Previous cellular, animal, and human studies suggest that increasing plasma HDL cholesterol may modulate insulin secretion. 5,[20][21][22] Cholesteryl ester transfer protein (CETP) inhibition increases plasma HDL cholesterol via a reduction in the transfer of neutral lipids (triglycerides and cholesteryl esters) between HDL and triglyceride-rich lipoprotein particles. The efficacy of this strategy to improve cardiovascular outcomes has not yet been determined, and there is controversy regarding whether CETP inhibition might produce a dysfunctional form of HDL cholesterol, which is less efficient at promoting reverse cholesterol transport than native HDL. 23 This controversy has arisen, in part, because of the early termination of 2 CETP inhibitor trials resulting from adverse events in the case of torcetrapib 24

BackgroundThe contribution of pro-inflammatory markers to cardiovascular (CV) risk and vascular calcification in chronic kidney disease (CKD) remains largely to be elucidated. We investigated the association between plasma levels of several biomarkers and calcification volume in three different vascular beds in CKD Stages 3 and 4 patients.MethodsThis is a cross-sectional, exploratory study in patients with an estimated glomerular filtration rate (eGFR) ≥20 and ≤45 mL/min/1.73 m2 and serum phosphorus ≥3.5 and <6.0 mg/dL enrolled in a previously published randomized, double blind, placebo-controlled single-centre trial. Ethylenediaminetetraacetic acid (EDTA) plasma samples were collected at baseline before patients received study medication and analysed for the presence of a number of biomarkers. Coronary artery calcium (CAC), thoracic aortic calcification (TAC) and abdominal aortic calcification (AAC) volumes were measured using standard electron-beam computed tomography protocols. Associations were adjusted for age, sex, smoking, body mass index, diabetes mellitus status, low-density lipoprotein cholesterol (LDL-C), systolic blood pressure and eGFR.ResultsAssociations with CAC were found for β2-microglobulin (B2M), fibroblast growth factor 23 (FGF23), interleukin-8 (IL-8) and IL-18. AAC was associated with: B2M, FGF23 and IL-2 receptor alpha (IL-2 RA). TAC was associated with: B2M, FGF23, IL-2 RA, IL-18 and tumour necrosis factor receptor type I. For most of the analysed biomarkers, there were non-significant trends of associations with calcification.ConclusionsThis exploratory study found that elevated plasma levels of several inflammatory biomarkers are significantly associated with arterial calcification in CKD Stages 3 and 4 patients. A greater understanding of inflammation and calcification in CKD patients may help the development of CV risk-assessment algorithms for better management of these patients.

The registry provides the first detailed data about the reality of treatment of IBD patients in Germany and reveals the necessity for networking among attending physicians in order to implement guidelines-conformed treatment.

To enable early detection of DIN and to ensure patients' safety through appropriate risk minimization and mitigation strategies, future research should focus on identification and validation of novel predictive biomarkers of kidney injury and development of DIN-specific classification and staging system. This could help in reducing the current high rate of attrition during drug development, and reduce marketing and post-marketing withdrawals of nephrotoxic drugs.