title: Oral phosphate supplementation corrects hypophosphatemia and normalizes plasma FGF23 and 25-hydroxyvitamin D3 levels in women with chronic metabolic acidosis.
abstract: BACKGROUND
  Chronic metabolic acidosis (CMA) is known to induce renal phosphate wasting and hypophosphatemia by enhancing bone resorption and inhibiting renal phosphate reabsorption. However, nothing is known regarding changes in the plasma levels of phosphate-regulating hormones during CMA, especially in humans with normal kidney function.
  
  
  METHODS
  Fifteen healthy Thai female volunteers were given NH (4)Cl orally for 7 days to induce CMA with or without oral phosphate supplementation. Blood and 24-h urine specimens were collected prior to and after CMA induction. Plasma concentrations and fractional excretion of calcium and inorganic phosphate as well as plasma levels of fibroblast growth factor (FGF) 23, 25(OH)D (3), 1,25(OH) (2)D (3) and intact parathyroid hormone (iPTH) were determined.
  
  
  RESULTS
  CMA led to hypophosphatemia and hypocalcemia with increases in the fractional excretion of calcium and phosphate. Plasma concentrations of FGF23, 25(OH)D (3) and iPTH were decreased, whereas that of 1,25(OH) (2)D (3) was increased. After oral phosphate supplementation, CMA-induced changes in the concentrations of the studied ions, FGF23 and 25(OH)D (3), but not those of 1,25(OH) (2)D (3) and iPTH, were diminished.
  
  
  CONCLUSIONS
  The CMA-induced hypophosphatemia was likely to initiate a negative feedback response, thereby leading to reduction in the plasma levels of hyperphosphaturic hormones, FGF23 and PTH. An increase in the plasma 1,25(OH) (2)D (3) level, despite diminishing 25(OH)D (3) storage pool, may help enhance the intestinal phosphate absorption. Oral phosphate supplementation abolished the effects of CMA on FGF23 and 25(OH)D (3) levels, suggesting that the plasma phosphate concentration is the primary regulator of the plasma levels of these hormones during CMA.
authors.affiliation: Consortium for Calcium and Bone Research, Faculty of Science, Mahidol University, Bangkok 10400, Thailand.
authors.forename: S
authors.initials: S
authors.lastname: Domrongkitchaiporn
authors.forename: S
authors.initials: S
authors.lastname: Disthabanchong
authors.forename: R
authors.initials: R
authors.lastname: Cheawchanthanakij
authors.forename: K
authors.initials: K
authors.lastname: Niticharoenpong
authors.forename: W
authors.initials: W
authors.lastname: Stitchantrakul
authors.forename: N
authors.initials: N
authors.lastname: Charoenphandhu
authors.forename: N
authors.initials: N
authors.lastname: Krishnamra
mesh_terms: D000138:Acidosis / Q000139:chemically induced* / Q000150:complications / Q000188:drug therapy*; D000284:Administration, Oral; D000328:Adult; D000643:Ammonium Chloride; D002112:Calcifediol / Q000097:blood*; D002908:Chronic Disease; D005260:Female; D000089703:Fibroblast Growth Factor-23; D005346:Fibroblast Growth Factors / Q000097:blood*; D006801:Humans; D017674:Hypophosphatemia / Q000139:chemically induced / Q000188:drug therapy* / Q000209:etiology; D008875:Middle Aged; D010710:Phosphates / Q000627:therapeutic use*; D018709:Statistics, Nonparametric
chemical_list: C000717427:FGF23 protein, human; D010710:Phosphates; D000643:Ammonium Chloride; D005346:Fibroblast Growth Factors; D000089703:Fibroblast Growth Factor-23; D002112:Calcifediol