By Gunter Stein
In accordance with the complaints of the foreign Workshop on Nephrology held lately in Berlin, Germany, this remarkable quantity provides the most recent study and scientific findings at the pathophysiology of persistent renal failure crucial for the advance of recent healing ways.
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Additional info for Pathogenetic and Therapeutic Aspects of Chronic Renal Failure
6. Kasiske BL, O'Donnell MP, Schmitz PG, Kim Y, Keane WF. Renal injury of diet-induced hypercholesterolemia in rats. Kidney Int 1990; 37:880891. 7. Kasiske BL, O'Donnell MP, Cleary MP, Keane WF. Treatment of hyperlipidemia reduces glomerular injury in obese Zucker rats. Kidney Int 1988; 33:667672. 8. Kasiske BL, O'Donnell MP, Garvis WJ, Keane WF. Pharmacologic treatment of hyperlipidemia reduces glomerular injury in rat 5/6 nephrectomy model of chronic renal failure. Circ Res 1988; 62:367374. 9.
In another study, LDL reduction by lovastatin did not change proteinuria in nephrotic subjects. The glomerular filtration rate (GFR) significantly increased, but only in patients with an initial GFR exceeding 70 ml/min (43). The dramatic decrease in serum LDL induced by LDL apheresis was accompanied by a more than 50% reduction of proteinuria in approximately 50% of the patients with therapy-resistant nephrotic syndrome. In some patients, a significant decrease in serum creatinine occurred (44).
Maneuvers that deplete circulating monocytes have been shown to reduce the number of infiltrating macrophages and diminish glomerular injury (17). Macrophages can release reactive oxygen species (ROS) and oxidize low-density lipoprotein (LDL). Oxidized LDL can be trapped into the mesangium more efficiency and contributes Page 23 again to the recruitment of monocytes directly or through the induction of chemoattractants (1821). The uptake of oxidized LDL and other lipoproteins by macrophages and mesangial cells stimulates the release of growth factors and cytokines, resulting in a new cycle of mesangial cell proliferation (19,2126).