Treatment of hyperlipidemia in human renal disease.

Existing evidence suggests that dyslipidemia associated with long-lasting nephrotic syndrome and with chronic renal insufficiency may favor in the long run the occurrence of cardiovascular complications, and also aggravate glomerular damage with a pathological mechanism analogous to atherosclerosis. Correction of hypercholesterolemia and hypertriglyceridemia is therefore mandatory in both clinical conditions. This goal can be achieved with the combination of dietary intervention and the administration, even for long periods of time, of hypolipemic drugs (hydroxymethylglutaryl coenzyme A, HMGCoA, reductase inhibitors, to correct hypercholesterolemia in nephrotic syndrome, and fibric acids, to correct hypertriglyceridemia in uremic and dialyzed patients are the drugs of choice). In end-stage renal failure, the choice of the type of dialysis is also important. The value of extracorporeal LDL cholesterol removal is still to be proven.

Aminonucleoside nephrosis in rats. Ultrastructural findings in the glomerulus by concomitant influence of indomethacin and aminonucleoside.

The concomitant administration of Indomethacin reduced the biochemical signs of the nephrotic syndrome induced in rats by aminonucleoside; in the rats treated with both drugs a morphological picture suggesting activated function of podocytes was found at the electron microscopic examination of the renal glomerular structures, together with the lesions characteristic of the aminonucleoside nephrosis. The possibility is discussed that Indomethacin could modify the permeability of the glomerular capillary wall by stimulating the podocytes to synthesize basement membrane material.