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Renal aspects of calcium and phosphorus metabolism in preterm infants
1Service de Néonatologie, Université de Liège, Belgique.
Insights
This study on preterm infants highlights how kidney function impacts calcium and phosphorus balance. Proper milk formulas are crucial for growth, preventing issues like phosphate depletion or hyperphosphatemia.
Area of Science:
- Nephrology
- Pediatric Endocrinology
- Nutritional Science
Background:
- Preterm infants exhibit unique challenges in mineral metabolism.
- Renal handling of calcium and phosphorus is critical for growth and development in neonates.
Purpose of the Study:
- To analyze renal aspects of calcium and phosphorus metabolism in preterm infants.
- To correlate metabolic balance studies with renal function and vitamin D activation.
- To provide clinical guidance on optimizing mineral intake for preterm infants.
Main Methods:
- Analysis of over 200 metabolic balance studies in preterm infants.
- Assessment of renal vitamin D metabolism (1,25-dihydroxyvitamin D production).
- Evaluation of renal phosphate handling, including tubular reabsorption thresholds and fractional excretion.
Main Results:
- Renal 1,25-dihydroxyvitamin D production increases post-birth if 25-hydroxyvitamin D is sufficient.
- Preterm infant gut responds to active vitamin D metabolites.
- High plasma phosphate threshold (2.1 mmol/l) for tubular reabsorption.
- Low fractional phosphate excretion is linked to growth rate, not parathyroid function.
- Inadequate phosphorus intake causes phosphate depletion with increased urinary calcium.
- Excessive phosphorus intake can lead to hyperphosphatemia due to reduced GFR.
Conclusions:
- Renal function significantly influences calcium and phosphorus homeostasis in preterm infants.
- Growth rate is a key factor in renal phosphate regulation.
- Careful adjustment of the calcium:phosphorus ratio in milk is essential for optimal bone and soft tissue accretion.
Abstract:
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.