Lipoprotein abnormalities are a regular part of metabolic changes associated with chronic renal failure. The character of dyslipoproteinaemia changes with the severity of disorders of renal functions, from initial deviations in the composition and distribution of circulating lipoprotein particles (a decline of glomerular filtration to 0.7-0.8 ml/s) to differently expressed changes of plasma lipid concentrations in terminal renal failure. The basis of the pathogenetic mechanism of these lipid abnormalities is the negative effect of the uraemic environment on the formation and catabolism of triglyceride-risk lipoproteins and on the function of the reverse cholesterol transport. An important part is also played by the modification of lipoprotein particles by oxidation and glycation. To a different extent also the nutritional status is manifested via the unfavourable composition of dietary fats, reduced effectiveness of antioxidant factors and in some instances also carnitine deficiency. Haemodialysis treatment and in particular peritoneal dialysis modify these lipid abnormalities. From the quantitative aspect renal dyslipoproteinaemia is not very striking, despite this its quantitative changes are important. It may have a negative impact on the progression of renal disease by its participation in the development of glomerular sclerosis and tubulointerstitial fibrosis. As one of the important risk factors it participates also in the acceleration of atherosclerosis in patients with chronic renal failure and in their much higher cardiovascular mortality as compared with the general population. These factors justify efforts to influence uraemic dyslipoproteinaemia. Fibrates or statins are indicated in conjunction with the supporting effect of diet and modification of the dialysis regimen. In tables and figures some results assembled by the authors are presented obtained in a group of dialyzed patients (characteristic of the lipid profile under basal conditions on fasting and after an oral lipid load and experience with influencing dysliopoproteinaemia by fenofibrates and atorvastatin).