Dyslipidemia in chronic kidney disease

487 In 1836, Richard Bright commented on the “mil­ ky serum” of patients with (what today would be called) end­stage renal disease (ESRD) – almost certainly the first recognition of hyper­ lipidemia. The relation between heavy proteinu­ ria with dyslipidemia had been noted at the be­ ginning of the 20th century and indeed dyslip­ idemia in patients with nephrotic proteinuria differs in many respects from dyslipidemia in pa­ tients with chronic kidney disease (CKD) with non­nephrotic proteinuria, i.e. <3 g/day. Protei­ nuria per se is associated with dyslipidemia as dis­ cussed in detail by Kaysen.1,2 A more detailed dis­ cussion of the situation in nephrotic proteinuria is beyond the scope of this contribution. The causes of dyslipidemia are undoubtedly complex. An inter esting new hypothesis states that prenatal programming3, e.g. the result of in­ trauterine malnutrition, causes obesity, dyslipi­ demia, type 2 diabetes, and a deficit in nephron numbers, thus increasing in para llel cardiovas­ cular and renal risks (FIGURE)4. A potential fur­ ther contributor is impaired insulin resistance, a known component of meta bolic syndrome and type 2 diabetes, both of which are associated with dyslipidemia and kidney disease. Dyslipidemia in type 2 diabetes has recently been reviewed by Jandeleit­Dahm5 and by Krane6. Dyslipidemia7,8, and particularly the role of lipogenesis9 in non­ diabetic CKD, have recently been reviewed by Rutkowski. In the following we shall discuss: 1 the lipid profile in chronic kidney disease 2 the association of dyslipidemia with cardio­ vascular disease in CKD 3 the potential impact of dyslipidemia on pro­ gression of CKD 4 the available evidence from lipid lowering inter ventions in CKD.