Metabolic acidosis due to inapparent defects in renal acid excretion in a patient with chronic diarrhea.
In a patient with persistent diarrhea, renal acid excretion was examined because fecal alkali loss was insufficient to account for chronic metabolic acidosis. Bicarbonate wasting did not occur at physiologic serum concentrations, and the patient's ability to lower urine pH after an acid load was within normal limits. Glomerular filtration rate and the maximal rate of distal hydrogen ion secretion were unequivocally reduced, however, and ammonium excretion ws consequently inadequate. Unanticipated hypophosphaturia limited urinary titratable acidity. This case demonstrates that renal dysfunction may contribute significantly to acidosis associated with diarrhea and shows that defects in renal acid excretion may be superficially inapparent.
Phelps
K R
KR
Department of Medicine, King's County Hospital Center, New York, N.Y.
Uribarri
J
J
D000138:Acidosis / Q000209:etiology*; D000143:Acids / Q000652:urine; D058186:Acute Kidney Injury / Q000150:complications* / Q000652:urine; D000468:Alkalies / Q000032:analysis; D000641:Ammonia / Q000652:urine; D001639:Bicarbonates / Q000097:blood / Q000652:urine; D002908:Chronic Disease; D003967:Diarrhea / Q000150:complications* / Q000652:urine; D005243:Feces / Q000032:analysis; D005260:Female; D006801:Humans; D006863:Hydrogen-Ion Concentration; D008875:Middle Aged; D010710:Phosphates / Q000652:urine
D000143:Acids; D000468:Alkalies; D001639:Bicarbonates; D010710:Phosphates; D000641:Ammonia