Abstract: SA-PO0569
Discordant Tubular Phosphate Conservation in Metabolic Bone Disease of Prematurity in an Extremely Preterm Infant
Session Information
- Bones, Stones, and Mineral Metabolism: Research and Cases
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Bone and Mineral Metabolism
- 502 Bone and Mineral Metabolism: Clinical
Authors
- Shanavas, Rayhan Shahid, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States
- Rhee, Raju, Kerala Genome Data Centre, Thiruvananthapuram, Kerela, India
- Illaparambath, Rahul, IQRAA International Hospital and Research Centre, Kozhikode, KL, India
Introduction
Metabolic bone disease of prematurity is commonly monitored using serum calcium, phosphorus, and alkaline phosphatase (ALP). Persistent hypophosphatemia despite supplementation is often attributed to inadequate intake or skeletal demand, but renal phosphate handling may reveal a distinct physiology.
Case Description
A male infant born at 23+6 weeks' gestation developed progressive biochemical metabolic bone disease of prematurity despite fortified feeds and mineral supplementation. Initial screening on day 24 showed calcium 9.6 mg/dL, phosphorus 4.2 mg/dL, and ALP 599 IU/L. During NICU progression, phosphorus declined to 3.2 mg/dL while ALP rose to 1424 IU/L, with calcium remaining within reference range. Extended evaluation showed elevated intact parathyroid hormone of 219.3 pg/mL, 25-hydroxyvitamin D of 27.2 ng/mL, tubular reabsorption of phosphate of 78%, and tubular maximum phosphate reabsorption per glomerular filtration rate of 0.8 mmol/L. In the setting of hypophosphatemia, reduced tubular phosphate conservation suggested PTH-associated phosphaturic physiology rather than intake limitation alone. There was no evidence of generalized proximal tubular dysfunction, hypercalciuria, impaired kidney function, or nephrocalcinosis. Management was adjusted to calcium carbonate with increased divided oral phosphate dosing. Before discharge, phosphorus improved to 4.4 mg/dL and ALP began to decline, although PTH remained elevated, suggesting delayed endocrine recovery. Post-discharge follow-up showed gradual normalization of PTH and continued ALP improvement.
Discussion
Persistent hypophosphatemia in metabolic bone disease of prematurity may reflect inappropriate renal phosphate loss despite supplementation. Incorporating PTH, tubular reabsorption of phosphate, and TmP/GFR into evaluation may help distinguish inadequate mineral delivery from phosphaturic physiology and support more targeted mineral management in extremely preterm infants.