Contribution of Intestine, Bone, Kidney, and Dialysis to Extracellular Fluid Calcium Content
- 1 January 2010
- journal article
- review article
- Published by Ovid Technologies (Wolters Kluwer Health) in Clinical Journal of the American Society of Nephrology
- Vol. 5 (Supplement), S12-S22
- https://doi.org/10.2215/cjn.05970809
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 D3, 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.Keywords
This publication has 93 references indexed in Scilit:
- The emerging role of phosphate in vascular calcificationKidney International, 2009
- Association of Serum Phosphate with Vascular and Valvular Calcification in Moderate CKDJournal of the American Society of Nephrology, 2009
- Guidelines for the Management of Asymptomatic Primary Hyperparathyroidism: Summary Statement from the Third International WorkshopJournal of Clinical Endocrinology & Metabolism, 2009
- Endocrine functions of bone in mineral metabolism regulationJCI Insight, 2008
- Improving Global Outcomes in Mineral and Bone DisordersClinical Journal of the American Society of Nephrology, 2008
- Mortality effect of coronary calcification and phosphate binder choice in incident hemodialysis patientsKidney International, 2007
- Chronic Kidney Disease and the Risks of Death, Cardiovascular Events, and HospitalizationNew England Journal of Medicine, 2004
- Marked suppression of secondary hyperparathyroidism by intravenous administration of 1,25-dihydroxy-cholecalciferol in uremic patients.JCI Insight, 1984
- On the pathogenesis of hyperparathyroidism in chronic experimental renal insufficiency in the dogJCI Insight, 1971
- Metabolic balance studies in primary renal tubular acidosis: Effects of acidosis on external calcium and phosphorus balancesThe Journal of Pediatrics, 1966