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10.1111/sdi.12411 http://scihub22266oqcxt.onion/10.1111/sdi.12411 26303319!ä!26303319 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Semin+Dial 2015 ; 28 (6): 564-77 Nephropedia Template TP {{tp|p=26303319|t=2015. Pathophysiology of Calcium, Phosphorus, and Magnesium Dysregulation in Chronic Kidney Disease |pdf=|usr=}}{{26303319}} gab.com Text Pathophysiology of Calcium, Phosphorus, and Magnesium Dysregulation in Chronic Kidney Disease JO: Semin Dial http://www.kidney.de/pget.php?&tw=1&pmid=26303319 #FOAvip Calcium, phosphorus, and magnesium homeostasis is altered in chronic kidney disease (CKD). Hypocalcemia, hyperphosphatemia, and hypermagnesemia are not seen until advanced CKD 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 CKD is maintained by increased secretion of fibroblast growth factor 23 (FGF23) and PTH. 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, magnesium is not regulated by a hormone, but fractional excretion of magnesium increases as CKD progresses. As 60-70% 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. Besides abnormal bone morphology and vascular calcification, abnormalities in mineral homeostasis are associated with increased cardiovascular risk, increased mortality and progression of CKD. Twit Text FOAVip Pathophysiology of Calcium, Phosphorus, and Magnesium Dysregulation in Chronic Kidney Disease ????Semin Dial http://www.kidney.de/pget.php?&tw=1&pmid=26303319 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26303319 #FOAvip English Wikipedia <ref>{{Cite pmid|26303319}}</ref> Pathophysiology of Calcium, Phosphorus, and Magnesium Dysregulation in Chronic Kidney Disease #MMPMID26303319 Felsenfeld AJ; Levine BS; Rodriguez M Semin Dial 2015[Nov]; 28 (6): 564-77 PMID26303319show ga Calcium, phosphorus, and magnesium homeostasis is altered in chronic kidney disease (CKD). Hypocalcemia, hyperphosphatemia, and hypermagnesemia are not seen until advanced CKD 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 CKD is maintained by increased secretion of fibroblast growth factor 23 (FGF23) and PTH. 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, magnesium is not regulated by a hormone, but fractional excretion of magnesium increases as CKD progresses. As 60-70% 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. Besides abnormal bone morphology and vascular calcification, abnormalities in mineral homeostasis are associated with increased cardiovascular risk, increased mortality and progression of CKD. |*Renal Insufficiency, Chronic/complications/metabolism/physiopathology[MESH] |Calcium/*metabolism[MESH] |Disease Progression[MESH] |Fibroblast Growth Factor-23[MESH] |Glomerular Filtration Rate/*physiology[MESH] |Humans[MESH] |Kidney/*physiopathology[MESH] |Magnesium/*metabolism[MESH] |Metabolic Diseases/*etiology/metabolism[MESH]Pathophysiology of Calcium, Phosphorus, and Magnesium Dysregulation in(epmc).pdf DeepDyve Pubget Overpricing