Vitamin D intoxication in an anephric child.

Area of Science:

• Pediatric Endocrinology
• Nephrology
• Vitamin D Metabolism

Background:

• The primary synthesis of active vitamin D (1,25-dihydroxycholecalciferol) occurs in kidney tissue.
• Severe hypercalcemia was observed in a child lacking kidneys (anephric) despite vitamin D treatment.

Purpose of the Study:

• To investigate the cause of severe hypercalcemia in an anephric child treated with vitamin D.
• To identify the specific vitamin D metabolite responsible for the observed hypercalcemia.

Main Methods:

• Treatment with calcium-free peritoneal dialysis to reduce serum calcium.
• Administration of oral prednisolone and calcitonin to manage hypercalcemia.
• Monitoring of serum calcium and 25-hydroxyvitamin D (25-OHD) levels.

Main Results:

• Peritoneal dialysis acutely lowered serum calcium, suggesting enhanced bone resorption.
• Prednisolone provided temporary relief, but hypercalcemia recurred after discontinuation.
• Calcitonin effectively normalized serum calcium levels.
• Peak serum 25-hydroxyvitamin D (25-OHD) levels were significantly elevated (635 ng/ml) and decreased with a 10-day half-time.

Conclusions:

• High serum 25-hydroxyvitamin D (25-OHD) is the likely cause of hypercalcemia in this anephric child.
• 25-OHD may stimulate bone resorption, contributing to elevated calcium levels.
• While 25-OHD is implicated, the contribution of other vitamin D metabolites cannot be entirely ruled out.