# Metabolic Alkalosis: Generation, Maintenance, Chloride

Urine chloride provides a branch, not a diagnosis: combine <20 versus ≥20 with BP, volume, kidney function, and diuretic timing.

![Infographic: Metabolic Alkalosis: Generation, Maintenance, Chloride](https://urinenephrology.org/visual-reference/images/metabolic-alkalosis.png?v=20261003c)

## Generation is not maintenance

Vomiting, gastric drainage, diuretics, or alkali generate alkalosis. Chloride/potassium depletion, reduced GFR, or mineralocorticoid activity prevents bicarbonate excretion. Verify the blood-gas pattern if elevated bicarbonate could instead compensate for chronic respiratory acidosis.

## Urine chloride <20 mEq/L

A low value suggests chloride avidity: vomiting/NG suction, remote diuretic exposure, or a post-hypercapnic state are common explanations. Urine sodium may remain high during bicarbonaturia, so chloride is often more informative than sodium in this setting.

## Urine chloride ≥20 mEq/L

First ask about active or recent loop/thiazide treatment. With hypertension, evaluate mineralocorticoid or related sodium-retaining mechanisms. With normal/low BP and persistent renal losses, consider diuretics, Bartter/Gitelman physiology, or other salt-wasting causes.

## Low chloride does not order saline

If truly volume depleted, chloride-containing isotonic fluid and potassium chloride can correct maintenance factors. If congested with heart failure, low urine chloride does not justify routine saline. Review diuretic strategy, potassium/magnesium replacement, and selected alkalosis treatment with the team.

## Correct the sustaining abnormality

Stop ongoing gastric losses when possible, replace potassium and magnesium deficits, and review alkali/calcium intake. Persistent hypertensive alkalosis requires cause-directed evaluation; merely replacing potassium may not resolve continued mineralocorticoid-driven loss.

## Read a timed sample

Document diuretic timing and obtain urine before treatment when feasible. Repeat an inconsistent result; advanced CKD and mixed disorders reduce interpretability. Synthetic example: vomiting plus UCl 8 supports chloride depletion; UCl 55 after furosemide cannot by itself establish aldosterone excess.

## Supporting evidence

- [Clinical evidence and guidance](https://www.ccjm.org/content/91/6/345)
- [PubMed 35525634](https://pubmed.ncbi.nlm.nih.gov/35525634/)

## Source lessons

- [metabolic alkalosis](https://urinenephrology.org/2025_UDPA_Lectures_Live/electrolytes/acid-base/metabolic-alkalosis.html)
- [case18 enhanced](https://urinenephrology.org/2025_UDPA_Lectures_Live/cases/case18_enhanced.html)

Read alongside the full lessons; the findings and decisions shown here require the stated clinical context.