SALT SUPPLEMENTATION, GROWTH, AND NEPHROCALCINOSIS IN THE FUROSEMIDE-TREATED WEANLING RAT

Objective: Furosemide treatment in the human neonate is associated wit h sodium depletion, growth retardation, hypercalciuria and nephrocalci nosis. Dietary sodium intake is known to directly influence urinary ca lcium excretion. The objectives of this study were to create a rat mod el of furosemide-induced nephrocalcinosis and to test the effects of d ietary sodium supplementation on growth, electrolyte balance, calciuri a, and renal calcifications. Methods: Initially, 18 weanling Sprague-D awley rats were randomly divided into three groups. Groups A (control) and B were fed a basal diet. Group C was fed a sodium-enriched diet. Groups B and C received furosemide (40 mg/kg) intraperitoneally daily for 28 days. At the end of the study, serum, urine, and kidney samples were obtained for biochemical and histologic analyses. The three grou ps were then compared for differences in growth, electrolyte homeostas is, calcium excretion and nephrocalcinosis. Subsequently an additional 15 rats were studied to confirm our findings regarding urinary calciu m excretion and kidney calcifications. Results: Treatment with furosem ide without sodium supplementation (group B) resulted in decreased wei ght gain compared with group A (137.5 +/- 12.9 vs. 154.0 +/- 10.6 g; p < 0.05), hypokalemia (3.7 +/- 0.1 vs. 4.4 +/- 0.4 mEq/l; p < 0.05), a nd nephrocalcinosis (187.1 +/- 155 vs. 18.8 +/- 6.9 mu g Ca/g dry kidn ey; p < 0.05). Sodium supplementation (group C) normalized weight gain and corrected electrolyte abnormalities without increasing calciuria or nephrocalcinosis. Conclusions: We conclude that in this animal mode l, chronic furosemide treatment results in growth failure and developm ent of nephrocalcinosis. Sodium supplementation protects against the d eleterious effects of furosemide on weight gain and electrolyte homeos tasis with no adverse effect on nephrocalcinosis.