Renal aspects of calcium and phosphorus metabolism in preterm infants.
The aim of this study is to emphasize renal aspects of calcium and phosphorus metabolism from our data of more than 200 metabolic balance studies carried out in preterm infants. Renal production of 1,25-dihydroxyvitamin D increased rapidly after birth provided the concentration of the substrate, 25-hydroxyvitamin D, is adequate. The gut of preterm infants is able to respond to the active metabolite of vitamin D. Mean plasma phosphate threshold for tubular reabsorption of phosphate is high, about 2.1 mmol/l or 6.5 mg/dl. The low fractional excretion of phosphate cannot be explained by immature parathyroid function nor by renal unresponsiveness to parathormone, at least after the first days of life. It is probably due to regulating factors related to the high rate of growth. Because of reduced glomerular filtration rate, a too high phosphorus intake may result in hyperphosphatemia. Conversely, a too low phosphorus intake will lead to a phosphate depletion syndrome characterized by marked increase in urinary calcium excretion, no urinary phosphate, and hypophosphatemia. Preterm infants with chronic metabolic acidosis are able to acidify urine so that titratable acid is directly related to urinary excretion of phosphate. Clinical implications are that calcium:phosphorus ratio in milk must be adapted according to net bone and soft tissue retention.
D000138:Acidosis / Q000378:metabolism; D002118:Calcium / Q000378:metabolism* / Q000652:urine; D006801:Humans; D007231:Infant, Newborn; D007234:Infant, Premature / Q000378:metabolism*; D007668:Kidney / Q000378:metabolism*; D007684:Kidney Tubules / Q000378:metabolism; D010281:Parathyroid Hormone / Q000502:physiology; D010710:Phosphates / Q000378:metabolism; D010758:Phosphorus / Q000378:metabolism*; D014807:Vitamin D / Q000378:metabolism
D010281:Parathyroid Hormone; D010710:Phosphates; D014807:Vitamin D; D010758:Phosphorus; D002118:Calcium