In 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.