: How does amiloride increase calcium reabsorption in the kidneys? Amiloride is a potassium-sparing diuretic that acts on the distal convoluted tubule and collecting ducts to inhibit ENaC channels. I found studies that show

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Regarding calcium transport in the kidney:

In contrast with the proximal tubule and the thick ascending limb of
the loop of Henle, the distal tubule reabsorbs calcium exclusively via
the transcellular route.

See also: www.ncbi.nlm.nih.gov/pmc/articles/PMC4491294/
Also, calcium availability in blood (and hence for filtration in the kidney) is dependent on pH - higher pH will increase binding of calcium to albumine (this is happens e. g. in plasmapheresis when EDTA is added to your blood to prevent coagulation outside of your body); see also: www.kidney-international.org/article/S0085-2538(15)57007-5/pdf

In the distal convoluted tubule (DCT) and connecting tubule (CNT),
acidosis effects the expression of TRPV5, but also the luminal H+
concentration has direct effects on TRPV5 activity (H+ inhibits).

Consequently, bicarbonaturia, by increasing luminal pH increases TRPV5
activity. There is debate as to whether there is significant calcium
reabsorption from the collecting duct. However, ? intercalated cells
in this segment, when unable to secrete protons such as with dRTA,
will fail to acidify the urine altering the solubility of calcium
salts. In the proximal tubule, a high pH inhibits citrate reabsorption
(as observed in pRTA).

Patients with dRTA have long been appreciated to also have a disorder
of sodium wasting.73 The molecular details of how the vacuolar
H+-ATPase in the collecting duct contributes to sodium reabsorption
were recently described. In combination with pendrin and Slc4A8, the
H+-ATPase mediates thiazide-sensitive sodium reabsorption through the
?-intercalated cell under situations of volume depletion.72,88,89
Mutations in either disease causing subunits would therefore prevent
transcellular sodium reabsorption via this mechanism. Consequently,
patients with mutations in the H+-ATPase would be prone to volume
contraction and, as has been suggested for mutations in NCC, have
increased proximal tubular sodium and consequently calcium
reabsorption. Thus, if volume contracted, these patients would further
attenuate hypercalciuria induced by metabolic acidosis. However, it
should also be noted that volume contraction could exacerbate
nephrocalcinosis and nephrolithiasis by decreasing urinary flow
resulting in increased urine supersaturation of calcium, phosphate, or
oxalate.

Source: www.ncbi.nlm.nih.gov/pmc/articles/PMC5118493/