Intestinal absorption of calcium and the effect of renal insufficiency

Abstract

Normal mechanisms of calcium absorption have been shown to be dependent on a variety of mechanisms which can be altered in uremia. Absorption across the mucosa probably takes place in three steps, one at the mucosal surface sensitive to the lumenal calcium concentration and a brush border Ca dependent ATPase (alkaline phosphatase). Calcium transport then is linked to the presence of a calcium binding protein within the cell or at tight junctions and through the lateral intercellular spaces. Calcium ions also are found in close relationship with mitochondrial structures near the blood mucosal cell boundary suggesting that active transport (linked with Na+ and K+ activated ATPase) finally 'secretes the calcium' out of the cell into the circulation. Vitamin D in its finally active form 1,25 OH cholecalciferol affects all three steps particularly in the synthesis of calcium binding protein. Other factors in the transport of calcium depend on the concentration of parathyroid hormone, the degree of skeletal saturation with calcium and types of calcium salt presented to the mucosa. The various types of isotope tests used in studying absorption are discussed critically. In uremia the calcium content of the diet often suffers, the more severe the uremia the lower the absorption in the first segments of the gut possibly compensated in segments further down. Supplements of physiological doses of 1.25 DHCC restore absorption rapidly whereas hemodialysis does not. However, it is possible that uremia may affect calcium absorption even when the Vitamin D status of the patient is normal. The therapeutic advantages of using high oral loads of calcium salts and the active Vitamin D metabolite are discussed. (Parsons - London)