Secondary proximal tubular acidosis

Abstract Renal clearance and acid-base data from six patients with hyperchloremic acidosis associated with chronic renal disease are analyzed. A defective tubular threshold for bicarbonate absorption was identified in each. When the plasma (HCO 3 − ) fell below this threshold, all patients were able to excrete urine with pH 5.0, indicating the tubular capacity for ammonia and titratable acid excretion. Following acetazolamide infusion in one patient, there was an immediate increase in urine (HCO 3 − ) which substantiated the qualitative presence of tubular carbonic anhydrase. These data support a proximal tubular abnormality in association with the underlying renal disease. Although alkaline urine is the expected finding with such a defect, the reduced glomerular filtration and small bicarbonate load resulted in the intermittent excretion of acid urine. The presence of hypercholoremia associated with severe and recurrent acidosis distinguishes this group from the more commonly recognized patient with “uremic acidosis”. Appropriately, they may be classified as secondary proximal renal tubular acidosis. Sodium bicarbonate prevents and readily corrects the alkali deficit.