Niacin and progression of CKD.

Niacin is the oldest drug available for the treatment of dyslipidemia. It has been studied extensively and tested in clinical trials of atherosclerotic cardiovascular disease prevention and regression in the general population, but not specifically in patients with chronic kidney disease (CKD), who are at extremely high residual risk despite current therapy. Despite the current controversy about recent trials with niacin, including their limitations, there may be a place for this agent in select patients with CKD with dyslipidemia. Niacin has a favorable unique impact on factors affecting the rate of glomerular filtration rate decline, including high-density lipoprotein (HDL) particle number and function, triglyceride levels, oxidant stress, inflammation and endothelial function, and lowering of serum phosphorus levels by reducing dietary phosphorus absorption in the gastrointestinal tract. These effects may slow glomerular filtration rate decline and ultimately improve CKD outcomes and prevent cardiovascular risk. This review presents the clinically relevant concept that niacin holds significant potential as a renoprotective therapeutic agent. In addition, this review concludes that clinical investigations to assess the effect of niacin (in addition to aggressive low-density lipoprotein cholesterol lowering) on reduction of cardiovascular events in patients with CKD with very low HDL cholesterol (or those with identified dysfunctional HDL) and elevated triglyceride levels need to be considered seriously to address the high residual risk in this population.

Precision Medicine and Personalized Management of Lipoprotein and Lipid Disorders in Chronic and End-Stage Kidney Disease.

Precision medicine is an emerging field that calls for individualization of treatment strategies based on characteristics unique to each patient. In lipid management, current guidelines are driven mainly by clinical trial results that presently indicate that patients with non-dialysis-dependent chronic kidney disease (CKD) should be treated with a ß-hydroxy ß-methylglutaryl-CoA reductase inhibitor, also known as statin therapy. For patients with end-stage kidney disease (ESKD) being treated with hemodialysis, statin therapy has not been shown to successfully reduce poor outcomes in trials and therefore is not recommended. The two major guidelines dissent on whether statin therapy should be of moderate or high intensity in non-dialysis-dependent CKD patients, but often leave the prescribing clinician to make that decision. These decisions often are complicated by the increased concerns for adverse events such as myopathies in patients with advanced kidney disease and ESKD. In the future, there may be an opportunity to further identify CKD and ESKD patients who are more likely to benefit from lipid-modifying therapy as opposed to those who likely will suffer from its side effects using precision medicine tools. For now, data from genetics studies and subgroup analyses may provide insight for future research directions in this field and we review some of the work that has been published in this regard.

Optimizing diabetes management through glucose profiling: a case-based approach.

It is well documented that tight glucose control prevents the microvascular complications of diabetes, and many studies suggest that postprandial hyperglycemia may be associated with macrovascular complications. Maintaining target glucose values is challenging, as therapies are often not targeted to individual glucose excursion patterns. Postprandial SMBG values may be more tightly correlated to HbA1c than are fasting values. Studies of patients with pregnancies complicated by diabetes demonstrate that using SMBG around meals significantly improves glucose control and pregnancy outcomes. Adopting this model in type 2 diabetes may help achieve better glycemic control.