Hypophosphatemic effect of niacin extended release in ischemic kidney disease

Abstract

Ischemic nephropathy is an emerging cause of end stage renal disease, associated with many co-morbidities especially cardiovascular disease risk and derangement in calcium-phosphorus homeostasis resulting in hyperphosphatemia, influencing bones, a characteristic of advancing chronic kidney disease. The management of elevated serum phosphorus has been a challenge in this patient population with compromised kidney performance, as available phosphorus lowering agents possess many undesirable hazardous secondary effects and/or are very expensive. While niacin in different formulation is known to not only correct dyslipidemia but also reduce phosphorus level, but its clinical use restricted owing to side effects. The objective of present study is to evaluate such effect of niacin extended release (NER) in ischemic nephropathy. The chronic kidney disease patients fulfilling the pre-defined criteria were randomly categorized into two groups of equal size (n=60) and prescribed either atorvastatin 20 mg/day or NER 500 mg/day with the same dose of statin for four months. A control of 50 healthy characters matched was also incorporated for local reference range. Baseline and follow up phosphorus concentration was measured and means were compared using t-test at SPSS version 17 with 0.05 chosen alpha. There was no difference in the baseline levels in both groups while significant (p<0.001) hyperphosphatemia was observed in both units as compared with healthy controls. The administration of atorvastatin alone for four weeks showed an insignificant decrease in phosphorus, whereas, NER significantly reduced phosphorus (p<0.001). The mean percent change from baseline to follow up further endorsed the finding as statin alone brought -13.8 % reduction in phosphorus and NER -47 % from baseline. NER, at its lowest prescribed dose once a day was well tolerated by most of the patients and demonstrated significant goal achievement of phosphorus reduction. It is concluded that NER even at low doses in renal compromised dyslipidemic patients may be a promising approach to prevent the harmful vascular, valvular effects caused by hyperphosphatemia in addition to its principal target of HDL-C elevation.