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Oral phosphate-loading test for the assessment of distal urinary acidification in children
Insights
An oral phosphate load effectively elevates the urinary PCO2 gradient in children, similar to phosphate infusions. This method aids in diagnosing renal tubular acidosis by assessing hydrogen ion secretion defects.
Area of Science:
- Pediatric Nephrology
- Renal Physiology
- Acid-Base Balance
Background:
- Phosphate buffer system is crucial for acid-base balance.
- Urinary minus blood PCO2 gradient (U-B PCO2) indicates hydrogen ion secretion.
- Phosphate infusion elevates U-B PCO2 when urinary pH is near the phosphate pK (6.8).
Purpose of the Study:
- To evaluate the efficacy of an oral phosphate load in elevating U-B PCO2 in children.
- To assess the diagnostic utility of oral phosphate loading for renal tubular acidosis.
Main Methods:
- 18 healthy children (3-13 years) received an oral phosphate load.
- Urinary phosphate concentration, pH, and U-B PCO2 were measured.
- 4 children with distal renal tubular acidosis were also studied for comparison.
Main Results:
- Oral phosphate load increased urinary phosphate to 44.8 +/- 4.7 mmol/l and U-B PCO2 to 68.8 +/- 7.0 mm Hg.
- Children with urinary phosphate >20 mmol/l achieved U-B PCO2 >40 mm Hg.
- Children with distal renal tubular acidosis showed U-B PCO2 <20 mm Hg, indicating a secretory defect.
Conclusions:
- Oral phosphate loading is effective in elevating urinary PCO2 in children.
- This method is comparable to phosphate infusion for diagnostic purposes.
- Oral phosphate load can be widely applied in evaluating renal tubular acidosis.
Abstract:
Neutral phosphate infusion results in an elevated urinary minus blood PCO2 gradient (U-B PCO2), providing that the urinary pH is close to the pK (6.8) of the phosphate buffer system. The present investigation was designed to evaluate whether an oral phosphate load could achieve similar results in children. 18 normal children, aged 3-13 years, were studied. Following the oral phosphate load, the urinary phosphate concentration increased to 44.8 +/- 4.7 mmol/l (mean +/- SEM), and U-B PCO2 reached 68.8 +/- 7.0 mm Hg, with a urinary pH of 6.87 +/- 0.07. With a urinary phosphate concentration above 20 mmol/l, all children reached a U-B PCO2 above 40 mm Hg. 4 children with primary distal renal tubular acidosis were also studied. All exhibited a U-B PCO2 below 20 mm Hg despite values of urinary phosphate concentration at or above 20 mmol/l, indicating the presence of a true secretory defect in distal hydrogen ion secretion. The present study demonstrates that an oral phosphate load is as effective as a phosphate infusion in elevating the urinary PCO2 and, therefore, could have a wide application in the pathophysiologic evaluation of renal tubular acidosis.