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Reduced renal acid excretion in malnutrition: a result of phosphate depletion
Insights
Phosphate depletion in infants with malnutrition causes reduced acid excretion and bicarbonate loss. Supplementation corrects these issues, improving kidney function and weight gain.
Area of Science:
- Pediatric Nephrology
- Nutritional Science
- Biochemistry
Background:
- Protein-calorie malnutrition in infants can lead to metabolic acidosis.
- Acquired monosaccharide intolerance is a potential cause of malnutrition.
- Acid-base balance is crucial for infant growth and development.
Purpose of the Study:
- To investigate the mechanisms of metabolic acidosis in malnourished infants.
- To assess the role of phosphate depletion in renal acid excretion.
- To evaluate the impact of phosphate supplementation on acid-base balance.
Main Methods:
- Measured plasma bicarbonate, renal net acid excretion (NAE), titratable acidity (TA), and phosphate levels in malnourished infants.
- Administered intravenous and oral phosphate loads to assess response.
- Studied urinary bicarbonate excretion after partial and complete recovery.
Main Results:
- Malnourished infants exhibited reduced plasma bicarbonate and decreased NAE, with low titratable acidity.
- Phosphate depletion was indicated by reduced phosphate excretion and serum levels.
- Phosphate supplementation significantly increased NAE.
- Urinary bicarbonate loss was observed during partial recovery, suggesting a reabsorption defect.
Conclusions:
- Phosphate depletion contributes to reduced renal net acid excretion in malnourished infants.
- Defects in urinary buffer availability and bicarbonate reabsorption are linked to phosphate depletion.
- Phosphate repletion can improve acid-base balance and renal function in these infants.
Abstract:
Eleven infants recovering from protein-calorie malnutrition secondary to acquired monosaccharide intolerance were found to have reduced plasma bicarbonate concentration associated with inadequate weight gain. Renal net acid excretion (NAE) was decreased to a mean of 34.2 micronEq/1.73m2/min. Titratable acidity (TA) was markedly reduced, accounting for only 16% of NAE. This marked reduction in TA was associated with reduced mean phosphate (PO4) excretion (.074 mg/min) and a reduced mean serum PO4 (3.9 mg/dl), suggesting PO4 depletion. Two patients received intravenous phosphate loads, resulting in an increase in mean NAE from 35.1 to 89.7 microgEq/1.73m2/min. A similar response was seen after oral PO4 supplementation. Three patients were studied after partial correction of their acidosis. At a relatively low plasma bicarbonate concentration (mean = 16.6 mmoles/liter) significant amounts of bicarbonate were detected in the urine (mean = 8.7 micronEq/1.73m2/min), suggesting a defect in bicarbonate reabsorption. Five patients studied after complete recovery from malnutrition had normal NAE in response to ammonium chloride load. The reduction in NAE appears to be secondary to unavailability of urinary buffers and a reduction in bicarbonate reabsorption; both of these defects can be explained by phosphate depletion.