Disturbances of the lipid metabolism in chronic renal failure (CRF) are characterized by an accumulation of serum VLDL, IDL, and remnants and also by a decrease of the HDL pool, especially for HDL2. CRF is also associated with a decrease of apolipoproteins (apo) AI and AII in relation to a preferential decrease of lipoparticles (Lp) AI-AII by comparison with the anti-atherogenic Lp AI containing no AII. It is furthermore characterized by a marked increase of apo CIII, which is disproportionate with respect to the increase of apo CII and the variation of apo E, in relation with an accumulation of Lp B-CIII (and also Lp B-E and Lp B-C-E for hemodialyzed patients) in the whole spectrum of low density lipoproteins. The abnormal distribution of apo into the various classes of lipoproteins is the consequence firstly of the relative inefficacy of the lipolytic process implicated in TG-rich lipoprotein metabolism (LPL dysfunction), and secondly of the abnormal reverse cholesterol transport (anomalies of CETP and LCAT). The hormonal, nutritional, and iatrogenic factors implicated in the uremic dyslipoproteinemia are described and the implications of such abnormalities on cardiovascular disease and on the progression of renal disease are discussed.