Intestinal calcium absorption, serum phosphate, and parathyroid hormone in patients with chronic renal failure and osteodystrophy before and during hemodialysis

Abstract

In 34 patients with chronic renal failure (CRF), fractional 47calcium absorption (Fa47Ca) was measured by an external counting method. A significant correlation was found with impairment of renal function, as expressed by the creatinine clearance. There was also a significant correlation of Fa47Ca with the serum phosphate (SeP) level and of immunoreactive parathyroid hormone (iPTH) with renal function. When the relationship of both SeP and Fa47Ca with creatinine clearance was excluded, no partial correlation between SeP and Fa47Ca appeared to exist. A significant increase of Fa47Ca and serum Ca and a significant decrease of SeP and iPTH were found in 12 patients 2 to 15 months after they were put on intermittent hemodialysis. The possible influence of SeP on intestinal calcium absorption is discussed, and it is suggested that impairment of intestinal absorption of calcium is not a main factor in development of renal osteodystrophy.

Vitamin D and Renal Disease

“…This increase in intestinal calcitriol degradation could partially account for the blunted response to calcitriol treatment to increase intestinal calcium absorption [77]. It is unclear whether CKD increases 24-hydroxylase activity in tissues other than the intestine, and whether the increases in 24-hydroxylase result from a blunted suppression by high PTH, similar to that described earlier for PTH induction of renal 1a-hydroxylase [10]; from a direct induction of 24-hydroxylase by metabolic acidosis [78], by increases in FGF23 [7]; or in response to therapy with calcitriol or its less calcemic analogs.…”

“…Also, there are no epidemiological studies in the hemodialysis population suggesting a higher frequency of the 5 0 polymorphism affecting Cdx-2 binding to the VDR promoter, known to result in an intestine-specific reduction in VDR expression [159]. The increases in calcium absorption following dialysis [77,160] support an impaired VDR function, as either the removal of uremic toxins, or other dialysisdriven changes such as a decrease in serum phosphate or volume depletion suffice to restore the response to serum calcitriol [160].…”