title: 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.
authors.affiliation: Harold Simmons Center for Kidney Disease Research and Epidemiology, Division of Nephrology and Hypertension, University of California Irvine Medical Center, Orange, CA. Electronic address: estreja@uci.edu.
authors.forename: Elani
authors.initials: E
authors.lastname: Streja
authors.affiliation: Nephrology Section, Memphis Veterans Affairs Medical Center, Memphis, TN; Division of Nephrology, University of Tennessee Health Science Center, Memphis, TN.
authors.forename: Csaba P
authors.initials: CP
authors.lastname: Kovesdy
authors.affiliation: Infosphere Clinical Research, West Hills, CA; Providence Medical Group, West Hills, CA.
authors.forename: Dan A
authors.initials: DA
authors.lastname: Streja
authors.affiliation: Harold Simmons Center for Kidney Disease Research and Epidemiology, Division of Nephrology and Hypertension, University of California Irvine Medical Center, Orange, CA.
authors.forename: Hamid
authors.initials: H
authors.lastname: Moradi
authors.affiliation: Harold Simmons Center for Kidney Disease Research and Epidemiology, Division of Nephrology and Hypertension, University of California Irvine Medical Center, Orange, CA; Department of Medicine, UC Irvine School of Medicine, Irvine, CA.
authors.forename: Kamyar
authors.initials: K
authors.lastname: Kalantar-Zadeh
authors.affiliation: Department of Medicine, UC Irvine School of Medicine, Irvine, CA; Atherosclerosis Research Center, Long Beach Veteran Affairs Healthcare System, Long Beach, CA. Electronic address: moti.kashyap@va.gov.
authors.forename: Moti L
authors.initials: ML
authors.lastname: Kashyap
mesh_terms: D015897:Comorbidity; D003324:Coronary Artery Disease / Q000453:epidemiology; D018450:Disease Progression; D004730:Endothelium, Vascular / Q000187:drug effects; D006801:Humans; D000960:Hypolipidemic Agents / Q000494:pharmacology / Q000627:therapeutic use*; D009525:Niacin / Q000494:pharmacology / Q000627:therapeutic use*; D018384:Oxidative Stress / Q000187:drug effects; D051436:Renal Insufficiency, Chronic / Q000453:epidemiology / Q000503:physiopathology / Q000517:prevention & control*; D014280:Triglycerides / Q000097:blood
chemical_list: D000960:Hypolipidemic Agents; D014280:Triglycerides; D009525:Niacin
keywords: HDL function; Niacin; cardiovascular disease; chronic kidney disease; hyperphosphatemia; phosphorus absorption