Sodium's partner in salt, and the raw material for stomach acid.
Mechanisms, studies and evidence grades for each claim above.
Chloride (Cl⁻) is the second most abundant electrolyte in blood after sodium, and the main negatively charged one. Body fluids have to stay electrically neutral. So for every positive sodium ion held in the fluid outside cells, a negative ion has to go with it, and about two-thirds of the time that ion is chloride. That's why the two travel as table salt and why chloride is about 100 mmol/L in blood, against sodium's 140.1
Together, sodium and chloride make up most of the dissolved particles outside cells, so between them they decide where water sits and how much blood volume there is (see Sodium). In the kidney, the salt-absorbing transporters that loop and thiazide diuretics block carry chloride alongside sodium. In fact, a sensor in the kidney (the macula densa) reads chloride concentration to decide whether to switch on renin and save salt. When chloride is lost, by vomiting for example, the kidney acts as if salt is short even if sodium intake is fine.1
Chloride also flows through its own channels in many tissues. The best-known is CFTR, the channel that is broken in cystic fibrosis. It lets chloride, and water following it, onto the surfaces of the lungs, gut and sweat ducts. When it fails, mucus becomes thick and sticky.
↑ back to summaryStomach acid is hydrochloric acid, HCl, and the "Cl" comes straight from blood chloride. Parietal cells in the stomach lining make it in two separate streams. A proton pump (the H⁺/K⁺-ATPase, the target of PPI drugs like omeprazole) pushes hydrogen ions into the stomach, and chloride follows through its own channels. The two meet in the stomach as acid at a pH near 1, about a million times more acidic than blood.2
That acid is needed to:
Every gram of acid the stomach secretes leaves bicarbonate behind in the blood (the "alkaline tide" after a meal), and the pancreas neutralises it further down. Normally these balance out. Ongoing vomiting or stomach suction breaks that balance: acid and chloride are lost and the bicarbonate stays.2
↑ back to summaryChloride and bicarbonate are the two main negative ions in blood, and they trade places. When one goes up, the other usually goes down. That makes chloride a lever the kidney uses to control acidity:
Chloride as a warning sign. Low blood chloride turns out to predict outcomes. In patients admitted with heart failure, each 1 mmol/L drop in chloride went with about 6–7% higher one-year mortality. Chloride predicted death independently, while sodium lost its predictive value once chloride was accounted for.4 That points to chloride's central role in how the kidney senses salt and volume, which is mostly overlooked.
↑ back to summaryThe adequate intake is 2.3 g/day for adults, which is the chloride in about 3.8 g of salt, or ⅔ tsp. Almost all dietary chloride comes from salt, so anyone getting enough sodium also gets enough chloride. Dietary deficiency essentially doesn't happen. Low chloride comes from losses.
Low chloride (hypochloremia) comes from vomiting, stomach suction, loop and thiazide diuretics, and heavy sweating. It brings on metabolic alkalosis, and with it low potassium, weakness, cramps and fatigue. The kidney also responds as though volume is low and keeps holding salt.3 Long-term acid-blocking drugs reduce stomach acid without lowering blood chloride. Their side effects on B12, iron and magnesium absorption come from less acid, not from too little chloride.
On a routine metabolic panel: low chloride with high bicarbonate suggests vomiting or diuretics. High chloride with low bicarbonate suggests a large saline load, diarrhoea (which loses bicarbonate), or some kidney acid-handling disorders. Doctors use the anion gap, calculated from sodium, chloride and bicarbonate, to tell these apart.1
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