Urinary phosphate and cyclic AMP excretion following citrate-induced hypocalcemic stimulation of the neonatal parathyroid glands.
Sixteen neonates, ranging in gestational age from 27 to 41 weeks and in postnatal age from birth to 8 days, were evaluated for their renal response to an endogenous PTH stimulus in 22 separate experiments. The PTH stimulus was generated by the decreased serum ionized Ca that accompanies exchange transfusion with citrated blood. The neonates increased their serum PTH from 95.8 +/- 13.1 to 133.9 +/- 15.4 microliterEq/ml (mean +/- SEM) during the transfusion, while increasing their urinary cAMP from 0.77 +/- 0.11 to 1.45 +/- 0.22 nmol/ml, and their urinary P from 12.9 +/- 2.6 to 30.6 +/- 6.1 mg/dl in the four hours following the exchange transfusion. This response was not related to postnatal or gestational age. We speculate that lack of renal responsiveness to PTH does not play a major role in the pathogenesis of early neonatal hypocalcemia.
D002951:Citrates / Q000494:pharmacology*; D000242:Cyclic AMP / Q000652:urine*; D005078:Exchange Transfusion, Whole Blood; D005260:Female; D006801:Humans; D006996:Hypocalcemia / Q000503:physiopathology*; D007231:Infant, Newborn; D007232:Infant, Newborn, Diseases / Q000503:physiopathology*; D007477:Ions; D008297:Male; D010280:Parathyroid Glands / Q000187:drug effects*; D010281:Parathyroid Hormone / Q000097:blood / Q000502:physiology; D010710:Phosphates / Q000652:urine*; D013268:Stimulation, Chemical
D002951:Citrates; D007477:Ions; D010281:Parathyroid Hormone; D010710:Phosphates; D000242:Cyclic AMP