Niacin only modestly reduces serum phosphate levels in patients with chronic kidney disease (CKD) and cardiovascular disease, researchers concluded in a report published online in the Clinical Journal of the American Society of Nephrology.

In a subgroup analysis of the randomized AIM-HIGH (Atherothrombosis Intervention in Metabolic Syndrome with Low HDL/High Triglycerides: Impact on Global Health) trial, Joachim H. Ix, MD, of the University of California San Diego, and colleagues examined the effects of extended-release niacin (1500 or 2000 mg) or placebo in 352 participants with an estimated glomerular filtration rate (eGFR) below 60 mL/min/1.73 m2. Unlike phosphate binders, niacin inhibits an intestinal sodium phosphate co-transporter.

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Niacin therapy lowered plasma phosphate 0.08 mg/dL per year and 0.25 mg/dL over 3 years, compared with placebo. In the niacin group, plasma phosphate declined from 3.4 to 3.3 mg/dL at 3 years, whereas in the placebo group, it rose from 3.4 to 3.6 mg/dL.

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Niacin demonstrated no significant effect on other markers of mineral bone disorder, including intact fibroblast growth factor 23, parathyroid hormone, calcium, or vitamin D metabolites over 3 years.

Although niacin decreases phosphate concentrations, the observed effects were relatively modest in magnitude, according to the researchers.

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“These findings, in the context of prior studies, do not support use of niacin in isolation for the purposes of cardiovascular disease prevention in CKD,” Dr Ix and his team concluded. “However, future trials combining niacin or nicotinamide with phosphate binders or other phosphate-lowering therapies may provide new synergistic opportunities for attacking mineral bone disorders in patients with CKD.”

In an accompanying editorial, Tilman B. Drüeke, MD, and Ziad A. Massy, MD, PhD, noted that although the observed effect of niacin on phosphate was statistically significant, the clinical relevance “seems to be poor, at least when considered solely on the basis of changes in essentially normal plasma levels at baseline. Information on changes in urinary phosphate excretion might have helped to obtain a more favorable view of niacin’s effect on phosphate control.”


Malhotra R, Katz R, Hoofnagle A, Bostom A, et al. The effect of extended release niacin on markers of mineral metabolism in CKD. Clin J Am Soc Nephrol. doi: 10.2215/CJN.05440517

Drueke TB and Massy ZA. Lowering expectations with niacin treatment for CKD-MBD. Clin J Am Soc Nephrol. doi: 10.2215/CJN.12021017