Abstract
Excretion of acidic urine reflects the normal renal response to metabolic acidosis and is present from a very young age. We have studied urinary acidification (UA) daily during the hospital course of 16 infants with acute gastroenteritis and metabolic acidosis (MA). Urine pH on admission was higher than 5.5 in 14 (87%) patients. We hypothesized that inappropriate UA was due to Na deficiency and inadequate Na delivery to the distal nephron. Forty-one urinary samples were collected during MA. The mean pH of 24 samples with Na concentration<10 mmol/l was significantly higher than the pH of 17 samples with Na concentration > 10 mmol/l (6.04±0.06 vs 5.19±0.1, p<0.001). The urine ratios of titratable acid/creatinine and total acidity/creatinine were significantly higher in Na rich urine samples (p<0.02), whereas ammonium/creatinine ratio was not. Following administration of furosemide or correction of the Na deficit, appropriate acidification was observed. We conclude chat impaired UA is frequently found during MA in infants with acute gastroenteritis and is caused by a sodium deficit and not due to transient distal renal tubular acidosis.
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Izraeli, S., Rachmel, A., Frishberg, Y. et al. 1 TRANSIENT RENAL ACIDIFICATION DEFECT DURING ACUTE INFANTILE DIARRHEA – THE ROLE OR URINARY SODIUM. Pediatr Res 28, 277 (1990). https://doi.org/10.1203/00006450-199009000-00025
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DOI: https://doi.org/10.1203/00006450-199009000-00025