The question of primary lipid nephrotoxicity

Abstract

Half a century ago, Bagdade [1] reported hypertriglyceridaemia in haemodialysis patients. Since then, the serum lipoprotein patterns of the various forms of kidney disease have been amply documented. In patients with reduced kidney function, this pattern is characterized by increases in triglycerides, apolipoprotein CIII and remnant particles as well as decreases in high-density lipoprotein (HDL) cholesterol and apolipoprotein A1. Low-density lipoprotein (LDL) cholesterol and apolipoprotein B are generally reported to be similar to those of healthy individuals. This pattern, largely explained by delayed removal of triglyceride-rich lipoproteins and disturbed synthesis of apolipoproteins in the liver, is full-blown in end-stage renal disease but changes can be detected early in chronic kidney disease [2, 3]. The focus of lipoprotein research in nephrology has changed. Small studies, documenting and searching for pathophysiological mechanisms of dyslipoproteinaemia, have been replaced by large treatment trials and risk estimations with regard to cardiovascular disease and kidney function. This development is rational; the prevalence of chronic kidney disease is steadily increasing worldwide; there are many indications that dyslipoproteinaemia accelerates the progress of chronic kidney disease, and the cardiovascular risk is manifold in patients with reduced kidney function, increasing early in that process [4]. The entry of the statins has radically changed the treatment scene, even though the impact of lipid-modifying treatment in chronic kidney disease has not been fully elucidated.