Physiology · Renal, fluids and acid–base

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

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	≈100 %	Na⁺-coupled transporters by family
Bicarbonate	≈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.

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.

Add to my cards (4)

See it in 3D

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

Kidneys

In Biochemistry

← All of 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 (OpenStax (Rice University), 2022); 25.4 Microscopic Anatomy of the Kidney (OpenStax (Rice University), 2022); Proximal renal tubular acidosis: MedlinePlus Medical Encyclopedia (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).

Spotted a mistake?We are always improving for the community. Tell us what is wrong and our team will review it.Report a mistake

Representative model, for educational purposes only.