1. Urinary excretion of prostaglandin E2 is increased in patients with idiopathic hypercalciuria, but in order to conclude that hyperprostaglandinuria is a primary phenomenon, it must be demonstrated that high levels of urinary prostaglandin E2 can be dissociated from other factors, such as urine volume and natriuresis, and from the hypercalciuria itself.
2. We studied 10 patients with idiopathic hypercalciuria and 10 control subjects on high and low calcium diets providing daily calcium intakes of 30-35 mmol and 7.5-10 mmol, respectively, and similar sodium intakes. In addition, patients with idiopathic hypercalciuria and control subjects were studied during water restriction and water diuresis.
3. Urinary prostaglandin E2 excretion was more than twice as high in patients with idiopathic hypercalciuria than in control subjects on the low and high calcium diets as well as during water restriction and water diuresis (P<0.01).
4. Urinary prostaglandin E2 excretion was not affected by changes in urinary calcium excretion in patients with idiopathic hypercalciuria and in control subjects. Patients with idiopathic hypercalciuria on the low calcium diet and control subjects on the high calcium diet had similar levels of calciuria and natriuresis, yet urinary prostaglandin E2 excretion (mean ± SEM) was 11.62 ± 1.71 nmol/day in the patients with idiopathic hypercalciuria and 3.26 ± 0.48 nmol/day in the control subjects (P= 0.0006).
5. These results indicate that increased urinary prostaglandin E2 excretion is a cardinal characteristic of patients with idiopathic hypercalciuria.
