Evidence suggesting hyperoxaluria as a cause of nephrocalcinosis in phosphate-treated hypophosphataemic rickets.

Urinary excretion of oxalate and phosphate was measured in twelve vitamin-D-treated, phosphate-supplemented patients with X-linked hypophosphataemia (XLH; four children, eight adolescents and adults) to investigate possible causative factors of nephrocalcinosis other than calcium. Oxalate excretion correlated highly with urinary phosphate excretion and with intake of phosphate supplements corrected for body surface area. Young children received the highest relative doses of phosphate (range 2.27-10.8 g/1.73 m2 daily) and their urinary oxalate excretion was very high (0.94-3.38 mmol/1.73 m2 daily). The urinary oxalate excretion of untreated adults with XLH was within normal limits. Six patients had evidence of nephrocalcinosis on ultrasound. The high urinary oxalate excretion in phosphate-supplemented XLH may be seen as a special type of enteric hyperoxaluria, in which the conditions of calcium-oxalate crystal precipitation could be reached even at normal levels of urinary calcium excretion. Urinary excretion of both calcium and oxalate should therefore be monitored during treatment in young XLH patients.