Proximal tubule

The proximal tubules are part of the renal nephron, a system that begins at the renal end of Bowman's capsule to the beginning of the loop of Henle. It measures approximately 15 mm long and 55 nanometers in diameter. Its walls are composed of a single layer of cubic cells (simple cubic epithelium). These cells have on the luminal side widely developed microvilli called “brush borders” that provide a very large surface area for the main function of the proximal tubule: resorption. This consists of absorbing part of the filtered nutrients back into the blood and letting the ultrafiltrate continue in the loop of Henle.

The proximal tubule reabsorbs 40-60% of the glomerular ultrafiltrate. Glucose and amino acids are reabsorbed practically entirely along the proximal tubule, especially in the initial segments (S1 and S2), through specific cotransporter enzymes with sodium.

In the proximal tubule, between 60 and 70% of the filtered potassium (K) and 80% of the bicarbonate (HCO3) are also reabsorbed. As for water and salt—sodium chloride, formed by sodium (Na) and chlorine (Cl)—they are reabsorbed in a more variable way depending on the needs of regulating body volume; They are reabsorbed in isosmotic proportions, so that the osmolarity of the tubular fluid remains the same as that of the plasma throughout its journey. Sodium is reabsorbed both passively and actively via multiple transporters. Chlorine (Cl) is reabsorbed mainly passively in the last segment (S3) of the proximal tubule, by a chemical and electrical gradient, but also actively by a chloro-formate countertransporter. Water is passively reabsorbed paracellularly, by osmosis.

There are several mechanisms that intervene in ion exchange:

- Sodium-potassium ATPase pump: located in the basolateral membrane, towards the vessels and the interstitium. This pump removes three sodium ions from the cell into the interstitium and introduces two potassium ions. This exchange causes the operation of a sodium-hydrogenion antiporter.

- The sodium-hydrogen ion antiporter is located in the apical membrane, located towards the tubular lumen, and introduces sodium ions (demanded by the activity of the previous pump) exchanging them with protons. These protons will combine with bicarbonate ions from the tubular lumen and give rise to carbon dioxide.

- Carbonic anhydrase joins bicarbonate to hydrogen ions to form CO₂ and water. These diffuse into the cell through the apical membrane. Part of the CO₂ will pass into the blood and, another part, combines with water inside the cell, again producing carbonic acid, thanks to carbonic anhydrase. This acid will be ionized into bicarbonate ion that passes into the blood and into protons, which are used by the Na-H antiporter described above.

- Finally, there will be a passage of chlorine ions through paracellular diffusion, without the intervention of channels or pumps, and transcellular, exchanging by format. The step is facilitated by the fact that the reabsorption of sodium in the initial part of the tubule generates a potential difference, making the tubular lumen more negative due to the chlorine charges. This difference tends to be compensated by the reabsorption of chlorine (Cl), which diffuses by electrical gradient.