Renal calcium reabsorption

Renal calcium reabsorption is the physiological process by which the kidneys recover filtered calcium from the tubular fluid back into the systemic circulation, playing a vital role in maintaining whole-body calcium homeostasis [7, 11, 15]. This process occurs through two main pathways: passive paracellular transport, primarily in the proximal tubule and the thick ascending limb (TAL), and active transcellular transport in the distal convoluted tubule (DCT) and connecting tubule (CNT) [11, 13, 20]. Key molecular targets regulating this process include the Calcium-sensing receptor (CaSR), which inhibits reabsorption in response to high extracellular calcium; the Transient receptor potential vanilloid 5 (TRPV5) channel, which acts as the rate-limiting apical entry step for active reabsorption; and the Parathyroid hormone 1 receptor (PTH1R), which stimulates reabsorption in response to PTH [1, 5, 17]. Dysregulation of renal calcium handling is central to the pathogenesis of conditions such as nephrolithiasis (kidney stones), hypercalciuria, and chronic kidney disease-mineral and bone disorder (CKD-MBD) [5, 11, 18]. Pharmacological interventions include calcimimetics like cinacalcet that target CaSR, PTH analogs like teriparatide that target PTH1R, and diuretics such as thiazides that indirectly enhance calcium conservation [4, 7, 16, 20].

Other names

Renal calcium handlingTubular calcium reabsorptionRenal Ca2+ transportRenal calcium conservation

Modulation of renal calcium reabsorption occurs through several mechanisms: calcimimetics (e.g., cinacalcet) activate the calcium-sensing receptor (CaSR) to inhibit parathyroid hormone (PTH) secretion and directly modulate tubular transport; PTH analogs (e.g., teriparatide) activate the PTH1 receptor to increase apical TRPV5 channel activity; and thiazide diuretics indirectly enhance proximal calcium reabsorption by inhibiting the sodium-chloride symporter (NCC) [4, 7, 16, 20].