réabsorption

Réabsorption is the physiological process by which the kidneys reclaim water and solutes from the filtrate and return them to the bloodstream. In physiology, the term réabsorption is used to describe this reclaiming function in the nephron, where filtrate formed by glomerular filtration passes through renal tubules and substances are actively or passively transported back into peritubular capillaries. The proximal tubule accounts for the largest share, followed by the loop of Henle, distal tubule, and collecting duct. Substances commonly reabsorbed include water, glucose, amino acids, sodium, chloride, bicarbonate, potassium, and calcium.

Mechanisms: Sodium reabsorption drives most transport, via active transport and cotransport with glucose and amino acids. Water follows osmotically through aquaporin channels, especially in the proximal tubule and collecting duct under the influence of antidiuretic hormone (ADH). The loop of Henle reabsorbs NaCl via NKCC2 transporters; the distal tubule and collecting duct modify final composition under hormonal control. About 65-70% of filtered water and NaCl is reabsorbed in the proximal tubule; glucose and amino acids are nearly completely reabsorbed there; bicarbonate is also largely reabsorbed.

Hormonal regulation and clinical relevance: ADH increases water reabsorption in the collecting ducts; aldosterone increases Na+ reabsorption and K+ secretion in the distal nephron; atrial natriuretic peptide reduces Na+ reabsorption in the collecting ducts. Disruption of reabsorption can lead to polyuria and electrolyte imbalances. Diuretics alter reabsorption at specific nephron segments: loop diuretics inhibit NKCC2, thiazides inhibit NCC, and potassium-sparing diuretics affect ENaC or aldosterone pathways. In diseases such as diabetes mellitus, high filtrate glucose exceeds transport capacity, leading to glucosuria and osmotic diuresis.