å¡ CASE REPORT å¡ Renal Potassium Wasting in Distal Renal Tubular Acidosis: Role of Aldosterone Shigeaki Muto, Yasushi Asano, Hitoaki Okazaki* and Shogo Kano* Hie pathogenesis of renal potassium wasting and hypokalemia in classic renal tubular acidosis (type 1 RTA) remains uncertain. The prevailing theory is that K+-Na+ exchange is stimulated due to an inability of the distal tubule to establish a normal steep lumen-peritubular H+ gradient. We encountered a 42-year-old woman with type 1 RTA associated with Sjogren's syndrome, in whom renal potassium wasting and hypokalemia persisted despite sustained correction of systemic acidosis with alkali therapy and increased intake of potassium. In addition, plasma renin activity was markedly increased and the serum aldosterone level was upper-normal despite the hypokalemia. Increased intake of sodium resulted in suppression on the serum aldosterone and correction of renal potassium wasting and hypokalemia. This case shows that secondary hyperaldosteronism, possibly due to an impairment of sodium conservation in the distal tubule, may contribute to the loss of potassium from the distal tubule even after the correction of acidosis. (Internal Medicine 31: 1047-1051, 1992) Key words: hypokalemia, proton secretory defect, secondary hyperaldosteronism, Sjogren's syndrome

Intro duction Renal potassium wasting and hypokalemia commonly occur in distal renal tubular acidosis (type 1 RTA) (1-5), and are inferred to be a reversible consequence of the renal acidification defect (3-6). This is based on the observation that in patients with type 1 RTA, correction of systemic acidosis with alkali therapy can lead to a reduction in the urinary excretion of potassium and correction of In hypokalemia the present (2, paper 4, 6). we report a patient with type 1 RTA associated with Sjogren's syndrome, in whom renal potassium wasting and hypokalemia were observed to per sist despite sustained correction of systemic acidosis with alkali therapy and increased intake of potassium. On the other hand, increased sodium intake resulted in a decrease of serum aldosterone concentration and correction of renal potassium wasting and hypokalemia. We also discuss the pathogenesis Case Report of the renal potassium wasting in type 1 RTA.

1969, she had initially manifested Raynaud's phenomenon, and in 1977 she presented with swelling of the right parotid gland. Two years later, she presented with a similar lesion of the right parotid gland as well as a dry mouth, and was admitted to our hospital on May 7, 1979. Laboratory studies revealed the following values: serum potassium, 3.4 mEq/1; sodium, 136 mEq/1; chloride, WBC,or sugars. Urinalysis showed a pH of 7.0,97 andmEq/1; no proteins 3,700/mm3; of rheumatoid factor, 1 :40 (hemagglutination). Examination urinary sediments revealed 4-5 WBC and 1-2 RBC per high-power field without any casts. Arterial blood gas analysis on room air showed the following: oxygen tension (PO2) 85 mmHg, carbon dioxide tension (PCO2) 33.2 mmHg, HC