On the mechanism of renal potassium wasting in renal tubular acidosis associated with the Fanconi syndrome (type 2 RTA)

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Abstract

The mechanism of renal potassium wasting in renal tubular acidosis associated with the Fanconi syndrome (type 2 RTA) was investigated in 10 patients, each of whom had impaired proximal renal tubular reabsorption of bicarbonate as judged from a greater than 15-20% reduction of renal tubular bicarbonate reabsorption (THCO3-) at normal plasma bicarbonate concentrations. When the plasma bicarbonate concentration ([HCO3-]p) was experimentally increased to normal levels in three patients with a fractional potassium excretion (CK/Cin) of less than 1.0 during acidosis, CK/Cin and urinary potassium excretion (UKV/Cin) increased strikingly and concurrently with a striking increase in urinary sodium (UNaV/Cin) and bicarbonate (UHCO3-V/Cin) excretion. When [HCO3-]p was increased to normal levels in two patients with a CK/Cin of greater than 1.0 during acidosis and in whom UNaV/Cin and UHCO3-V/Cin were already markedly increased, CK/Cin did not increase further. When [HCO3-]p was decreased to subnormal levels in a patient given ammonium chloride, UKV/Cin, CK/Cin, and UHCO3-V/Cin decreased concurrently. In the six patients in whom [HCO3-]p was maintained at normal levels (oral alkali therapy) for 2 months or longer, CK/Cin was directly related to the urinary excretion rates of sodium and bicarbonate, hence was directly related to the magnitude of reduction of THCO3- at normal [HCO3-]p; CK/Cin was greater than 0.55 in all six patients and greater than 1.0 in four.

Authors

Anthony Sebastian, Elisabeth McSherry, R. Curtis Morris Jr.