Lipids and progressive kidney disease.
The nephrotic syndrome comprises proteinuria, oedema, albuminuria, hypoalbuminaemia, and hyperlipidaemia. Some of its manifestations are present throughout the course of progressive renal disease. Hyperlipidaemia is one of the most dramatic of the clinical manifestations of the syndrome, but has not been seen as relevant to the progression of renal disease. Recently, however, increasing interest has been shown in the lipid abnormalities of patients with persistent proteinuria, largely as a result of experimental data which have emphasised the connection between progressive disease and hyperlipidaemia in animal models. This review considers some aspects of the metabolic background against which the pathological changes in animal models of nephrotic syndrome take place. Attention is drawn to analogies between glomerular disease and atherosclerosis. Lack of information on the value of long-term lipid lowering therapy in patients with proteinuria, hyperlipidaemia, and progressive renal disease emphasises the need for long-term studies of lipid-lowering therapy in these individuals. A conceptual framework for understanding the role of lipids is discussed in relation to the underlying disease processes and possible therapeutic approaches in man.
Moorhead
J F
JF
Department of Nephrology, Royal Free Hospital, London, England, United Kingdom.
D000818:Animals; D001161:Arteriosclerosis / Q000378:metabolism; D015777:Eicosanoids / Q000096:biosynthesis; D005920:Glomerular Mesangium / Q000378:metabolism; D006949:Hyperlipidemias / Q000150:complications / Q000378:metabolism; D050356:Lipid Metabolism; D008264:Macrophages / Q000378:metabolism; D009404:Nephrotic Syndrome / Q000209:etiology / Q000378:metabolism*; D011507:Proteinuria / Q000150:complications
D015777:Eicosanoids