This case illustrates the complex interplay of aldosterone action, sodium and potassium balance, and acid–base regulation. The 2 key diagnostic steps were demonstration of suppressed plasma aldosterone and renin, and an inappropriate increase in urine potassium. Persons with decreased total body potassium should excrete no more than approximately 15 mmol of potassium daily. A timed urine collection, although definitive, is often not practical. The urine potassium concentration of 21 mmol/L was borderline increased but does not take into account urine flow rate or concentration. In fact, the urine was relatively dilute with an osmolality of 226 mOsm/kg. Thus, indirect measures that can allow assessment of potassium excretion are needed to assess an untimed urine sample. The authors report the result of the transtubular potassium gradient. This calculation relates the osmolality of the urine to the potassium concentration in plasma and urine. A typical result is 8–9, but the value should drop to <2 if the kidney is appropriately conserving potassium. The ratio of the urine potassium concentration to the creatinine concentration has also been suggested to be useful (1).
The principal cell in the cortical collecting duct is the final site in the nephron for sodium reabsorption via electrogenic sodium channels in the apical membrane. Aldosterone stimulates electrogenic sodium channel insertion, leading to increased sodium reabsorption. This action produces a more electronegative lumen voltage caused by Na+ entry, which promotes potassium excretion via separate potassium-specific channels. The negative luminal voltage also enhances acid (H+) secretion by intercalated cells in the same segment. Aldosterone additionally stimulates the H+-ATPase in intercalated cells, causing further H+ excretion and systemic bicarbonate gain (2). As demonstrated in this case, the marked increased activation of the mineralocorticoid receptor thus caused sodium retention (hypertension), potassium loss (hypokalemia), and acid loss (metabolic alkalosis).
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- © 2009 The American Association for Clinical Chemistry