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[Physiology](https://durgical.com/en/physiology/) · [Renal, fluids and acid–base](https://durgical.com/en/physiology/#s-renal)

# Renal handling of H⁺ and bicarbonate

- Mechanism
- Exam priority: medium

The kidney reclaims all filtered bicarbonate and makes new bicarbonate by excreting the acid that metabolism produces.

Updated 2026-11-01

Also called: Net acid excretion, Ammoniagenesis, Titratable acid

**See it in 3D:** [Kidneys](https://durgical.com/en/anatomy/kidney/)

## Key points

- Reclaiming is not generating: reabsorbing filtered HCO₃⁻ only avoids losing it; new bicarbonate appears when H⁺ is excreted with phosphate or NH₃.
- ≈80–90 % of filtered HCO₃⁻ is reclaimed in the proximal tubule (NHE3 + carbonic anhydrase).
- Collecting duct α-intercalated cells: apical H⁺-ATPase and H⁺/K⁺-ATPase, stimulated by aldosterone. β cells secrete HCO₃⁻ (pendrin).
- NH₄⁺ (from glutamine) is the adaptable route; titratable acid is limited by filtered phosphate.
- Minimum urine pH ≈4.5: free H⁺ hardly counts; what is excreted is bound to buffers.
- H⁺ secretion rises with acidosis, high PCO₂, volume contraction (angiotensin II, aldosterone) and hypokalaemia.

## What it is

Thousands of mmol of bicarbonate are filtered each day, and metabolism produces fixed acids the lungs cannot remove. The kidney does two jobs: reclaim filtered bicarbonate (mainly in the proximal tubule) and generate new bicarbonate by excreting H⁺ bound to urinary buffers: phosphate (titratable acid) and ammonia (as NH₄⁺). Ammonium is the route that can rise several-fold in chronic acidosis.

## How it works, step by step

- In the tubular cell, carbonic anhydrase forms H⁺ and HCO₃⁻ from CO₂ and water.
- H⁺ goes into the lumen (NHE3 proximally; H⁺ pumps in the collecting duct) and HCO₃⁻ crosses the basolateral membrane into blood.
- If the secreted H⁺ meets filtered HCO₃⁻, that bicarbonate is merely reclaimed (no net gain).
- If it binds HPO₄²⁻ and leaves as H₂PO₄⁻, the HCO₃⁻ that entered the blood is new: titratable acid.
- The proximal tubule deaminates glutamine, producing NH₄⁺ (to urine) and new HCO₃⁻ (to blood).
- NH₃ is recycled in the medulla and, in the collecting duct, traps H⁺ as NH₄⁺, which cannot cross back.
- In chronic acidosis ammoniagenesis rises over days; it is the main renal defence.

### The nephron: segments, transporters and diuretics

**Na⁺ reabsorbed** ≈ 65–70% **Water reabsorbed** ≈ 65–70%

#### Proximal tubule

- **What it does:** Reabsorbs ≈ 65–70% of filtered Na⁺ and water (isosmotically), nearly all glucose and amino acids, ≈ 80% of HCO₃⁻ and most K⁺ and phosphate. Secretes organic acids and bases (many drugs) and makes NH₄⁺ from glutamine.
- **Transporters:** NHE3 (Na⁺/H⁺) with carbonic anhydrase; SGLT2 (early segment, ≈ 90% of glucose) and SGLT1; NaPi-2a (phosphate); basolateral Na⁺/K⁺-ATPase.
- **Hormones:** Ang II stimulates NHE3 (more Na⁺ and HCO₃⁻: contraction alkalosis); PTH inhibits NaPi-2a (phosphaturia) and activates 1α-hydroxylase (active vitamin D).
- **Drugs:** Carbonic anhydrase inhibitors (1), SGLT2 inhibitors (2) and osmotic diuretics (3, with the thin descending limb).
- **Disorders:** Fanconi syndrome (loses glucose, amino acids, phosphate and HCO₃⁻); type 2 (proximal) renal tubular acidosis; familial renal glucosuria (SGLT2).

- Glomerulus and arterioles
- Proximal tubule
- Thin descending limb
- Thin ascending limb
- Thick ascending limb
- Distal convoluted tubule
- Collecting tubule and duct
- Juxtaglomerular apparatus (macula densa)
- Cortex
- Medulla
- Interstitial osmolality (≈ 300 → 1200 mOsm/kg)

Illustrative schematic drawn by Durgical (a long-loop juxtamedullary nephron); proportions and percentages are approximate and not for clinical decisions.

### The nephron: segments, transporters and diuretics

**Na⁺ reabsorbed** ≈ 2–5% **Water reabsorbed** variable (ADH)

#### Collecting tubule and duct

- **What it does:** Fine tuning: reabsorbs ≈ 2–5% of Na⁺, secretes K⁺ and H⁺ and reabsorbs water as ADH allows (urine from ≈ 50 to ≈ 1200 mOsm/kg). Principal cells handle Na⁺, K⁺ and water; intercalated cells handle acid–base.
- **Transporters:** Principal: ENaC, ROMK and BK (K⁺ secretion; BK is flow-driven), apical AQP2 (ADH) and basolateral AQP3/4. α-intercalated: H⁺-ATPase and H⁺/K⁺-ATPase (secrete acid). β-intercalated: pendrin (secrete HCO₃⁻). Inner medulla: urea transporters (ADH).
- **Hormones:** Aldosterone (more ENaC, ROMK, Na⁺/K⁺-ATPase and H⁺-ATPase); ADH via the V2 receptor → cAMP → AQP2 insertion; atrial natriuretic peptide curbs Na⁺ reabsorption.
- **Drugs:** ENaC blockers (6) and mineralocorticoid receptor antagonists (7): K⁺-sparing (risk of hyperkalemia). V2 receptor antagonists (8, vaptans): aquaretics.
- **Disorders:** Liddle syndrome (overactive ENaC: hypertension, hypokalemia, low renin and aldosterone); nephrogenic diabetes insipidus (V2 or AQP2, lithium); type 1 distal renal tubular acidosis (H⁺ secretion fails: urine pH > 5.5, hypokalemia, stones) and type 4 (hypoaldosteronism: hyperkalemia); SIADH (excess ADH).

- Glomerulus and arterioles
- Proximal tubule
- Thin descending limb
- Thin ascending limb
- Thick ascending limb
- Distal convoluted tubule
- Collecting tubule and duct
- Juxtaglomerular apparatus (macula densa)
- Cortex
- Medulla
- Interstitial osmolality (≈ 300 → 1200 mOsm/kg)

Illustrative schematic drawn by Durgical (a long-loop juxtamedullary nephron); proportions and percentages are approximate and not for clinical decisions.

## Equations

**Net acid excretion**NAE = UNH4·V + TA·V − UHCO3·V

**U NH4 ·V**
ammonium excreted

**TA**
titratable acid

**U HCO3 ·V**
bicarbonate lost in urine

At steady state, NAE matches daily fixed-acid production.

**Filtered bicarbonate**Filtered load = GFR × [HCO3−]p

180 L/day × 24 mmol/L ≈ 4300 mmol/day to be reclaimed.

## Approximate figures

| Parameter | Value | Note |
| --- | --- | --- |
| Fixed-acid production (Western diet) | ≈50–100 mmol/day | sulfuric and phosphoric acid from protein |
| Filtered HCO₃⁻ | ≈4300 mmol/day | |
| Minimum urine pH | ≈4.5 | |
| Ammonium excreted | ≈30–40 mmol/day; many times more in chronic acidosis | |

Approximate values for a healthy adult at rest; each laboratory sets its own ranges.

## Renal tubular acidoses: where it fails

| Type | Defect | Urine pH | Plasma K⁺ |
| --- | --- | --- | --- |
| [Distal (type 1)](https://durgical.com/en/conditions/normal-anion-gap-metabolic-acidosis/) | H⁺ not secreted in the collecting duct | > 5.5 always | Low |
| [Proximal (type 2)](https://durgical.com/en/conditions/normal-anion-gap-metabolic-acidosis/) | Lower threshold for HCO₃⁻ reclamation |
- Distal RTA goes with nephrocalcinosis and stones: alkaline urine, hypercalciuria and low urinary citrate.
- In chronic kidney disease too few nephrons make ammonium: metabolic acidosis appears, first with a normal and later a high anion gap.
- Hyperkalaemia suppresses ammoniagenesis and hypokalaemia stimulates it: potassium and acid travel together.

## Memory aid

“Reclaiming is getting your change back; generating is earning new money”: the proximal tubule returns filtered bicarbonate, while phosphate and ammonium pay out new bicarbonate.

## Test yourself

Think of the answer, then tap the question to see it.

## Why can reabsorbing filtered bicarbonate not by itself correct a metabolic acidosis?

It only prevents loss of what was already in plasma. To correct acidosis the kidney must generate new HCO₃⁻ by excreting H⁺ as titratable acid or as NH₄⁺.

## Which acid-excretion route rises most in chronic metabolic acidosis, and where does it come from?

Ammonium: the proximal tubule deaminates more glutamine, sending NH₄⁺ to urine and new HCO₃⁻ to blood. Titratable acid barely rises because it depends on filtered phosphate.

## A child with hyperchloraemic acidosis has a urine pH of 6.5 despite the acidosis, plus hypokalaemia and nephrocalcinosis. Which RTA fits?

Distal (type 1): the collecting duct cannot secrete H⁺ and urine never drops below 5.5; alkaline urine and hypercalciuria favour calcium deposition.

## Why does volume contraction tend to maintain an alkalosis?

Angiotensin II increases proximal NHE3 and aldosterone stimulates distal H⁺ secretion: the kidney reclaims all the HCO₃⁻ instead of excreting the excess.

[Add to my cards (4)](https://durgical.app/estudiar/?add=/en/physiology/renal-handling-of-h-and-bicarbonate/)

## See it in 3D

The structures of Durgical's 3D anatomy where it happens.

- [Kidneys](https://durgical.com/en/anatomy/kidney/)

## Related topics

- [Buffers and the Henderson–Hasselbalch equation](https://durgical.com/en/physiology/buffers-and-the-henderson-hasselbalch-equation/)
- [Proximal tubule transport](https://durgical.com/en/physiology/proximal-tubule-transport/)
- [Distal tubule and collecting duct](https://durgical.com/en/physiology/distal-tubule-and-collecting-duct/)
- [Metabolic acidosis, the anion gap and compensation](https://durgical.com/en/physiology/metabolic-acidosis-the-anion-gap-and-compensation/)
- [Metabolic alkalosis and its compensation](https://durgical.com/en/physiology/metabolic-alkalosis-and-its-compensation/)
- [Potassium balance](https://durgical.com/en/physiology/potassium-balance/)

## Related conditions

- [Normal anion gap (hyperchloraemic) metabolic acidosis](https://durgical.com/en/conditions/normal-anion-gap-metabolic-acidosis/)
- [Metabolic alkalosis](https://durgical.com/en/conditions/metabolic-alkalosis/)
- [Hypokalaemia](https://durgical.com/en/conditions/hypokalaemia/)
- [Chronic kidney disease](https://durgical.com/en/conditions/chronic-kidney-disease/)

## In Biochemistry

- [Bicarbonate–CO₂ buffer system](https://durgical.com/en/biochemistry/topics/bicarbonate-co-buffer-system/)
- [Ammonia (ammonium)](https://durgical.com/en/biochemistry/molecules/ammonia/)
- [Glutamine](https://durgical.com/en/biochemistry/molecules/glutamine/)

[← All of physiology](https://durgical.com/en/physiology/)

Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.

Sources: [26.4 Acid-Base Balance](https://openstax.org/books/anatomy-and-physiology-2e/pages/26-4-acid-base-balance) (OpenStax (Rice University), 2022); [Distal renal tubular acidosis: MedlinePlus Medical Encyclopedia](https://medlineplus.gov/ency/article/000493.htm) (MedlinePlus, US National Library of Medicine, 2024); [Proximal renal tubular acidosis: MedlinePlus Medical Encyclopedia](https://medlineplus.gov/ency/article/000497.htm) (MedlinePlus, US National Library of Medicine, 2024); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 31). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016).

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Representative model, for educational purposes only.

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License: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Cite as: DurgiPedia (durgical.com), https://durgical.com/en/physiology/renal-handling-of-h-and-bicarbonate/