During the past 5 years, we have identified idiopathic
hypercalciuria in five of seven patients referred for evaluation of
renal glycosuria between 1985 and 1991. The children, all boys, ranged in age from 6 to 12 years. Endocrine function was normal, and none of the patients had
hyperparathyroidism,
hypercalcemia,
renal tubular acidosis, or other secondary causes of
hypercalciuria. The
calcium/
creatinine ratio in a fasting urine specimen was elevated in all five children who had
hypercalciuria, with a mean value (+/- SD) of 0.34 +/- 0.06 (normal, < 0.2). In one child who had
renal colic with spontaneous passage of gravel-like material, the idiopathic
hypercalciuria persisted after 1 week on a diet containing 2000 mg of
sodium and 300 mg of
calcium. On the basis of studies that examined the site along the nephron responsible for
hypercalciuria in rats with
streptozocin-induced diabetes, we speculate that in children with
renal glycosuria, there is defective reabsorption of
glucose and
calcium in the straight portion of the proximal tubule or in the collecting duct. It is likely that a similar mechanism accounts for the idiopathic
hypercalciuria in children with
diabetes mellitus.