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Hypocalcemia, hyperphosphatemia, and hypermagnesemia are not seen until advanced\n                    <jats:styled-content style=\"fixed-case\">CKD<\/jats:styled-content>\n                    because adaptations develop. Increased parathyroid hormone (PTH) secretion maintains serum calcium normal by increasing calcium efflux from bone, renal calcium reabsorption, and phosphate excretion. Similarly, renal phosphate excretion in\n                    <jats:styled-content style=\"fixed-case\">CKD<\/jats:styled-content>\n                    is maintained by increased secretion of fibroblast growth factor 23 (\n                    <jats:styled-content style=\"fixed-case\">FGF<\/jats:styled-content>\n                    23) and PTH. However, the phosphaturic effect of\n                    <jats:styled-content style=\"fixed-case\">FGF<\/jats:styled-content>\n                    23 is reduced by downregulation of its cofactor Klotho necessary for binding\n                    <jats:styled-content style=\"fixed-case\">FGF<\/jats:styled-content>\n                    23 to\n                    <jats:styled-content style=\"fixed-case\">FGF<\/jats:styled-content>\n                    receptors. Intestinal phosphate absorption is diminished in\n                    <jats:styled-content style=\"fixed-case\">CKD<\/jats:styled-content>\n                    due in part to reduced levels of 1,25 dihydroxyvitamin D. Unlike calcium and phosphorus, magnesium is not regulated by a hormone, but fractional excretion of magnesium increases as\n                    <jats:styled-content style=\"fixed-case\">CKD<\/jats:styled-content>\n                    progresses. As 60\u201370% of magnesium is reabsorbed in the thick ascending limb of Henle, activation of the calcium\u2010sensing receptor by magnesium may facilitate magnesium excretion in\n                    <jats:styled-content style=\"fixed-case\">CKD<\/jats:styled-content>\n                    . Modification of the\n                    <jats:styled-content style=\"fixed-case\">TRPM<\/jats:styled-content>\n                    6 channel in the distal tubule may also have a role. Besides abnormal bone morphology and vascular calcification, abnormalities in mineral homeostasis are associated with increased cardiovascular risk, increased mortality and progression of\n                    <jats:styled-content style=\"fixed-case\">CKD<\/jats:styled-content>\n                    .\n                  <\/jats:p>","DOI":"10.1111\/sdi.12411","type":"journal-article","created":{"date-parts":[[2015,8,25]],"date-time":"2015-08-25T02:04:08Z","timestamp":1440468248000},"page":"564-577","source":"Crossref","is-referenced-by-count":168,"title":["Pathophysiology of Calcium, Phosphorus, and Magnesium Dysregulation in Chronic Kidney Disease"],"prefix":"10.1111","volume":"28","author":[{"given":"Arnold J.","family":"Felsenfeld","sequence":"first","affiliation":[{"name":"Department of Medicine VA Greater Los Angeles Healthcare System and the David Geffen School of Medicine at UCLA Los Angeles California"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Barton 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