Background And Objectives: Niacin administration lowers the marked hyperphosphatemia that is characteristic of renal failure. We examined whether niacin administration also reduces serum phosphorus concentrations in patients who have dyslipidemia and are free of advanced renal disease.
Design, Setting, Participants, & Measurements: We performed a post hoc data analysis of serum phosphorus concentrations that had been determined serially (at baseline and weeks 4, 8, 12, 18, and 24) among 1547 patients who had dyslipidemia and were randomly assigned in a 3:2:1 ratio to treatment with extended release niacin (ERN; 1 g/d for 4 weeks and dose advanced to 2 g/d for 20 weeks) combined with the selective prostaglandin D2 receptor subtype 1 inhibitor laropiprant (L; n = 761), ERN alone (n = 518), or placebo (n = 268).
Results: Repeated measures analysis revealed that ERN-L treatment resulted in a net mean (95% confidence interval) serum phosphorus change comparing ERN-L with placebo treatment of -0.13 mmol/L (-0.15 to -0.13 mmol/L; -0.41 mg/dl [-0.46 to -0.37 mg/dl]). These results were consistent across the subgroups defined by estimated GFR of <60 or > or =60 ml/min per 1.73 m(2), a serum phosphorus of >1.13 mmol/L (3.5 mg/dl) versus < or =1.13 mmol/L (3.5 mg/dl), the presence of clinical diabetes, or concomitant statin use.
Conclusions: We have provided definitive evidence that once-daily ERN-L treatment causes a sustained 0.13-mmol/L (0.4-mg/dl) reduction in serum phosphorus concentrations, approximately 10% from baseline, which is unaffected by estimated GFR ranging from 30 to > or =90 ml/min per 1.73 m(2) (i.e., stages 1 through 3 chronic kidney disease).
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http://dx.doi.org/10.2215/CJN.07341009 | DOI Listing |
Indian J Orthop
January 2025
Dayanand Medical College and Hospital, Tagore Nagar, civil lines, Ludhiana, Punjab 141001 India.
Purpose: There is paucity of guidelines with inadequate data available about the extent and prevention of bone and joint disease in beta-thalassemic patients in Indian population. This study aims to determine bone and joint involvement in beta-thalassemic patients. It evaluates serum biochemical parameters of bone formation and resorption and correlates with the symptomatology in these patients.
View Article and Find Full Text PDFPediatr Rep
December 2024
Department of Pediatrics, "Victor Babes" University of Medicine and Pharmacy, 300041 Timisoara, Romania.
Background: Pediatric chronic kidney disease (CKD) requires reliable biomarkers for early detection and monitoring. Neutrophil gelatinase-associated lipocalin (NGAL) has emerged as a potential marker due to its responsiveness to renal impairment and involvement in mineral metabolism.
Objectives: To evaluate serum NGAL levels in pediatric CKD patients and explore correlations with estimated glomerular filtration rate (eGFR), ferritin, calcium-phosphorus (Ca*P) product, and total serum protein.
Clin Transl Sci
January 2025
University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
Despite the widespread use of currently available serum phosphate management options, elevated serum phosphate is common in patients with end-stage kidney disease on dialysis. Characteristics of currently available phosphate binders that lead to poor patient experiences such as large drug volume size of required daily medication (e.g.
View Article and Find Full Text PDFProbl Radiac Med Radiobiol
December 2024
State Institution «National Research Center for Radiation Medicine, Hematology and Oncology of the National Academy of Medical Sciences of Ukraine», 53 Yuriya Illienka Street, Kyiv, 04050, Ukraine.
Parathyroids are the key regulators of calcium-phosphorus metabolism. By means of parathyroid hormone they respond to any changes in the serum level of calcium and phosphorus ions and determine the integrity of skeleton, affecting almost all systems and cells where calcium and phosphorus are involved in metabolism and/or signaling.Disorders of parathyroid function are associated with significant complications accompanying secondary hyperparathyroidism.
View Article and Find Full Text PDFMol Genet Metab Rep
December 2024
School of Medicine, Urmia University of Medical Sciences, Urmia, West Azerbaijan, Iran.
Objectives: Phenylketonuria is a hereditary condition caused by the deficiency of the enzyme phenylalanine hydroxylase, leading to abnormal phenylalanine metabolism. Managing phenylketonuria involves implementing dietary interventions to control phenylalanine levels and prevent complications. However, these treatments can lead to long-lasting negative effects, including impacts on bone health and abnormal biochemical test findings.
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