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Distal convoluted and connecting tubule: calcium reabsorption

Target organ · TRPV5 Calbindin-D28k Thiazide

The only nephron segment where calcium reabsorption is hormonally regulated. Calcium enters through the apical TRPV5 channel, is ferried across by calbindin-D28k and is extruded basolaterally by NCX1 and PMCA1b. PTH increases TRPV5 expression and keeps it in the membrane, reclaiming the last 8-10% of filtered calcium.

Traced from the start

  1. Fall in ionised calciumRise in ionised calcium
  2. Calcium-sensing receptor on parathyroid chief cells
  3. Parathyroid hormone
  4. Distal convoluted and connecting tubule: calcium reabsorption

Detail

Where calcium is reabsorbed
About 65% passively in the proximal tubule with sodium and water, about 25% paracellularly in the thick ascending limb through claudin-16/19 driven by the lumen-positive potential, and the final 8-10% actively in the distal tubule
Transporters
Apical TRPV5, cytosolic calbindin-D28k, basolateral NCX1 and PMCA1b
Stimulated by
PTH, and calcitriol, which induces TRPV5 and calbindin; alkalosis increases and acidosis decreases TRPV5 activity
Diuretics
Thiazides block NCC in the distal tubule and increase calcium reabsorption, causing hypocalciuria; loop diuretics abolish the lumen-positive potential in the thick ascending limb and cause calciuria

When it goes wrong

Thiazide diuretic

Mild hypercalcaemia with reduced urinary calcium; used deliberately in idiopathic hypercalciuric stone formers, but it can unmask primary hyperparathyroidism

Loop diuretic used for hypercalcaemia

Calciuresis, but only once the patient is volume-replete; given to a dehydrated patient it worsens the hypercalcaemia, so saline comes first

Bartter syndrome, or an activating calcium-sensing receptor mutation

Hypercalciuria with nephrocalcinosis, the mirror image of the hypocalciuria of familial hypocalciuric hypercalcaemia

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