Introduction: I report the case of a premature neonate who developed a transient hyperphosphatemia at 1 month of age with associated hyperuremia, hypercreatininemia and hyperparathyroidism.
Case report: This baby girl was born by emergency caesarean section for maternal APH at 27+6 weeks. She had an uneventful neonatal period with minimal ventilation. She was treated with ibuprofen, amilorone and frusemide for a PDA with associated heart failure. Her enteral feeds had been increased and fortified due to poor weight gain and she was taking caffeine citrate, erythromycin, ranitidine, sodium chloride supplements and vitamins. At 1 month of age she developed a hyperphosphatemia (phosphate 3.93 mmol/l) with associated hyperuremia (urea 14.3 mmol/l) and hypercreatininemia (creatinine 58 μmol/l). Potassium remained on the higher end of normal (5.1 mmol/l) and sodium was stable on supplements (134 mmol/l). Urine output was good and weight gain was a little below target. Wrist and knee X-rays, ultrasound kidneys and gas were all normal. Frusemide was changed to chlorthiazide, fortifier was stopped and calcium supplements were started (despite normal calcium 2.53 mmol/l and adjusted calcium 2.63 mmol/l). Following this the phosphate levels returned to normal.
Conclusion: Despite thorough investigations we were not able to identify a cause for this hyperphosphataemia. Parathyroid hormone resistance was considered which may have been driven by relative hypocalcaemia even though the serum calcium levels were normal. One possible explanation was the frusemide causing a hypocalcaemia which in term caused the hyperparathyroidism but resistance to the parathyroid hormone occurs to avoid calcium depleting the bones which explains the normal calcium.
12 - 14 Nov 2014
British Society for Paediatric Endocrinology and Diabetes