Effects of Hypercholesterolemia on Renal Hemodynamics: Study in Patients with Nephrotic Syndrome

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Abstract
Experimental and clinical studies have demonstrated a positive relationship between hyperlipidemia and rate of progression of renal disease, suggesting that lipids can induce or aggravate glomerular injury mainly by interacting with mesangial cells. Nevertheless, recently, it has been demonstrated that increased cholesterol levels can also induce endothelial cell dysfunction. Thus, since endothelium is known to play a major role in modulating the vascular tone, we have tested the possibility that hypercholesterolemia impairs the renal hemodynamics in patients with active nephrotic syndrome and elevated serum cholesterol levels. In this single-blind, nonrandom study, 12 patients were treated with pravastatin (group T, treated, n = 12) and 8 with placebo (group C, controls, n = 8). The controls were studied after the pravastatin group had been completed. Before starting the treatment the patients underwent basal determinations including routine laboratory investigations and PAH and inulin clearances. The same determinations were repeated after 48 h, and 6 and 12 weeks from the beginning of the treatment. The study at 48 h was performed to see if pravastatin had a direct, cholesterol-independent effect on renal function. The following basal results were reported (mean ± SEM; group T vs. group C): serum cholesterol (mmol/l) 9.7 ± 0.4 vs. 9.1 ± 0.3 (NS); proteinuria (g/24 h):6.2 ± 0.2 vs. 7.0 ± 0.7 (NS); PAH clearance (ml/min): 353 ± 21 vs. 385 ± 31 (NS); inulin clearance (ml/min): 62.5 ± 7.7 vs. 67 ± 9.3 (NS). After 48 h, no changes were observed in both groups. Subsequently, in group T, the following percentage changes of basal levels were observed: serum cholesterol -21.4 ± 3.2% at 6 weeks (p PAH were significantly greater in group T (at 6 weeks: p

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