Abstract
Calcium, phosphorus and magnesium homeostasis is altered in CKD. Hypocalcemia, hyperphosphatemia and hypermagnesemia are not seen until advanced CKD because adaptations develop. Increased parathyroid hormone secretion maintains S[Ca] within normal limits by increasing calcium efflux from bone, renal calcium reabsorption and phosphate excretion. Similarly, renal phosphate excretion in CKD is maintained by increased secretion of parathyroid hormone and fibroblast growth factor 23 (FGF23). However, the phosphaturic effect of FGF23 is reduced by downregulation of its cofactor Klotho, necessary for binding FGF23 to FGF receptors. Intestinal phosphate absorption is diminished in CKD due in part to reduced levels of 1,25 dihydroxyvitamin D. Unlike calcium and phosphorus, renal magnesium handling is not regulated by a hormone, but fractional excretion of magnesium increases as CKD progresses. Because 60 to 70% of magnesium is reabsorbed in the thick ascending limb of Henle, activation of the calcium-sensing receptor by magnesium may facilitate magnesium excretion in CKD. Modification of the TRPM6 channel in the distal tubule may also have a role in renal magnesium handling. Besides abnormal bone morphology and vascular calcification, abnormalities in mineral homeostasis are associated with increased cardiovascular risk, increased mortality and progression of CKD.
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