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2015 ; 3
(11
): ä Nephropedia Template TP
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Vasopressin regulates renal calcium excretion in humans
#MMPMID26620256
Hanouna G
; Haymann JP
; Baud L
; Letavernier E
Physiol Rep
2015[Nov]; 3
(11
): ä PMID26620256
show ga
Antidiuretic hormone or arginine vasopressin (AVP) increases water reabsorption
in the collecting ducts of the kidney. Three decades ago, experimental models
have shown that AVP may increase calcium reabsorption in rat kidney. The
objective of this study was to assess whether AVP modulates renal calcium
excretion in humans. We analyzed calcium, potassium, and sodium fractional
excretion in eight patients affected by insipidus diabetes (nephrogenic or
central) under acute vasopressin receptor agonist action and in 10 patients
undergoing oral water load test affected or not by inappropriate antidiuretic
hormone secretion (SIADH). Synthetic V2 receptor agonist (dDAVP) reduced
significantly calcium fractional excretion from 1.71% to 0.58% (P < 0.05) in
patients with central diabetes insipidus. In patients with nephrogenic diabetes
insipidus (resistant to AVP), calcium fractional excretion did not change
significantly after injection (0.48-0.68%, P = NS). In normal subjects undergoing
oral water load test, calcium fractional excretion increased significantly from
1.02% to 2.54% (P < 0.05). Patients affected by SIADH had a high calcium
fractional excretion at baseline that remained stable during test from 3.30% to
3.33% (P = NS), possibly resulting from a reduced calcium absorption in renal
proximal tubule. In both groups, there was a significant correlation between
urine output and calcium renal excretion. In humans, dDAVP decreases calcium
fractional excretion in the short term. Conversely, water intake, which lowers
AVP concentration, increases calcium fractional excretion. The correlation
between urine output and calcium excretion suggests that AVP-related antidiuresis
increases calcium reabsorption in collecting ducts.
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