NORMAL PROSTAGLANDINURIA E(2) IN GITELMANS SYNDROME, THE HYPOCALCIURIC VARIANT OF BARTTERS-SYNDROME

In familial Bartter's syndrome, hyperprostaglandinuria is considered a constant feature and prostanoid synthetase inhibition often positivel y influences the disease course, The urinary calcium excretion disting uishes two clinically and biochemically different variants, namely, cl assic Bartter's syndrome (normocalciuric or hypercalciuric variant; ur inary calcium to creatinine greater than or equal to 35.3 mg/mg 10(-3) ) and Gitelman's syndrome (hypocalciuric variant; urinary calcium to c reatinine <35.3 mg/mg 10(-3)). In the hypocalciuric variant of Bartter 's syndrome prostanoid synthetase inhibition is of little benefit. Sin ce the production of prostanoids has not been extensively studied in G itelman's syndrome, the urinary excretion of prostaglandin E(2) was as sessed by radioimmunoassay in 11 untreated patients with Gitelman's sy ndrome (aged 10 to 21 years; five females and six males) and in 11 hea lthy controls (aged 11 to 20 years; five females and six males). The u rinary excretion of prostaglandin E(2) was similar in both study group s. The study provides the rationale for the poor effect of prostanoid synthetase inhibition in the hypocalciuric variant of Bartter's syndro me. The assessment of urinary excretion of prostaglandin E(2) does not represent a diagnostic sine qua non in the context of familial Bartte r's syndrome. (C) 1995 by the National Kidney Foundation, Inc.