Transient renal acidification defect during acute infantile diarrhea: the role of urinary sodium.

Abstract

We studied urinary acidification daily during the hospital course of 16 infants with acute gastroenteritis and metabolic acidosis. Urine pH value on admission was higher than 5.5 in 14 (87%) patients. We hypothesized that inappropriate urinary acidification was due to sodium deficiency and inadequate sodium delivery to the distal nephron. Forty-one urinary samples were collected during metabolic acidosis. The mean pH of 24 urine samples with sodium concentration less than 10 mmol/L was significantly higher than the pH of 17 samples with sodium concentration greater than 10 mmol/L (6.04 +/- 0.06 vs 5.19 +/- 0.1; p less than 0.001). The urine ratios of titratable acid to creatinine and of total acidity to creatinine were significantly higher in urine samples containing more sodium (p less than 0.02), whereas the ammonium/creatinine ratio was not. After administration of furosemide or correction of the sodium deficit, appropriate acidification was observed. We conclude that impaired urinary acidification is frequently found during metabolic acidosis in infants with acute gastroenteritis and results from a sodium deficit rather than from transient distal renal tubular acidosis.

• Authors: S Izraeli, A Rachmel, Y Frishberg, A Erman, B Flasterstein, M Nitzan, G Boner
• Journal: The Journal of pediatrics (J Pediatr) Vol. 117 Issue 5 Pg. 711-6 (Nov 1990) ISSN: 0022-3476 [Print] United States
• PMID: 2231202 (Publication Type: Comparative Study, Journal Article)

Chemical References

• Furosemide
• Sodium

Topics

• Acidosis, Renal Tubular (etiology)
• Acute Disease
• Age Factors
• Diarrhea, Infantile (complications, metabolism, therapy)
• Fluid Therapy
• Furosemide (administration & dosage, pharmacology)
• Humans
• Hydrogen-Ion Concentration
• Infant
• Injections, Intravenous
• Sodium (deficiency, metabolism, urine)
• Time Factors