Renal potassium handling in a patient with surreptitious vomiting.

Sir, We read with great interest the recently published Teaching Point ‘The tell-tale urinary chloride’ w1x. While differential diagnosis of this intriguing case was properly managed, focusing on urinary chloride concentration and the coexisting metabolic alkalosis, the teaching points reported are not clearly stated. Concerning the first point: we should note that gastric losses were unlikely to contribute significantly to hypokalaemia, since only small amounts of potassium were present in gastric fluid (about 5 to 10 mEqul). Most of the potassium deficit was initially due to urinary losses w2x. Concerning the second point: it is mentioned that the elevated potassium excretion was due to hypovolaemia and hyperaldosteronism. However, hypovolaemia is frequently associated with a marked decrease in distal fluid delivery, thereby diminishing potassium secretion despite the hypovolaemia-induced secondary hyperaldosteronism w3x. Kaliuria is due to the coexistent metabolic alkalosis and consequently to the elevation of plasma bicarbonate and the filtered bicarbonate load. The excess filtered bicarbonate exceeds reabsorptive capacity, which cannot increase acutely. As a result, NaHCO3 and water delivery to the distal nephron are enhanced; the ensuing reabsorption of some of this sodium in the cortical collecting tubule (which is stimulated by the coexistent aldosterone excess) is accompanied by increased potassium secretion, since bicarbonate acts as a non-reabsorptive anion w2x. However, the potassium wasting is generally transient; within 48 to 78 h proximal sodium and bicarbonate reabsorption rise in response to the hypovolaemia, less bicarbonate is delivered distally and potassium secretion falls w2x.