Tubulusreabsorption

Tubulusreabsorption, or tubular reabsorption, is the process by which filtered substances in the nephron filtrate are reclaimed from the tubular lumen and returned to the bloodstream. It is a major function of the renal tubules and is essential for maintaining fluid, electrolyte, and acid–base balance. In a healthy kidney, about two thirds of filtered water and sodium are reabsorbed, most of it in the proximal tubule. Under normal conditions, nearly all filtered glucose and amino acids are reabsorbed as well.

Reabsorption occurs through two main pathways: transcellular routes, where solutes cross tubular epithelial cells, and paracellular routes, where solutes pass between cells. Reabsorption is driven by active transport, especially the basolateral Na+/K+-ATPase, which creates a sodium gradient that powers the uptake of many solutes into tubule cells. Water follows the reabsorbed solutes by osmosis, often through aquaporin channels in cells along the nephron.

Segment-specific reabsorption includes:

- Proximal tubule: bulk reabsorption of Na+, water, bicarbonate, and other solutes; reabsorption of nearly all glucose and amino acids; significant bicarbonate handling.

- Loop of Henle: descending limb reabsorbs water; thick ascending limb reabsorbs Na+, K+, and Cl− via the NKCC2 cotransporter, generating medullary osmotic gradients.

- Distal tubule: Na+ reabsorption via the NaCl cotransporter (NCC); regulated entry of Na+ by aldosterone.

- Collecting duct: principal cells reabsorb Na+ through ENaC channels (under aldosterone control) and reabsorb water in response to vasopressin/ADH; intercalated cells participate in acid-base balance.

Hormonal regulation adjusts reabsorption to maintain homeostasis: aldosterone increases Na+ reabsorption, ADH promotes water reabsorption, and atrial natriuretic peptide reduces Na+ reabsorption. Clinically, changes in reabsorption affect urine composition and are targets of diuretics.