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The proximal tubule is the segment of the nephron in which begins from the renal (tubular) pole of the Bowman's capsule to the beginning of loop of Henle. At this location, the glomerular parietal epithelial cells (PECs) lining bowman’s capsule abruptly transition to proximal tubule epithelial cells (PTECs). The proximal tubule can be further classified into the proximal convoluted tubule ( PCT) and the proximal straight tubule ( PST).
The cytoplasm of the cells is densely packed with mitochondria, which are largely found in the basal region within the infoldings of the basal plasma membrane. The high quantity of mitochondria gives the cells an acidophilic appearance. The mitochondria are needed in order to supply the energy for the active transport of sodium ions out of the cells to create a concentration gradient which allows more sodium ions to enter the cell from the luminal side. Water passively follows the sodium out of the cell along its concentration gradient.
Cuboidal epithelial cells lining the proximal tubule have extensive lateral interdigitations between neighboring cells, which lend an appearance of having no discrete cell margins when viewed with a light microscope.
Agonist resorption of the proximal tubular contents after interruption of circulation in the capillaries surrounding the tubule often leads to disturbance of the cellular morphology of the proximal tubule cells, including the ejection of cell nuclei into the tubule lumen.
This has led some observers to describe the lumen of proximal tubules as occluded or "dirty-looking", in contrast to the "clean" appearance of distal tubules, which have quite different properties.
Based on ultrastructure, it can be divided into three segments, S1, S2, and S3.
| Proximal tubule | convoluted | S1 (2025). 9781416023289, Elsevier/Saunders. ISBN 9781416023289 | Higher cell complexity |
| S2 | |||
| straight | |||
| Lower cell complexity | |||
In relation to the morphology of the kidney as a whole, the convoluted segments of the proximal tubules are confined entirely to the renal cortex.
Some investigators on the basis of particular functional differences have divided the convoluted part into two segments designated S1 and S2.
Straight segments descend into the outer renal medulla. They terminate at a remarkably uniform level and it is their line of termination that establishes the boundary between the inner and outer stripes of the outer zone of the renal medulla.
As a logical extension of the nomenclature described above, this segment is sometimes designated as S3.
Fluid in the filtrate entering the proximal convoluted tubule is reabsorbed into the peritubular capillaries. This is driven by sodium transport from the lumen into the blood by the Na+/K+-ATPase in the basolateral membrane of the epithelial cells.
Sodium reabsorption is primarily driven by this P-type ATPase – 60–70% of the filtered sodium load is reabsorbed in the proximal tubule through active transport, solvent drag, and paracellular electrodiffusion. Active transport is mainly through the sodium/hydrogen antiporter NHE3. Paracellular transport increases transport efficiency, as determined by oxygen consumed per unit of Na+ reabsorbed, thus playing a part in maintaining renal oxygen homeostasis.
| Mass movement of water and occurs both through the cells and between them, passively via [[aquaporin]]s (transcellular transport) and between cells through tight junctions ([[paracellular]]). | |
| | sodium || approximately two-thirds | Mass movement of sodium occurs through the cells, by secondary active transport on the apical membrane, followed by active resorption across the basolateral membrane via the Na+/K+-ATPase. (2025). 9781461437840, Springer. ISBN 9781461437840 The solutes are absorbed isotonicity, in that the osmotic potential of the fluid leaving the proximal tubule is the same as that of the initial glomerular filtrate.
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| [[Glucose]], [[amino acids]], inorganic [[phosphate]], and some other solutes are resorbed via secondary active transport through co-transporters driven by the sodium gradient out of the nephron. | |
| Most of the filtered potassium is resorbed by two paracellular mechanisms – [[solvent drag]] and simple diffusion. | |
| Paracellular fluid reabsorption sweeps some urea with it via solvent drag. As water leaves the lumen, the concentration of urea increases, which facilitates diffusion in the late proximal tubule. | |
| Parathyroid hormone reduces reabsorption of [[phosphate]] in the proximal tubules, but, because it also enhances the uptake of phosphate from the [[intestine]] and [[bone]]s into the blood, the responses to PTH cancel each other out, and the serum concentration of phosphate remains approximately the same. | |
| Acidosis increases absorption. Alkalosis decreases absorption. |
Most of the ammonium that is excreted in the urine is formed in the proximal tubule via the breakdown of glutamine to alpha-ketoglutarate. This takes place in two steps, each of which generates an ammonium anion: the conversion of glutamine to glutamate and the conversion of glutamate to alpha-ketoglutarate. The alpha-ketoglutarate generated in this process is then further broken down to form two bicarbonate anions, which are pumped out of the basolateral portion of the tubule cell by co-transport with sodium ions.
PTECs also participate in the progression of tubulointerstitial injury due to glomerulonephritis, ischemia, interstitial nephritis, vascular injury, and diabetic nephropathy. In these situations, PTECs may be directly affected by protein (e.g., proteinuria in glomerulonephritis), glucose (in diabetes mellitus), or cytokines (e.g., interferon-γ and tumor necrosis factors). There are several ways in which PTECs may respond: producing cytokines, chemokines, and collagen; undergoing epithelial mesenchymal trans-differentiation; necrosis or apoptosis.
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