Bedside testing of CAPD fluid for bilirubin to aid diagnosis of visceral perforation.

of several large clinical trials, with cardiovascular disease (CVD) end-points, in the general population [2]. In the above-mentioned post hoc analyses, apart from the increased risk for type I errors [2], there are several limitations. Renal failure patients were excluded [1] and results regarding CKD progression are often based on fewer patients than initially included in the study [3]; glomerular filtration rate is indirectly estimated; adjustment for main factors influencing CKD progression is often incomplete and, when it is, changes the initial results [4], while data for albuminuria or microalbuminuria are frequently absent [5]. If the negative results of the ASCOT-LLA [6], VA-HIT [7] and ALERT [8] studies are added to these limitations, a motivated, based on post hoc analyses, reconsideration of the CPG seems, up to now, less urgent. On the other hand, considering the impressive results achieved by statin treatment in studies with CVD end-points in the general population and taking into account the dyslipidaemia patterns in CKD patients, a few points of interest in this particular population are worth highlighting. The main target, regarding lipids, in the majority of the studies in the general population, was elevated low-density lipoproteins (LDL) and total cholesterol (tChol). At initial stages of CKD, a similar dyslipidaemic pattern—due to nephrotic syndrome or to common causes of CKD such as diabetes, atherosclerosis, etc.—is frequently observed. Results based on studies in the general population can potentially be extrapolated (regarding hypolipidaemic treatment for CVD prevention) in CKD patients with a similar dyslipidaemic profile. The improvement of cardiovascular status—at least the haemodynamic benefit—should also be important for the stabilization or retardation of CKD progression. Furthermore, the pleiotropic effects of these drugs and specifically their actions on endothelial function, oxidative stress, inflammation, etc. might also be beneficial in slowing progression of CKD in this subgroup of patients. In contrast, in patients with severe CKD in whom the dyslipidaemic pattern approaches that of patients with end-stage renal failure (ESRF) in renal replacement treatment (who usually have elevated triglycerides, low high-density lipoproteins and normal or low tChol and LDL), extrapola-tion of the general population study results might no longer be appropriate (mainly because this dyslipidaemic profile does not exist in the populations included in these studies). Furthermore, hypertriglyceridaemia is better treated with fibrates or hypolipidaemic drugs other than statins, which do not seem to have any beneficial effects on CKD progression [7]. Moreover, cholesterol lowering in this subgroup of …