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http://dx.doi.org/10.1016/s0140-6736(73)91351-2 | DOI Listing |
Clin Exp Nephrol
December 2016
Department of Internal Medicine and Rehabilitation Science, Tohoku University Graduate School of Medicine, Sendai, Japan.
Background: Proteinuria plays an essential role in the progression of tubulointerstitial damage, which causes end-stage renal disease. An increased load of fatty acids bound to albumin reabsorbed into proximal tubular epithelial cells (PTECs) contributes to tubulointerstitial damage. Fibrates, agonists of peroxisome proliferator-activated receptor α (PPARα), have renoprotective effects against proteinuria whereas the effects of these compounds on fatty acid metabolism in the kidney are still unknown.
View Article and Find Full Text PDFJpn J Pharmacol
January 1996
Department of Pharmacology, Meijo University, Nagoya, Japan.
The possibility that hyperlipidemia and an increase of mononuclear cells in the glomeruli could participate in the pathogenesis of minimal change glomerulopathy was evaluated in puromycin aminonucleoside (PAN) nephrosis in rats. Significant increases in intraglomerular CD4-, IL-2-receptor (R)- and ED-1-positive cells were found in PAN rats. Urinary protein excretion and mononuclear cells in the glomeruli of 1% cholesterol diet-fed rats significantly increased, compared with standard diet feeding.
View Article and Find Full Text PDFAm J Nephrol
January 1991
Columbia-Presbyterian Medical Center, New York, N.Y.
Hyperlipidemia is common in patients with glomerular proteinuria. It may contribute to atherosclerotic complications and accelerate glomerular damage. Early trials of the fibric acid derivative clofibrate led to a myositis syndrome causing many nephrologists to abandon attempts at treatment of nephrotic hyperlipidemia.
View Article and Find Full Text PDFThe results of integrated estimations of a complex of lipid indices are presented. Their abnormalities are considered to be atherosclerosis risk factors in the evolution of glomerulonephritis and its different variants, types and stages. The quantitative and qualitative peculiarities of the indicated abnormalities are revealed, in particular, their major expressiveness in chronic form, nephrotic variant and in the stage of renal failure.
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