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10.1210/jc.2014-1308 http://scihub22266oqcxt.onion/10.1210/jc.2014-1308 C4184071!4184071!24960544     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24960544&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Clin+Endocrinol+Metab 2014 ; 99 (10): E1830-7 Nephropedia Template TP {{tp|p=24960544|t=2014. Activation of FGF-23 Mediated Vitamin D Degradative Pathways by Cholecalciferol |pdf=|usr=}}{{24960544}} gab.com Text Activation of FGF-23 Mediated Vitamin D Degradative Pathways by Cholecalciferol JO: J Clin Endocrinol Metab http://www.kidney.de/pget.php?&tw=1&pmid=24960544 #FOAvip Context:: The optimal circulating concentration of 25(OH) vitamin D is controversial. Objective:: The aim was to investigate if FGF-23 and 24,25(OH)2D can guide cholecalciferol replacement. Design:: Oral cholecalciferol (10,000 IU weekly) administered to subjects with 25(OH)D levels < 20 ?g/mL and eGFR > 60 mL/min/1.73 m2 (n = 25), chronic kidney disease (CKD) (n = 27), or end stage renal disease (ESRD) (n = 14). Setting:: The study was conducted at the Veterans Affairs clinics. Main Outcome Measure:: Serum FGF-23, PTH, 25(OH)D, 1,25(OH)2D, 24,25(OH)2D, calcium, and phosphorous concentrations, and urinary excretion of calcium and phosphorus at baseline and after 8 weeks of treatment. Results:: Cholecalciferol treatment increased concentrations of serum 25(OH)D by (19.3 ± 8 ?g/mL, P = .001; 12.2 ± 9 ?g/mL, P = .0001) and 24,25(OH)2D (1.14 ± 0.89 ?g/mL, P = .0024; 1.0 ± 0.72 ?g/mL P = .0002), and reduced serum PTH (?11 ± 21 pg/mL, P = .0292; ?42 ± 68 pg/mL, P = .0494) in normal and CKD subjects, respectively. Cholecalciferol increased serum FGF-23 levels only in normal subjects (44 ± 57 ?g/mL, P = .01). Increments in serum 25(OH)D positively correlated with serum FGF-23 and 24,25(OH)2D and negatively correlated with PTH. In ESRD, cholecalciferol administration increased 25(OH)D by (16.6 ± 6.6 ?g/mL P ? .05) without changing 24,25(OH)2D, FGF-23 or PTH levels. Conclusion:: Modest elevations of serum 25(OH)D levels after cholecalciferol treatment are sufficient to induce compensatory degradative pathways in patients with sufficient renal reserves, suggesting that optimal circulating 25(OH)D levels are approximately 20 ?g/mL. In addition, catabolism of 25(OH)D may also contribute to the low circulating vitamin D levels in CKD, since elevations of FGF-23 in CKD are associated with increased 24,25(OH)2D after cholecalciferol administration. Twit Text FOAVip Activation of FGF-23 Mediated Vitamin D Degradative Pathways by Cholecalciferol ????J Clin Endocrinol Metab http://www.kidney.de/pget.php?&tw=1&pmid=24960544 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24960544 #FOAvip English Wikipedia <ref>{{Cite pmid|24960544}}</ref> Activation of FGF-23 Mediated Vitamin D Degradative Pathways by Cholecalciferol #MMPMID24960544 Alshayeb H; Showkat A; Wall BM; Gyamlani GG; David V; Quarles LD J Clin Endocrinol Metab 2014[Oct]; 99 (10): E1830-7 PMID24960544show ga Context:: The optimal circulating concentration of 25(OH) vitamin D is controversial. Objective:: The aim was to investigate if FGF-23 and 24,25(OH)2D can guide cholecalciferol replacement. Design:: Oral cholecalciferol (10,000 IU weekly) administered to subjects with 25(OH)D levels < 20 ?g/mL and eGFR > 60 mL/min/1.73 m2 (n = 25), chronic kidney disease (CKD) (n = 27), or end stage renal disease (ESRD) (n = 14). Setting:: The study was conducted at the Veterans Affairs clinics. Main Outcome Measure:: Serum FGF-23, PTH, 25(OH)D, 1,25(OH)2D, 24,25(OH)2D, calcium, and phosphorous concentrations, and urinary excretion of calcium and phosphorus at baseline and after 8 weeks of treatment. Results:: Cholecalciferol treatment increased concentrations of serum 25(OH)D by (19.3 ± 8 ?g/mL, P = .001; 12.2 ± 9 ?g/mL, P = .0001) and 24,25(OH)2D (1.14 ± 0.89 ?g/mL, P = .0024; 1.0 ± 0.72 ?g/mL P = .0002), and reduced serum PTH (?11 ± 21 pg/mL, P = .0292; ?42 ± 68 pg/mL, P = .0494) in normal and CKD subjects, respectively. Cholecalciferol increased serum FGF-23 levels only in normal subjects (44 ± 57 ?g/mL, P = .01). Increments in serum 25(OH)D positively correlated with serum FGF-23 and 24,25(OH)2D and negatively correlated with PTH. In ESRD, cholecalciferol administration increased 25(OH)D by (16.6 ± 6.6 ?g/mL P ? .05) without changing 24,25(OH)2D, FGF-23 or PTH levels. Conclusion:: Modest elevations of serum 25(OH)D levels after cholecalciferol treatment are sufficient to induce compensatory degradative pathways in patients with sufficient renal reserves, suggesting that optimal circulating 25(OH)D levels are approximately 20 ?g/mL. In addition, catabolism of 25(OH)D may also contribute to the low circulating vitamin D levels in CKD, since elevations of FGF-23 in CKD are associated with increased 24,25(OH)2D after cholecalciferol administration. äActivation of FGF-23 Mediated Vitamin D Degradative Pathways by Cholec(epmc).pdf DeepDyve Pubget Overpricing