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

# Proximal tubule transport

- Mechanism
- Exam priority: medium

The first part of the tubule takes back two-thirds of the filtered salt and water and nearly all the glucose and amino acids.

Updated 2026-11-01

Also called: Proximal convoluted tubule, Isosmotic reabsorption

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

## Key points

- Reabsorbs ≈65–67 % of filtered Na⁺, water, K⁺ and Ca²⁺; the fluid leaving is still isosmotic (≈300 mOsm/kg).
- Glucose and amino acids: ≈100 % by Na⁺ cotransport (SGLT2 early, SGLT1 late).
- Bicarbonate: ≈80–90 % via Na⁺/H⁺ exchange (NHE3) and carbonic anhydrase; angiotensin II stimulates it.
- PTH inhibits phosphate reabsorption (NaPi-IIa) here: phosphaturia.
- Global failure = Fanconi syndrome: glucosuria with normal blood glucose, aminoaciduria, phosphaturia and proximal (type 2) renal tubular acidosis.
- Glomerulotubular balance: the proximal tubule reabsorbs a nearly fixed percentage of the filtered load even when GFR changes.

## What it is

The proximal tubule is the kidney’s bulk reclaimer: it reabsorbs about two-thirds of the filtered sodium and water, nearly 100 % of glucose and amino acids, and most of the bicarbonate. Its engine is the basolateral Na⁺/K⁺-ATPase, which keeps cell sodium low so that other solutes can ride in with sodium. Because the epithelium is highly water-permeable, what leaves is almost isosmotic. It also secretes organic acids and bases and makes ammonium.

## How it works, step by step

- The basolateral Na⁺/K⁺-ATPase pumps Na⁺ out: cell Na⁺ stays low and the interior negative.
- That gradient drives apical cotransporters: Na⁺-glucose, Na⁺-amino acid, Na⁺-phosphate.
- The Na⁺/H⁺ exchanger secretes H⁺; in the lumen H⁺ + HCO₃⁻ form CO₂, which enters the cell and is rebuilt into HCO₃⁻ that exits to blood.
- As solutes leave, water follows through aquaporin-1 and between cells: reabsorption is isosmotic.
- Water leaves faster than Cl⁻ early on, so luminal Cl⁻ rises and is reabsorbed down its gradient, between cells, in the late segment.
- High oncotic and low hydrostatic pressure in the peritubular capillary pull the reabsorbate into the blood.
- The straight segment secretes organic acids and bases, and makes NH₄⁺ and new bicarbonate from glutamine.

### 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.

## What the proximal tubule reclaims (approx. % of filtered load)

| Substance | % reabsorbed | How |
| --- | --- | --- |
| Glucose | ≈100 % | Apical SGLT2 and SGLT1; basolateral GLUT |
| [Amino acids](https://durgical.com/en/conditions/cystinuria/) | ≈100 % | Na⁺-coupled transporters by family |
| [Bicarbonate](https://durgical.com/en/conditions/normal-anion-gap-metabolic-acidosis/) | ≈80–90 % | NHE3 + carbonic anhydrase |
| Na⁺ and water | ≈65–67 % | Na⁺/K⁺-ATPase, NHE3, cotransporters; aquaporin-1 |
| Phosphate | ≈80 % | NaPi-IIa/IIc; inhibited by PTH |
| Ca²⁺ and K⁺ | ≈65 % | Mostly paracellular, dragged with water |
| Small filtered proteins | nearly all | Endocytosis (megalin–cubilin) |

## Clinical notes

- Cystinuria: the transporter for cystine and the dibasic amino acids (cystine, ornithine, lysine, arginine) fails: cystine stones.
- Hartnup disease: neutral amino acids (tryptophan) are not reabsorbed: a pellagra-like picture.
- Proximal (type 2) RTA: the bicarbonate threshold drops; urine can still be acidified once plasma bicarbonate has fallen.
- SGLT2 inhibitors and carbonic anhydrase inhibitors act here; the latter cause alkaline urine and mild hyperchloraemic acidosis.

## Memory aid

The proximal tubule is the vacuum cleaner: it takes two-thirds of the salt and water and everything valuable (glucose, amino acids, bicarbonate), leaving the fine-tuning to the rest of the nephron.

## Test yourself

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

## Why does tubular fluid osmolality barely change along the proximal tubule even though so much sodium is reabsorbed?

The proximal epithelium is very water-permeable (aquaporin-1 and the paracellular path): water follows solute almost immediately, so reabsorption is isosmotic.

## A patient has glucosuria with normal blood glucose, phosphaturia, aminoaciduria and a normal anion gap acidosis. Where is the defect?

In the proximal tubule as a whole (Fanconi syndrome): the sodium-coupled transport of this segment fails.

## Why does volume contraction increase proximal bicarbonate reabsorption?

Angiotensin II stimulates proximal NHE3 and Na⁺/K⁺-ATPase, and the higher filtration fraction raises peritubular oncotic pressure; both increase Na⁺ and HCO₃⁻ recovery.

## What happens to luminal chloride concentration along the proximal tubule, and why does it matter?

It rises, because HCO₃⁻ and water are reabsorbed ahead of Cl⁻ early on. That gradient then drives passive paracellular Cl⁻ reabsorption in the late segment.

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## See it in 3D

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

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

## Related topics

- [Glucose transport maximum and renal threshold](https://durgical.com/en/physiology/glucose-transport-maximum-and-renal-threshold/)
- [Renal handling of H⁺ and bicarbonate](https://durgical.com/en/physiology/renal-handling-of-h-and-bicarbonate/)
- [Tubular secretion of organic acids and bases](https://durgical.com/en/physiology/tubular-secretion-of-organic-acids-and-bases/)
- [Transport in the loop of Henle](https://durgical.com/en/physiology/transport-in-the-loop-of-henle/)
- [Where and how diuretics act](https://durgical.com/en/physiology/where-and-how-diuretics-act/)
- [Primary and secondary active transport](https://durgical.com/en/physiology/primary-and-secondary-active-transport/)

## Related conditions

- [Cystinuria](https://durgical.com/en/conditions/cystinuria/)
- [Hartnup disease](https://durgical.com/en/conditions/hartnup-disease/)
- [Normal anion gap (hyperchloraemic) metabolic acidosis](https://durgical.com/en/conditions/normal-anion-gap-metabolic-acidosis/)

## In Biochemistry

- [Na⁺/K⁺-ATPase (sodium pump)](https://durgical.com/en/biochemistry/enzymes/na-k-atpase/)
- [Glucose](https://durgical.com/en/biochemistry/molecules/glucose/)
- [Membrane transport](https://durgical.com/en/biochemistry/topics/membrane-transport/)
- [Bicarbonate–CO₂ buffer system](https://durgical.com/en/biochemistry/topics/bicarbonate-co-buffer-system/)

[← 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: [25.6 Tubular Reabsorption](https://openstax.org/books/anatomy-and-physiology-2e/pages/25-6-tubular-reabsorption) (OpenStax (Rice University), 2022); [25.4 Microscopic Anatomy of the Kidney](https://openstax.org/books/anatomy-and-physiology-2e/pages/25-4-microscopic-anatomy-of-the-kidney) (OpenStax (Rice University), 2022); [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. 28). 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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