Vomiting and the Renal Potassium Cascade
Most potassium lost during repeated vomiting does not come from the vomit itself — it comes from the kidney dumping potassium over days as a side effect of metabolic alkalosis, volume depletion, and aldosterone activation. This is why simple oral potassium supplementation cannot fix the deficit.
The potassium concentration in gastric secretions is small, around 5-10 mEq/L. If direct loss from vomit were the whole story, severe hypokalemia would require implausibly large vomited volumes. The actual cascade runs through the kidney. Step one: vomiting loses hydrochloric acid (H+ plus Cl-), water, and a little potassium. Step two: losing H+ produces metabolic alkalosis (blood becomes too basic) and losing water produces hypovolemia. These two states together activate the classic renal emergency response. Step three: the kidney prioritizes saving sodium and bicarbonate, and dumps potassium as the price. The mechanism: hypovolemia triggers an aldosterone surge, and aldosterone reabsorbs sodium in exchange for either potassium or hydrogen ions dumped into urine. The body is simultaneously alkalotic and would prefer to retain hydrogen, but aldosterone wins the competition. Potassium becomes the electrolyte that loses the vote. Chloride depletion makes everything worse. Without chloride, the kidney pairs sodium with bicarbonate instead, retaining more bicarbonate, worsening alkalosis, and dumping still more potassium. This is chloride-responsive metabolic alkalosis, and it explains why IV saline is given before potassium replacement in clinical settings: you cannot correct the potassium until the chloride is restored. A classic diagnostic clue is paradoxical aciduria — urine that is acidic even though the body is alkaline, because the kidney is desperately dumping hydrogen alongside potassium to save sodium. The magnesium catch closes the loop. Potassium is excreted via ROMK channels in the kidney that require magnesium to close. When magnesium is low (which chronic GI loss patients usually are), the channels stay open and potassium leaks out regardless of oral supplementation. The clinical rule: hypokalemia cannot be corrected without first correcting hypomagnesemia. This is why "just take potassium pills" cannot fix the deficit when the underlying volume, chloride, and magnesium status are not also addressed. Fasting, by contrast, does not produce this cascade — no HCl loss means no alkalosis means no aldosterone surge, and electrolytes stay stable for weeks if normal mineral intake continues.