HYPERCHLOREMIC ACIDOSIS IN CHRONIC OBSTRUCTIVE UROPATHY
1972 Volume 63 Issue 3 Pages 187-199
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1972 Volume 63 Issue 3 Pages 187-199
Hyperchloremic acidosis is not rarely observed in patients with chronic obstructive uropathy. The mechanisms for these alteration have not been clearly estalbished. As an approach to elucidating the underlying mechanisms of electrolytes abnormalities, measurements of serum electrolytes and the response of acid excretion in the urine to administration of ammonium chloride have been evaluated. The present report deals with 17 patients with obstructive uropathy who showed hyperchloremic acidosis (chloride: higher than 111mEq/L, more than twice in 4-5 weeks; bicarbonate: less than 22mEq/L). For the purpose of comparison, 8 patients with obstructive uropathy as well as normochloremic acidosis were studied as controls.
The observed difference on the serum electrolytes was that serum sodium concentration was within the normal range in the patients with hyperchloremic acidosis. On the contrary, low level of serum sodium concentration was encountered in the patients with normochloremic acidosis.
The considered possibility was that a decrease of serum bicarbonate concentration was compensated by an increase of serum chloride concentration, because measurement of serum phosphate and sulfate concentration showed no significant increase, if present at all, regardless the existence of acidosis. As might be obvious in the patients with normochloremic acidosis, electroneutrality is maintained by a decrease of serum sodium concentration, compensating a decrease of serum bicarbonate concentration.
Impairment of hydrogen ion excretion was encountered on oral ammonium chloride loading in both acidotic patients, which was manifest especially in the patients with hyperchloremic acidosis.
It is suggested that the pattern of acid excretion is not only due to simple loss of functioning nephrons, but also due to spxcific defects in tubular acid excretion.
Thus, hyperchloremic acidosis in chronic obstructive uropathy might be attributed to specific tubular defects which produce a situation compatible with that found in renal tubular acidosis. The development of hyperchloremia might become evident when the serum sodium concentration is within the normal range.
