Reducing lipids for CV protection in CKD patients-current evidence

Lipid parameters are altered in the earliest stages of primary kidney disease, some even when measured glomerular filtration rate (GFR) is still normal. The main problem is that routinely measured lipid parameters are deceivingly normal except low high-density lipoprotein (HDL) and moderately elevated triglycerides (TGs) (>150 mg per 100 ml). Behind this unimpressive spectrum, serious anomalies are hidden: increased very low-density lipoprotein (VLDL) and chylomicron remnants, accumulation of delipidated small dense low-density lipoprotein (LDL), post translational modification of lipoproteins, abnormal concentrations of Lp(a) and nonprotective HDL. A routine parameter with some predictive value is the concentration of non-HDL cholesterol. Several of these abnormal lipoprotein particles stimulate cellular free oxygen radical formation which in turn induce inflammation and impact on endothelial function. A bone of contention is the indication for treatment with statins in endstage renal disease. Poor survival is paradoxically predicted by low cholesterol. This appears to be the result of confounding by microinflammation. One controlled interventional study in hemodialysed type 2 diabetics, the 4-D study, failed to show a significant benefit on the primary cardiovascular endpoint. We discuss potential explanations for this 'negative' outcome and the implications for statin treatment.