Niacin and Progression of CKD

Abstract

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.

Gut microbiota and inflammation in chronic kidney disease and their roles in the development of cardiovascular disease

“…Conversely, the species found to be decreased in CKD are among those that strengthen gut barrier function [16,36,37]; produce anti-inflammatory [46,71,73,109], NO [16,47], CDCA, UDCA [50,[83][84][85], GABA [60,61,110], Ach [65,107,108], and the vitamin B complex [17, 52-54, 81, 82]; increase the production of gut hormones with anti-inflammatory properties [57][58][59][76][77][78][79]; increase anti-inflammatory vagal activity [90,93,97]; and decrease pro-inflammatory renal sympathetic activity. Interestingly, CKD is associated with gut barrier dysfunction, an increase in uremic toxins [101], elevated renal sympathetic activity [111], lower group B vitamin levels [112][113][114] and NO [115], and a reduction in vagal activity [116], which may stem from the gut dysbiosis found in patients with CKD. Therefore, we can suggest that a healthy gut microbiota can protect from CKD, whereas gut dysbiosis takes part in the development and progression of CKD through a number of pathways that manipulate host inflammatory activity.…”

Imaging niacin trafficking with positron emission tomography reveals in vivo monocarboxylate transporter distribution

“…Based on these results, [ 11 C]niacin might be a valuable tool for imaging renal, cardiac and liver function in humans, particularly in light of clinical studies suggesting a benefit of niacin use in pathologies such as chronic kidney [ 36 , 37 ] and liver diseases [ 38 ] and atherosclerosis [ 39 , 40 ].…”

Pleiotropic effects of niacin: Current possibilities for its clinical use

“…Niacin has a unique favorable impact on factors affecting the rate of glomerular filtration decline, including number of high-density lipoprotein (HDL) particles and their function, triacylglycerol levels, oxidative stress, inflammation and endothelial function. It also lowers serum phosphorus levels by reducing dietary phosphorus absorption in the gastrointestinal tract (106). Niacin has been observed to work best in patients with lipid-profile characteristics of CKD, i.e., patients with raised VLDL-TG and decreased HDL (107,20).…”