Endogenous digoxin-like substance in the urine of preterm infants with late hyponatremia

Kovács, Lajos; Bircák, J; Lichardus, B

doi:10.1007/bf02467374

Cited by 1 publication

(1 citation statement)

References 6 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Studies in the perinatal period have re vealed tissue distribution of EOLS with the highest content in the fetal/neonatal adrenals followed by the gut and the brain [13,14] and there have been reports indicating that plas ma levels and urinary excretion of EOLS inversely correlate with gestational and post natal ages [15][16][17][18], Moreover, significant pos itive correlation has been found between neo natal EOLS and fractional sodium excretion implying that EOLS might be involved in sodium and volume regulation during the ear ly postnatal life [19][20][21].…”

Section: Introductionmentioning

confidence: 99%

Urinary Excretion of Endogenous Ouabain-Like Substance in Furosemide-Treated Neonates: Its Relation to Renal Excretory Pattern and Endocrine Factors

Sulyok¹,

Adamovits

Worgall

et al. 1997

Neonatology

View full text Add to dashboard Cite

The present study was undertaken to define the possible role of endogenous ouabain-like substance (EOLS) in controlling renal excretory pattern, in mediating the renal responses to furosemide and in inducing endocrine reactions in furosemide-treated neonates. Ten newborn infants with mean birthweight of 2,752 g and mean gestational age of 37.1 weeks were given furosemide in a dose of 1 mg/kg. Prior to and following furosemide therapy, urine was collected for a period of 12 h and analyzed for creatinine, osmolality, sodium and potassium, as well as for EOLS, arginine vasopressin (AVP), aldosterone and endothelin-1 (ET-1). In response to furosemide administration, urine flow rate and urinary osmolar, sodium and potassium excretion increased significantly, whereas creatinine excretion remained unchanged. Furthermore, following furosemide therapy, urinary excretion of EOLS (148.7 ± 70.8 vs. 200.1 ± 98.1 pg/kg/h) and AVP (19.5 ± 5.4 vs. 27.8 ± 7.8 pg/kg/h) tended to increase, whereas ET-1 (36.0 ± 5.6 vs. 61.4 ± 8.7fmol/kg/h, p < 0.01) and aldosterone (507 ± 120 vs. 751 ± 203 ng/kg/h, p < 0.05) increased significantly. Prior to furosemide, urinary EOLS excretion was found to correlate positively with diuresis (r = 0.80, p < 0.01), sodium (r = 0.91, p < 0.001), creatinine (r = 0.75, p < 0.001), osmolar (r = 0.96, p < 0.001), ET-1 (r = 0.90, p < 0.001) and AVP (r = 0.92, p < 0.001) excretion. After furosemide, urinary EOLS excretion significantly correlated only with diuresis (r = 0.69, p < 0.05), ET-1 (r = 0.77, p < 0.01) and AVP (r = 0.92, p < 0.001). Urinary EOLS proved to be independent of aldosterone excretion irrespective of furosemide administration. It is concluded that urinary EOLS excretion is closely related to neonatal renal excretory pattern and it may have a role in controlling diuresis and natriuresis. The renal response to furosemide appears to be independent of EOLS, although interdependent endocrine reactions can be induced by furosemide which may modulate the production rate and urinary excretion of EOLS.

show abstract