Calciumreabsorption

Calcium reabsorption is the process by which calcium ions filtered by the glomerulus are transported from the tubular lumen back into the bloodstream. It maintains extracellular calcium levels and supports bone mineralization, contributing to overall calcium homeostasis.

The reabsorption of calcium occurs along several segments of the nephron. In the proximal tubule, roughly 60–70% of filtered calcium is reabsorbed, primarily via a combination of transcellular and paracellular routes driven by solvent drag as water is reabsorbed. The thick ascending limb of the loop of Henle reabsorbs about 20–25% of filtered calcium, largely through a paracellular pathway that follows the lumen-positive transepithelial voltage generated by NKCC2, ROMK, and the claudins 16 and 19 in tight junctions.

The distal convoluted tubule reabsorbs about 8–10% through a regulated transcellular mechanism. Calcium enters apical tubule cells via the TRPV5 channel, binds to the cytosolic carrier calbindin-D28k, and is extruded basolaterally by NCX1 and PMCA1b. Hormonal regulation is prominent in this segment, with parathyroid hormone (PTH) upregulating TRPV5 and the basolateral pumps, thereby increasing calcium reabsorption. Calcitriol (1,25-dihydroxyvitamin D3) also supports renal calcium reabsorption, in part by modulating TRPV5 and calcium-handling proteins.

A small, variable portion is reabsorbed in the collecting duct, where the rate is influenced by hormones and physiologic state, but it generally represents a minor contribution.

Clinical relevance: diuretics influence calcium handling—thiazides reduce urinary calcium loss by enhancing reabsorption, while loop diuretics increase calcium excretion by inhibiting the thick ascending limb. Abnormal reabsorption can affect calcium balance and bone health.