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Transient renal acidification defect during acute infantile diarrhea: the role of urinary sodium
S Izraeli1, A Rachmel, Y Frishberg
1Department of Pediatrics A, Beilinson Medical Center, Petah Tiqva, Israel.
Insights
Infants with acute gastroenteritis and metabolic acidosis often show impaired urinary acidification due to sodium deficiency. Correcting this sodium deficit leads to appropriate urine acidification, suggesting it
Area of Science:
- Pediatric Nephrology
- Gastroenterology
- Acid-Base Balance
Background:
- Metabolic acidosis in infants with acute gastroenteritis can impair kidney function.
- Urinary acidification is crucial for acid-base homeostasis.
- Previous studies suggest distal renal tubular dysfunction, but the role of sodium deficiency is unclear.
Purpose of the Study:
- To investigate the relationship between sodium levels and urinary acidification in infants with acute gastroenteritis and metabolic acidosis.
- To determine if sodium deficiency is the primary cause of impaired urinary acidification in this population.
Main Methods:
- Daily urine pH monitoring in 16 infants during hospitalization.
- Analysis of 41 urine samples for sodium concentration, titratable acid, total acidity, and ammonium levels relative to creatinine.
- Comparison of urinary acidification parameters between samples with low (<10 mmol/L) and adequate (≥10 mmol/L) sodium concentrations.
Main Results:
- On admission, 87% of infants had a urine pH > 5.5.
- Urine pH was significantly higher in samples with low sodium concentration (6.04 ± 0.06) compared to those with adequate sodium (5.19 ± 0.1).
- Higher sodium concentrations correlated with increased titratable acid and total acidity to creatinine ratios, but not ammonium to creatinine ratio.
Conclusions:
- Impaired urinary acidification in infants with acute gastroenteritis and metabolic acidosis is frequently associated with sodium deficit.
- This condition results from inadequate sodium delivery to the distal nephron, not transient distal renal tubular acidosis.
- Correction of sodium deficit or furosemide administration restored appropriate urinary acidification.
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.