THE HYPONATREMIA OF NEONATAL URINARY ASCITES - CLINICAL OBSERVATIONS,EXPERIMENTAL CONFIRMATION AND PROPOSED MECHANISM

Citation
Hs. Clarke et al., THE HYPONATREMIA OF NEONATAL URINARY ASCITES - CLINICAL OBSERVATIONS,EXPERIMENTAL CONFIRMATION AND PROPOSED MECHANISM, The Journal of urology, 150(2), 1993, pp. 778-781
Citations number
20
Categorie Soggetti
Urology & Nephrology
Journal title
ISSN journal
00225347
Volume
150
Issue
2
Year of publication
1993
Part
2
Pages
778 - 781
Database
ISI
SICI code
0022-5347(1993)150:2<778:THONUA>2.0.ZU;2-O
Abstract
A case of neonatal urinary ascites with severe hyponatremia is reporte d. Critical review of the literature on neonatal urinary ascites, whic h included determination of serum electrolytes, revealed a 70% inciden ce of hyponatremia. In an attempt to explain the mechanism of the hypo natremia, urinary ascites was produced in rats by creation of either a unilateral (uretero-peritoneal) or bilateral (vesicoperitoneal) shunt . Hyponatremia did not occur in the unilateral group but it was profou nd in the bilateral group. At 48 hours postoperatively renin was uncha nged in the unilateral group but it was significantly elevated in the bilateral group. Aldosterone was elevated in the unilateral group and markedly elevated in the bilateral group. Urine entering the peritonea l cavity equilibrates with plasma. The proposed mechanism of hyponatre mia in the bilateral group is autodialysis with intraperitoneal urine containing progressively lower sodium concentration secondary to incre ased renin and aldosterone.