title: Renal excretion of calcium and phosphorus in premature infants with incipient late metabolic acidosis.
abstract: BACKGROUND
  Premature infants receiving alimentation with cow milk-based formulas run a considerably high risk of incipient late metabolic acidosis, an early stage developing of manifest late metabolic acidosis. Is bone metabolism involved in pathophysiologic mechanisms characterizing this early stage of retention acidosis?
  
  
  METHODS
  Urinary ionography was performed in 10 premature infants with spontaneous development of incipient late metabolic acidosis (indicated by urine pH < 5.4 on 2 consecutive days) and 10 pair-matched premature infants with normal values of urine pH; both groups were receiving full oral nutrition with the same standard formula. Moreover, in 37 premature infants with incipient late metabolic acidosis who were randomly allocated to oral therapy with 2 mmol. kg(-1). d(-1) of either NaHCO 3 or NaCl over a period of 7 days, urinary excretion of calcium and phosphorus was assessed on day 1 and day 7.
  
  
  RESULTS
  Incipient late metabolic acidosis was accompanied by increased phosphaturia in premature infants receiving full oral nutrition. Seventeen premature infants receiving NaCl therapy (19 treatment periods) showed increased calciuria from day 1 to day 7, whereas, in 20 premature infants receiving NaHCO 3 therapy (23 treatment periods), calcium or phosphorus excretion in urine did not increase.
  
  
  CONCLUSIONS
  The data of urinary calcium and phosphorus excretion in premature infants support the hypothesis that bone mineralization may already be impaired in the early stage of incipient late metabolic acidosis.
authors.affiliation: Pediatric Clinic and Research Institute of Child Nutrition, Beurhausstrasse 40, D-44137 Dortmund, Germany. kalhoff@klinikendortmund.de
authors.forename: H
authors.initials: H
authors.lastname: Kalhoff
authors.forename: L
authors.initials: L
authors.lastname: Diekmann
authors.forename: S
authors.initials: S
authors.lastname: Rudloff
authors.forename: F
authors.initials: F
authors.lastname: Manz
mesh_terms: D000141:Acidosis, Renal Tubular / Q000188:drug therapy / Q000503:physiopathology / Q000652:urine*; D001846:Bone Development / Q000502:physiology*; D001842:Bone and Bones / Q000378:metabolism*; D002118:Calcium / Q000652:urine*; D006801:Humans; D006863:Hydrogen-Ion Concentration; D007223:Infant; D007230:Infant, Low Birth Weight; D007231:Infant, Newborn; D007234:Infant, Premature; D007235:Infant, Premature, Diseases / Q000188:drug therapy / Q000503:physiopathology / Q000652:urine*; D007668:Kidney / Q000502:physiology; D010758:Phosphorus / Q000652:urine*; D017693:Sodium Bicarbonate / Q000627:therapeutic use; D012965:Sodium Chloride / Q000627:therapeutic use
chemical_list: D010758:Phosphorus; D012965:Sodium Chloride; D017693:Sodium Bicarbonate; D002118:Calcium