Neonatal parathyroid secretion and renal receptor maturation in premature infants.
16 premature infants with normal trophicity were studied during the 1st week of life using serum parathormone (IPTH) dosage and evaluation of renal tubule maturation by the effect of exogenous parathormone (PTE) on urinary elimination of 3':5'-cyclic adenosine monophosphate (cAMP). As of the 1st day, IPTH levels reached or surpassed those in the adult. Prematurity thus does not appear to influence parathormone response. Given the specificity of the dosage antiserum, it appears reasonable that the PTH detected is biologically active. After PTE, urinary elimination of cAMP does not appreciably increase until the 6th day, while still remaining much lower than adult levels. The lower the weight of the premature infant, the less intense the response of the kidney. It thus seems possible that the later development of renal parathormone receptor in the premature infant may be a factor responsible for neonatal hypocalcemia with hyperphosphatemia.
D001835:Body Weight; D000242:Cyclic AMP / Q000652:urine; D005260:Female; D005865:Gestational Age; D006801:Humans; D007231:Infant, Newborn; D007234:Infant, Premature; D007668:Kidney / Q000254:growth & development* / Q000502:physiology; D007684:Kidney Tubules / Q000254:growth & development; D008297:Male; D010281:Parathyroid Hormone / Q000097:blood / Q000378:metabolism*; D010710:Phosphates / Q000652:urine; D011956:Receptors, Cell Surface / Q000502:physiology*
D010281:Parathyroid Hormone; D010710:Phosphates; D011956:Receptors, Cell Surface; D000242:Cyclic AMP