This response is important clinically, since it allows measurement of urinary potassium excretion to distinguish between extrarenal and renal losses as the cause of otherwise unexplained hypokalemia. Potassium excretion should be less than 25 meq/day with extrarenal losses (or with diuretic therapy if the effect of the drug has worn off) . In comparison, a higher value indicates at least some component of renal potassium wasting as might be seen with diuretic therapy, one of the forms of primary hyperaldosteronism (including Bartter's syndrome), or during the bicarbonaturic phase in a patient with vomiting.
The following renal abnormalities, most of which are reversible with potassium repletion, can be induced by hypokalemia .
Sodium wasting is particularly likely to occur during the first few days of vomiting, but can also be seen with chronic metabolic alkalosis if the degree of alkalosis is sufficiently severe that the increase in net bicarbonate reabsorptive capacity induced by volume and chloride depletion is insufficient to reabsorb all of the filtered bicarbonate . Early in the course of vomiting, for example, the plasma bicarbonate concentration and therefore the filtered bicarbonate load are increased; however, the ability to enhance bicarbonate reabsorption takes 3 to 4 days to reach its maximum. Thus, there will be increased NaHCO3 delivery to the collecting tubules; at this site, some of the excess sodium is reabsorbed in exchange for potassium in the collecting tubules. The net effect is that the urine will have the following composition:
- High urine sodium and potassium concentrations. These potassium losses are the major cause of hypokalemia with vomiting, since the concentration of potassium in gastric secretions is only 5 to 10 meq/L.
- Urine pH above 7.0 due to the bicarbonaturia.