Hypercalciuria during experimental vitamin K deficiency in the rat.
Vitamin K promotes the formation of gamma-carboxylated glutamate (GLA) in several protein species. GLA residues have a high affinity for the Ca ion. In the present study, we tested the hypothesis that experimental vitamin K deficiency in rats could induce changes in Ca metabolism. Vitamin K depletion, which was associated with a reduction in urinary GLA excretion, induced within 7 days a significant increase in cumulative urinary Ca excretion that persisted throughout the 21 days of study. The hypercalciuria of vitamin K-deficient rats was corrected on vitamin K supplementation. No concomitant changes were observed in intestinal Ca absorption determined by a balance technic or of skeletal resorption and apposition rates determined by bone histomorphometry. Plasma Ca, but not total protein concentration, of vitamin k-depleted rats showed a transient decrease at day 15 that disappeared at day 21. plasma sodium, phosphate and 1,25(OH)2 vitamin D concentration, and urinary phosphate, sodium, and creatinine excretion remained unchanged. In conclusion, vitamin k deficiency in the rat induced hypercalciuria that could be of renal origin. Its possible relationship to vitamin K-dependent renal GLA protein remains to be clarified.
D015055:1-Carboxyglutamic Acid / Q000652:urine; D000818:Animals; D002117:Calcitriol / Q000097:blood; D002118:Calcium / Q000097:blood / Q000378:metabolism / Q000652:urine*; D003404:Creatinine / Q000652:urine; D007408:Intestinal Absorption; D008297:Male; D010710:Phosphates / Q000378:metabolism; D051381:Rats; D012964:Sodium / Q000378:metabolism; D014813:Vitamin K Deficiency / Q000150:complications*
D010710:Phosphates; D015055:1-Carboxyglutamic Acid; D012964:Sodium; D003404:Creatinine; D002117:Calcitriol; D002118:Calcium