IN TWO PATIENTS WITH CLASSIC
RENAL TUBULAR ACIDOSIS (RTA) AND IN TWO PATIENTS WITH RTA ASSOCIATED WITH THE
FANCONI SYNDROME, RENAL POTASSIUM WASTING PERSISTED DESPITE SUSTAINED CORRECTION OF
ACIDOSIS: (a) during moderate degrees of
hypokalemia, daily urinary excretion of
potassium exceeded 80 mEq in each patient; (b) during more severe degrees of
hypokalemia, daily urinary excretion of
potassium exceeded 40 mEq in two patients and 100 mEq in another. These urinary excretion rates of
potassium are more than twice those observed in
potassium-depleted normal subjects with even minimal degrees of
hypokalemia. The persistence of renal
potassium wasting may have resulted in part from
hyperaldosteronism, since urinary
aldosterone was frankly increased in two patients and was probably abnormally high in the others relative to the degree of their
potassium depletion. The
hyperaldosteronism persisted despite sustained correction of
acidosis, a normal
sodium intake, and no reduction in measured plasma volume, and was not associated with
hypertension; its cause was not defined. In the two patients with classic RTA, neither renal
potassium wasting nor
hyperaldosteronism could be explained as a consequence of a gradient restriction on renal H(+) - Na(+) exchange because the urinary pH remained greater than, or approximately equal to, the normal arterial pH or considerably greater than the minimal urinary pH attained during
acidosis. The findings provide no support for the traditional view that renal
potassium wasting in either classic RTA or RTA associated with the
Fanconi syndrome is predictably corrected solely by sustained correction of
acidosis with
alkali therapy.