• M Paillard, P Houillier, and P Borensztein.
• Service de Physiologie Clinique, Université Pierre et Marie Curie, Unité INSERM 356, Hôpital Broussais, Paris.
• Ann Pediatr (Paris). 1993 Feb 1;40(2):81-9.

AbstractIn normal adults eating diets with standard protein contents, urinary excretion of NH4 approximates 40 mmol/24 hours and urinary pH is variable. In patients with metabolic acidosis, a urinary pH under 5.5 suggests an extra-renal cause whereas a urinary pH above 5.5 suggests a renal disorder, although there are many exceptions to this rule of thumb. However, urinary excretion of NH4 is always above 70 mmol/24 hours in extra-renal acidosis and less than or equal to 40 mmol/24 hours in renal acidosis; the two situations can readily be differentiated by determining the urinary anion gap which is absent in the former case and present in the latter. Acidosis due to nephron loss is readily diagnosed on the basis of advanced renal failure with an elevation in nonassayed plasma anions, contrasting with the increased serum chloride level found in tubular acidosis. Oral NaHCO3 loading followed by determination of the fractional excretion of HCO3 or, preferably, of the TmHCO3 normalized for glomerular filtration rate differentiates proximal tubular acidosis (decreased TmHCO3) from distal tubular acidosis (normal or increased TmHCO3). In the latter case, decreased serum potassium levels suggest distal tubular acidosis due to defective H(+)-ATPase or H+/K(+)-ATPase pump function (no increase in urinary PCO2 after oral NaHCO3 loading) or to inability of the kidney to develop a normal H+ gradient (normal increase in urinary PCO2). Increased serum potassium levels suggest conditions involving either hypoaldosteronism or alterations in transepithelial voltage or pseudo-hypoaldosteronism. The incidence of distal tubular acidosis with increased serum potassium levels is rising, whereas tubular acidosis with low serum potassium levels remains infrequent.

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