498747/
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There is experimental evidence to suggest that hypercholesterolaemia may play a pathogenetic role in progressive glomerular injury. We investigated the effect of cholesterol-lowering therapy on the progression of diabetic nephropathy in 34 patients with non-insulin-dependent diabetes mellitus. Patients were randomly assigned in a single-blind fashion 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 years. Renal function was assessed by serially measuring the serum creatinine, glomerular filtration rate (using Cr51-EDTA), and 24-h urinary protein excretion. Lovastatin treatment was associated with significant 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 and 18%, respectively. Beneficial effects on serum triglyceride, HDL-cholesterol and apo A1 levels were also observed. Lp(a) showed no significant change in both groups. Glomerular filtration rate deteriorated significantly in the placebo group after 24 months (p < 0.025) but showed no significant change in the lovastatin-treated patients. The increase in serum creatinine was statistically significant (p < 0.02) in placebo-treated patients at 12 and 24 months, and in the lovastatin group after 24 months. Twenty-four hour urinary protein excretion increased in both groups (p < 0.05). Lovastatin treatment was not associated with significant elevations in liver or muscle enzymes. We conclude that effective normalisation of hypercholesterolaemia may retard the progression of diabetic nephropathy.
CLINICAL PROBLEM: To examine the evidence supporting the recent National Cholesterol Education Program (NCEP) recommendation that low to moderate levels of cholesterol should be aggressively managed in patients with coronary heart disease (CHD). METHODS: Cohort studies and clinical trials with angiographic or clinical endpoints, that included CHD patients with low to moderate levels of cholesterol, were systematically identified through a MEDLINE search and critically reviewed. SYNOPSIS: None of the cohort studies show that a moderate level of cholesterol confers significantly increased risk of CHD death, although a pooled relative risk of 1.14 (95% CI 1.08 to 1.4) suggests that there may be a slight excess risk. Of five angiographic trials of CHD patients with moderate levels of cholesterol, two demonstrated no improvement in angiographic endpoints with intensive lipid-lowering therapy and the other three are difficult to interpret since they included other interventions in addition to the cholesterol-lowering regimen. No large clinical trial with clinical endpoints has been reported for CHD patients with low to moderate levels of cholesterol. RECOMMENDATIONS: The recommendation to treat CHD patients who have low to moderate levels of cholesterol with diet or drugs is not based on convincing evidence of efficacy. This is in clear contrast to the recommendation for CHD patients with high levels of cholesterol, for whom there is definitive clinical trial evidence of benefit from cholesterol-lowering therapy. While we await clinical trial results for CHD patients with low to moderate levels of cholesterol, clinicians and patients must consider the possible disadvantages of therapy in relation to the uncertain benefit.