Is the Calcium Correct? Measuring Serum Calcium in Dialysis Patients
ABSTRACT Abnormalities in calcium concentration are frequent in patients receiving dialysis therapy. Most cases of both hypo- and hypercalcemia are mild and asymptomatic. There is concern, however, that, on the one hand, hypocalcemia can drive hyperparathyroidism and eventually lead to gland hypertrophy and autonomous function. Hypercalcemia, on the other hand, can be associated with increased extraosseous calcium and phosphate deposition leading to vascular calcification with an attendant mortality and morbidity. Calcium exists in three main forms in the blood: the physiologically active free or ionized fraction (terms often used interchangeably), a protein bound fraction, and a fraction complexed to other anions. Although the ionized calcium can readily be measured using ion-specific electrodes, it is the total calcium that is most commonly measured because of sample handling and cost concerns. As it is the free or ionized form that is biologically active (and therefore of most relevance), a number of adjustment formulae have been derived to "correct" the total calcium for changes in albumin, protein, and complexing ion concentrations. These formulae show good statistical correlation with measured ionized calcium in populations studied as a whole, but are generally poor predictors of true ionized hypo- or hypercalcemia in individual patients. International guideline committees in nephrology recommend frequent assessment of calcium levels in dialysis patients and recommend that these levels be kept within the normal reference range. These guidelines are less clear on which measurement of calcium should be used to guide clinical decision making. This review examines the merits of making any adjustment to the total calcium measurement, and suggests when it is appropriate to measure the ionized or free calcium.
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- "It is generally agreed that the ionized (or free) calcium is the form that is biologically active. Because of this, free calcium (Ca++) is a more useful index than total calcium and provides a better indication of calcium status [15-17]. Ionized calcium can be measured directly with the use of calcium-specific electrodes. "
ABSTRACT: Chronic kidney disease is associated with disruption of the endocrine system that distorts the balance between calcitriol, calcium, phosphate and parathyroid hormone in the calcium regulation system. This can lead to calcification of the arterial tree and increased risk of cardiovascular disease and death. In this study we develop a health metric, based on biomarkers involved in the calcium regulation system, for use in identifying patients at high risk for future high-cost complications. This study is a retrospective observational study involving a secondary analysis of data from the kidney disease registry of a regional managed care organization. Chronic kidney disease patients in the registry from November 2007 through November 2011 with a complete set of observations of estimated glomerular filtration rate, calcitriol, albumin, free calcium, phosphate, and parathyroid hormone were included in the study (n = 284). Weibull regression model was used to identify the most significant lab tests in predicting "waiting time to hospitalization". A multivariate linear path model was then constructed to investigate direct and indirect effects of the biomarkers on this outcome. The results showed negative significant direct effects of phosphate and parathyroid hormone on "waiting time to hospitalization". Base on this result, the risk of hospitalization increases 16.8% for each 0.55 mg/dl increase in phosphate level and 13.5% for each 0.467 increase in the natural logarithm of parathyroid hormone. Positive indirect effects of calcitriol surrogate (calcidiol), free calcium, albumin and estimated glomerular filtration rate were observed but were relatively small in magnitude. Variables involved in the calcium regulation system should be included in future efforts to develop a quality of care index for Chronic Kidney disease patients.BMC Nephrology 07/2013; 14(1):154. DOI:10.1186/1471-2369-14-154 · 1.52 Impact Factor
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ABSTRACT: Chronic kidney disease–mineral and bone disorders (CKD-MBD) is a term introduced by the Kidney Disease: Improving Global Outcomes (KDIGO) work group on mineral and bone disorder as a syndrome of interrelated biochemical, bone, and vascular abnormalities encountered in CKD. Biochemical abnormalities in CKD represent primary indicators for the diagnosis and management of CKD-MBD. This review discusses each abnormality separately, with references to both the Kidney Dialysis Outcomes Quality Initiative (KDOQI) Clinical Practice Guidelines for Bone Metabolism and Disease in Chronic Kidney Disease and KDIGO Guidelines for Mineral and Bone Disorder. Selected references to the association between biochemical abnormalities and adverse clinical outcomes in CKD population are provided.Clinical Reviews in Bone and Mineral Metabolism 09/2011; 10(3). DOI:10.1007/s12018-011-9122-6
Article: Ionized calcium[Show abstract] [Hide abstract]
ABSTRACT: Calcium is the most abundant mineral in the human body. While most of the body's calcium is sequestered in the skeleton, the free, hydrated cation in solution is a key physiologic mediator in a host of metabolic and regulatory processes. The free cation concentration in the extracellular fluid, historically referred to as "ionized calcium" in clinical medicine, is frequently assayed in patients with suspected or known derangements of calcium metabolism. There is controversy in the literature as to whether direct measurement of ionized calcium, measurement of total (free plus chelated or protein-bound) calcium, or adjustment of total calcium for albumin concentration is the best or most practical clinical measure of calcium, as the three methods differ in costs and clinical sensitivities. This manuscript will review calcium biochemistry and homeostasis, compare the utilities of different methods of assessing calcium homeostasis, and discuss appropriate utilization of ionized calcium testing.Clinica chimica acta; international journal of clinical chemistry 04/2011; 412(9-10):696-701. DOI:10.1016/j.cca.2011.01.004 · 2.76 Impact Factor