Medservatory
USMLE Step 1Renal & acid–baseEP 11 of 21

Vomiting metabolic alkalosis: why the urine turns acid

Vomiting removes gastric acid and chloride, leaving a hypochloraemic, hypokalaemic metabolic alkalosis. Yet the urine is acid, a finding called paradoxical aciduria.

  • 5:36 video
  • 3 min read
  • 4 sources
  • Published 27 Oct 2026
Video lesson · 5:36 · Watch on YouTubeSeries: Acid–Base Disorders & ABG Interpretation · @medservatory
Chapters (12)
By the end of this lesson

Trace how loss of gastric HCl, volume depletion and aldosterone produce a hypochloraemic, hypokalaemic metabolic alkalosis with paradoxical aciduria.

The short version

  1. Vomiting loses hydrochloric acid, so bicarbonate rises while chloride and volume fall.
  2. Aldosterone, low volume and low potassium keep the kidney reabsorbing bicarbonate and secreting hydrogen ions, so the urine is acid despite alkaline blood (paradoxical aciduria).
  3. Urine chloride is low, below about 20 mEq/L, which marks a chloride-responsive alkalosis.
  4. Saline restores volume and chloride, and potassium is replaced; the kidney can then excrete the extra bicarbonate.

Vomiting metabolic alkalosis and the acid-urine paradox

A man has been vomiting for five days. His blood pH is 7.51 and his bicarbonate is 38. With alkaline blood, his urine should be alkaline. But his urine pH is 5.

Alkaline blood with acid urine is called paradoxical aciduria. This lesson traces how vomiting causes a hypochloraemic, hypokalaemic metabolic alkalosis, and why the urine turns acid.[3]

The stomach: acid out, bicarbonate in (the alkaline tide)

A parietal cell makes hydrochloric acid. It pumps hydrogen ions into the stomach, and chloride goes with them. A bicarbonate goes the other way, into the blood. That is the alkaline tide.[2]

In a healthy person, that gain is short-lived. But if the acid is vomited out, the bicarbonate stays behind and the chloride is gone.[2]

Generation and maintenance: vomiting supplies both

An alkalosis needs a generating event and a maintenance factor, as in the previous lesson (EP 10). Vomiting supplies both.[1][4]

  1. Step 1: generationVomiting removes hydrochloric acid, hydrogen and chloride together. The blood keeps the bicarbonate, so bicarbonate rises and chloride falls.[1][2][3]
  2. Step 2: volumeGastric fluid is lost too, so the extracellular volume contracts. Low volume switches on the renin–angiotensin–aldosterone system.[2][3]
  3. Step 3: maintenanceA healthy kidney would simply excrete the extra bicarbonate. This one does not. Volume depletion and low potassium are the most common stimuli for the kidney to reabsorb more bicarbonate.[1]

Chloride depletion and a lower filtration rate also stop the kidney clearing bicarbonate.[2][4]

Aldosterone, hydrogen secretion and the potassium loop

Aldosterone is the hormone that holds on to sodium. In the collecting duct it pulls sodium in through sodium channels, and the price is potassium and hydrogen ions pushed out into the urine.[2][3][4]

  • The collecting duct secretes more hydrogen ions, and each one secreted means bicarbonate is reabsorbed.[1][2]
  • The same sodium reabsorption pulls potassium into the urine, so the kidney loses potassium.[2][3]
  • Low potassium pushes the proximal tubule to reabsorb even more bicarbonate.[2][4]

So low chloride, low volume and low potassium form a loop that locks the alkalosis in.[2][4]

Paradoxical aciduria: acid urine despite alkaline blood

Here is the paradox. The kidney is secreting hydrogen ions because it is saving sodium and bicarbonate. The urine turns acid even though the blood is alkaline.[2][3]

The picture is therefore high bicarbonate, low chloride, low potassium and acid urine.[2][3]

Urine chloride and treatment of hypochloraemic metabolic alkalosis

Urine chloride is low, below about 20 mEq/L. That marks a chloride-responsive alkalosis, the type from the previous lesson.[1][2]

Some sources use a lower cut-off of 10 mEq/L rather than 20.[4]

The fix follows the mechanism. Saline restores volume and chloride, and potassium is replaced. Once volume and chloride return, the kidney can excrete the extra bicarbonate.[1][4]

Worked check: the numbers in the practice case

Henderson–Hasselbalch
pH = 6.1 + log( HCO₃⁻ / (0.03 × PaCO₂) )

HCO₃⁻ 38 mEq/L and PaCO₂ 49 mm Hg

Does the pH fit the bicarbonate and PaCO₂?
  1. 0.03 × 49 = 1.47
  2. 38 / 1.47 = 25.9
  3. 6.1 + log 25.9 = 7.51, which matches the measured pH

The serum anion gap (Na⁺ − [Cl⁻ + HCO₃⁻], without K⁺) is 137 − (88 + 38) = 11 mEq/L, which is normal. Urine chloride is 4 mEq/L, so the alkalosis is chloride-responsive, and the urine potassium of 32 mEq/L, which is inappropriately high for a serum potassium of 2.8 mEq/L, points to renal potassium loss. Alkaline blood with a urine pH of 5.0 is paradoxical aciduria.[1][2][3]

Practice question

Original · USMLE style
Your turnQB-MS-S1-REN-011-01

A 29-year-old man comes to the emergency department because of 5 days of vomiting after a stomach illness. He has had no diarrhea and takes no medications. His pulse is 112/min. Blood pressure is 98/62 mm Hg supine and 84/52 mm Hg standing. Laboratory studies show:

Results
Serum Na⁺137 mEq/L
Serum K⁺2.8 mEq/L
Serum Cl⁻88 mEq/L
Serum HCO₃⁻38 mEq/L
Serum urea nitrogen34 mg/dL
Serum creatinine1.1 mg/dL
Arterial pH (room air)7.51
Arterial PCO₂ (room air)49 mm Hg
Urine Na⁺12 mEq/L
Urine K⁺32 mEq/L
Urine Cl⁻4 mEq/L
Urine pH5.0
Urine ketonesnegative
Which of the following best explains this patient's urine pH?
Pick one option. Your answers stay on this device.

Common questions

What is paradoxical aciduria?

It is acid urine in a patient whose blood is alkaline. In vomiting, the kidney secretes hydrogen ions because it is saving sodium and bicarbonate, so the urine turns acid.

Why does vomiting cause metabolic alkalosis?

Vomiting removes gastric hydrochloric acid, hydrogen and chloride together. The blood keeps the bicarbonate, so bicarbonate rises and chloride falls.

Why is vomiting alkalosis hypokalaemic?

Low volume switches on aldosterone, which pulls sodium in at the collecting duct and pushes potassium and hydrogen ions out into the urine, so the kidney loses potassium.

What is the alkaline tide?

When a parietal cell pumps hydrogen ions and chloride into the stomach, a bicarbonate goes the other way, into the blood. In a healthy person that gain is short-lived.

How is vomiting-induced metabolic alkalosis treated?

Saline restores volume and chloride, and potassium is replaced. Once volume and chloride return, the kidney can excrete the extra bicarbonate.

Transcript

Read the full narration, by chapter662 words

0:00Alkaline blood, acid urine?

A man has been vomiting for 5 days. His blood pH is 7.51, and his bicarbonate is 38. So his urine should be alkaline. But his urine pH is five. Alkaline blood, acid urine. That's called paradoxical aciduria. Today we trace how vomiting causes hypochloraemic, hypokalaemic metabolic alkalosis, and why the urine turns acid.

0:28The stomach: acid out, bicarbonate in (alkaline tide)

Start in the stomach. A parietal cell makes hydrochloric acid. It pumps hydrogen ions into the stomach, and chloride goes with them. And a bicarbonate goes the other way, into the blood. That's the alkaline tide. In a healthy person, that gain is short-lived. But if you vomit the acid out, that bicarbonate stays behind, and the chloride is gone.

0:52Recap: generation and maintenance

Last lesson, we saw that an alkalosis needs a generating event and a maintenance factor. Vomiting supplies both. Here's how.

1:02Step 1: generation (HCl lost)

Step one, generation. Vomiting removes hydrochloric acid, hydrogen and chloride together. The blood keeps the bicarbonate. So bicarbonate rises, and chloride falls.

1:15Step 2: volume loss, RAAS and the collecting duct

Step two, volume. Gastric fluid is lost too, so the extracellular volume contracts. Low volume switches on the renin angiotensin aldosterone system. Aldosterone is the hormone that holds on to sodium. In the collecting duct it pulls sodium in through sodium channels, and the price is potassium and hydrogen ions pushed out into the urine.

1:40Step 3: maintenance (volume, K⁺, Cl⁻, GFR)

Step three, maintenance. A healthy kidney would simply excrete the extra bicarbonate. This one won't. Volume depletion and low potassium are the most common stimuli for the kidney to reabsorb more bicarbonate. Chloride depletion and a lower filtration rate also stop the kidney clearing bicarbonate.

2:01Aldosterone drive and the potassium loop

Now add the aldosterone drive. The collecting duct secretes more hydrogen ions, and each one secreted means bicarbonate is reabsorbed. That sodium reabsorption also pulls potassium into the urine, so the kidney loses potassium. And low potassium makes it worse: it pushes the proximal tubule to reabsorb even more bicarbonate. So low chloride, low volume and low potassium form a loop that locks the alkalosis in.

2:32The paradox: acid urine despite alkaline blood

And there's the paradox. The kidney is secreting hydrogen ions, because it is saving sodium and bicarbonate. The urine turns acid, even though the blood is alkaline. So the picture is: high bicarbonate, low chloride, low potassium, and acid urine.

2:51Urine chloride and treatment

Urine chloride is low, below about 20 mEq/L. That marks a chloride-responsive alkalosis, the type from last lesson. The fix follows the mechanism. Saline restores volume and chloride, and potassium is replaced. Once volume and chloride return, the kidney can excrete the extra bicarbonate.

3:13Practice question

Your turn. A 29-year-old man has had 5 days of vomiting after a stomach illness. He has no diarrhea and takes no medicines. His pulse is 112, and his blood pressure drops when he stands. Serum sodium 137, potassium 2.8, chloride 88, bicarbonate 38. Arterial pH 7.51, PaCO2 49. Urine sodium 12, potassium 32, chloride 4, pH 5.0, ketones negative. Which of the following best explains his acid urine? A, excretion of filtered bicarbonate that exceeds tubular reabsorption. B, aldosterone-driven sodium reabsorption with potassium and hydrogen secretion. C, defective distal hydrogen secretion. D, excretion of ketoacids. E, carbonic anhydrase inhibition. Pause here and decide. A is out: excess bicarbonate in the urine would make it alkaline, but his kidney is reabsorbing bicarbonate hard. C is out: defective distal hydrogen secretion gives alkaline urine and a low blood bicarbonate. His is high. D is out: ketoacids would lower his bicarbonate, and his urine ketones are negative. E is out: a carbonic anhydrase inhibitor wastes bicarbonate, and he takes no medicines. So the answer is B: aldosterone drives sodium in, and potassium and hydrogen out. His urine chloride of four confirms a chloride-responsive state. Three things to keep.

5:03High-yield recap

One: vomiting loses hydrochloric acid, so bicarbonate rises while chloride and volume fall. Two: aldosterone, low volume and low potassium keep the kidney reabsorbing bicarbonate and secreting hydrogen, so the urine is acid. Three: urine chloride is low, and saline plus potassium corrects it.

5:27Next lesson: compensation in metabolic alkalosis

Next up: how the lungs compensate for a metabolic alkalosis, and the expected rise in PaCO2.

Sources

Numbers in the text, e.g. [1], point here
  1. Lewis JL III. Metabolic Alkalosis. MSD Manual Professional Version. msdmanuals.com/professional/endocrine-and-metabolic-disorders/acid-base-regulation-and-disorders/metabolic-alkalosis
  2. Do et al. Metabolic Alkalosis Pathogenesis, Diagnosis, and Treatment: Core Curriculum 2022. pmc.ncbi.nlm.nih.gov/articles/PMC10947768/
  3. Case report: hypokalaemic hypochloraemic metabolic alkalosis with paradoxical aciduria. pmc.ncbi.nlm.nih.gov/articles/PMC5778228/
  4. LITFL. Metabolic Alkalosis. litfl.com/metabolic-alkalosis/

The practice question is original and its patient is synthetic. Every fact is checked against the sources above in independent accuracy reviews. Always follow your local guidelines and your own laboratory’s ranges.

Image credits. Illustrations: Servier Medical Art (smart.servier.com), licensed under CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/); adapted (recoloured, outlined, resized): stomach, nephron, urine sample container. All other diagrams are original; example lab values are illustrative.

Corrections. None so far. Spotted an error? Email info@medservatory.com with the lesson code MS-S1-REN-011.

For exam study only, not medical advice. Read the medical disclaimer.

In this series

Playlist on YouTube
← Previous · EP 10Metabolic alkalosis: generation, maintenance and urine chloride
  1. EP 01ABG interpretation, made simple5:35
  2. EP 02Anion gap explained: high vs normal gap metabolic acidosis5:25
  3. EP 03Winters' formula: the expected PaCO₂ in metabolic acidosis5:10
  4. EP 04Delta ratio: find the hidden second acid–base disorder5:09
  5. EP 05New bicarbonate: how the kidney excretes acid with ammonium5:23
  6. EP 06High anion gap metabolic acidosis causes, sorted by the anion5:54
  7. EP 07Osmolar gap: how toxic alcohols hide from the anion gap5:31
  8. EP 08Urine anion gap: telling diarrhea from RTA5:33
  9. EP 09Renal tubular acidosis: tell RTA types 1, 2 and 4 apart5:24
  10. EP 10Metabolic alkalosis: generation, maintenance and urine chloride5:30
  11. EP 11Vomiting metabolic alkalosis: why the urine turns acid5:36
  12. EP 12Bartter vs Gitelman: NKCC2, NCC and urine calcium5:21
  13. EP 13Respiratory acidosis compensation: acute vs chronic5:22
  14. EP 14Respiratory alkalosis compensation: acute vs chronic5:33
  15. EP 15Metabolic alkalosis compensation: the expected PaCO₂5:12
  16. EP 16Salicylate poisoning acid-base: a classic mixed disorder5:31
  17. EP 17Type A vs type B lactic acidosis: split it by mechanism5:33
  18. EP 18DKA anion gap explained: from high gap to hyperchloraemic acidosis5:42
  19. EP 19Acidosis and hyperkalemia: how pH shifts potassium5:43
  20. EP 20ABG interpretation in 6 steps: the acid-base algorithm5:32
  21. EP 21Acid-base practice cases: three ABG vignettes, one algorithm5:44