title: Contribution of intestine, bone, kidney, and dialysis to extracellular fluid calcium content.
abstract: Calcium (Ca) balance is the net of Ca intake and output from the body over a period of time. The concept of Ca balance does not consider the redistribution of Ca that often occurs in patients with chronic kidney disease (CKD), especially those who are on dialysis, which is often in the form of soft tissue and/or vascular calcification. In this article, we consider movement of Ca with respect to the extracellular fluid (ECF) and develop a mathematical formulation for Ca homeostasis with respect to the ECF that includes input and output from the diet, the bone, the kidney, and dialysis. We consider calcium homeostasis in healthy individuals and in patients with excess parathyroid hormone, excess 1,25-dihydroxyvitamin D(3), and metabolic acidosis; patients who have CKD and are not on dialysis; and, finally, patients who have CKD and are on dialysis. On the basis of a number of assumptions, dialysis patients with a daily intake of >37.5 mmol of elemental Ca (1.5 g) have movement of Ca into the ECF even without supplemental activated vitamin D. Addition of activated vitamin D, which increases intestinal Ca absorption and can increase resorption of Ca from bone, leads to the movement of Ca into the ECF at virtually all levels of intake; however, there are numerous unanswered questions regarding Ca homeostasis in patients with CKD, including how much of the Ca, administered as a phosphate binder, is absorbed and what is the fate of this absorbed Ca. Until these pressing questions are answered with well-designed experiments, we do not know whether we are doing more harm than good for our dialysis patients by administering additional Ca as a phosphate binder, especially when they also receive activated vitamin D.
authors.affiliation: Departments of Medicine and of Pharmacology and Physiology, University of Rochester School of Medicine, Rochester, New York, USA. david_bushinsky@urmc.rochester.edu
authors.forename: David A
authors.initials: DA
authors.lastname: Bushinsky
mesh_terms: D000138:Acidosis / Q000378:metabolism; D000818:Animals; D001842:Bone and Bones / Q000378:metabolism*; D002117:Calcitriol / Q000009:adverse effects; D002118:Calcium / Q000009:adverse effects / Q000378:metabolism*; D002614:Chelating Agents / Q000009:adverse effects; D002908:Chronic Disease; D019587:Dietary Supplements / Q000009:adverse effects; D045604:Extracellular Fluid / Q000378:metabolism*; D006706:Homeostasis; D006801:Humans; D007413:Intestinal Mucosa / Q000378:metabolism*; D007668:Kidney / Q000378:metabolism*; D007674:Kidney Diseases / Q000378:metabolism / Q000628:therapy*; D008954:Models, Biological; D010281:Parathyroid Hormone / Q000378:metabolism; D006435:Renal Dialysis; D018570:Risk Assessment; D013997:Time Factors
chemical_list: D002614:Chelating Agents; D010281:Parathyroid Hormone; D002117:Calcitriol; D002118:Calcium