Calcium absorption in renal failure is markedly impaired, and is associated with a deficiency in 1,25 dihydrocholecalciferol (1,25 DHCC). Previous' absorption studies on the effect of 1,25 DHCC or 1α HCC were done by the radioactive calcium test meal which reflects isotopic and not necessarily net calcium absorption, did not define the mechanisms of absorption or the site within the GI tract from which absorption takes place. The purpose of the experiments was to study the effects of one week of therapy with 2 μg of 1α HCC orally per day in correcting calcium malabsorption by using the segmental perfusion technique. Fifteen patients (8 jejunals, 7 ileals) were perfused for 1.75 hr before and after 1α HCC with calcium gluconate solutions of 0, 1, 5, 10, 15 or 20 mM/l which also contained 50 mM/l NaCl, 5 mM/l KCl, and polyethylene glycol 0.5%. The results showed: in the jejunum 1α HCC caused the average calcium absorption rates to increase at all 4 luminal concentrations, (p<.005); in the jejunum the control studies at 1 mM/l showed calcium movement from blood to lumen (secretion) whereas treatment with 1α HCC revealed movement from lumen to blood (absorption); calcium absorption in the ileum was markedly depressed at all concentrations and 1α HCC increased the average absorption rates (p 0.0001 to < 0.025 for the 5 to 20 mM/l solutions). Calcium absorption in both segments is markedly depressed in patients with renal failure. The defect is corrected by 1α HCC, which in addition to absorption against electrochemical gradient, points to an active transport system in both segments in humans.
|Original language||English (US)|
|State||Published - Jan 1 1975|
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