Plasma FGF23 levels increase rapidly after acute kidney injury
暂无分享,去创建一个
D. Leaf | M. Wolf | S. Waikar | H. Jüppner | R. Pereira | D. Goltzman | A. Havasi | P. Pajevic | Marta Christov | M. Wolf
[1] Herbert Chase,et al. FGF-23 levels in patients with AKI and risk of adverse outcomes. , 2012, Clinical journal of the American Society of Nephrology : CJASN.
[2] Huiliang Xie,et al. Fibroblast growth factor 23 and Inflammation in CKD. , 2012, American Society of Nephrology. Clinical Journal.
[3] Hai Qing,et al. Demonstration of osteocytic perilacunar/canalicular remodeling in mice during lactation , 2012, Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research.
[4] H Lester Kirchner,et al. Increased risk of death and de novo chronic kidney disease following reversible acute kidney injury. , 2012, Kidney international.
[5] Jason R. Stubbs,et al. Longitudinal evaluation of FGF23 changes and mineral metabolism abnormalities in a mouse model of chronic kidney disease , 2012, Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research.
[6] A. Kapsoritakis,et al. Neutrophil gelatinase-associated lipocalin (NGAL) in inflammatory bowel disease: association with pathophysiology of inflammation, established markers, and disease activity , 2012, Journal of Gastroenterology.
[7] H. Jüppner,et al. Mineral abnormalities and long-term graft function in pediatric renal transplant recipients: a role for FGF-23? , 2011, Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association.
[8] Huiliang Xie,et al. Fibroblast growth factor 23 in patients undergoing peritoneal dialysis. , 2011, Clinical journal of the American Society of Nephrology : CJASN.
[9] E. Farrow,et al. Iron deficiency drives an autosomal dominant hypophosphatemic rickets (ADHR) phenotype in fibroblast growth factor-23 (Fgf23) knock-in mice , 2011, Proceedings of the National Academy of Sciences.
[10] E. Farrow,et al. Parathyroid hormone receptor signaling in osteocytes increases the expression of fibroblast growth factor-23 in vitro and in vivo. , 2011, Bone.
[11] A. Cheung,et al. FGF-23 associates with death, cardiovascular events, and initiation of chronic dialysis. , 2011, Journal of the American Society of Nephrology : JASN.
[12] W. Sellers,et al. FGF receptors control vitamin D and phosphate homeostasis by mediating renal FGF‐23 signaling and regulating FGF‐23 expression in bone , 2011, Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research.
[13] V. Shalhoub,et al. Direct and indirect effects of parathyroid hormone on circulating levels of fibroblast growth factor 23 in vivo. , 2011, Kidney international.
[14] Leah R. Padgett,et al. Iron modifies plasma FGF23 differently in autosomal dominant hypophosphatemic rickets and healthy humans. , 2011, The Journal of clinical endocrinology and metabolism.
[15] Shuang Huang,et al. Heme oxygenase-1 induction contributes to renoprotection by G-CSF during rhabdomyolysis-associated acute kidney injury. , 2011, American journal of physiology. Renal physiology.
[16] Jiang He,et al. Fibroblast growth factor 23 and risks of mortality and end-stage renal disease in patients with chronic kidney disease. , 2011, JAMA.
[17] Chi-yuan Hsu,et al. FGF-23 and PTH levels in patients with acute kidney injury: A cross-sectional case series study , 2011, Annals of intensive care.
[18] Huiliang Xie,et al. Fibroblast growth factor 23 is elevated before parathyroid hormone and phosphate in chronic kidney disease. , 2011, Kidney international.
[19] M. Wolf,et al. Elevated fibroblast growth factor 23 is a risk factor for kidney transplant loss and mortality. , 2011, Journal of the American Society of Nephrology : JASN.
[20] S. Casier,et al. Impaired GFR is the most important determinant for FGF-23 increase in chronic kidney disease. , 2011, Clinical biochemistry.
[21] S. Harris,et al. Targeted ablation of the PTH/PTHrP receptor in osteocytes impairs bone structure and homeostatic calcemic responses. , 2011, The Journal of endocrinology.
[22] V. Jorgetti,et al. FGF-23 as a predictor of renal outcome in diabetic nephropathy. , 2011, Clinical journal of the American Society of Nephrology : CJASN.
[23] G. Hampson. Circulating Fibroblast Growth Factor-23 Increases Following Intermittent Parathyroid Hormone (1–34) in Postmenopausal Osteoporosis: Association with Biomarker of Bone Formation , 2011, Calcified Tissue International.
[24] R. Elashoff,et al. Calcitriol and doxercalciferol are equivalent in controlling bone turnover, suppressing parathyroid hormone, and increasing fibroblast growth factor-23 in secondary hyperparathyroidism. , 2011, Kidney international.
[25] M. Kuro-o,et al. Klotho deficiency is an early biomarker of renal ischemia-reperfusion injury and its replacement is protective. , 2010, Kidney international.
[26] Masaaki Inaba,et al. Increased osteocyte death and mineralization inside bone after parathyroidectomy in patients with secondary hyperparathyroidism , 2010, Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research.
[27] J. Silver,et al. PTH increases FGF23 gene expression and mediates the high-FGF23 levels of experimental kidney failure: a bone parathyroid feedback loop. , 2010, American journal of physiology. Renal physiology.
[28] M. Kemper,et al. Fibroblast growth factor 23 and bone metabolism in children with chronic kidney disease. , 2010, Kidney international.
[29] R. Elashoff,et al. The calcemic response to continuous parathyroid hormone (PTH)(1-34) infusion in end-stage kidney disease varies according to bone turnover: a potential role for PTH(7-84). , 2010, The Journal of clinical endocrinology and metabolism.
[30] O. Mäkitie,et al. Long-Term Clinical Outcome and Carrier Phenotype in Autosomal Recessive Hypophosphatemia Caused by a Novel DMP1 Mutation , 2010, Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research.
[31] J. Bacchetta,et al. The influence of glomerular filtration rate and age on fibroblast growth factor 23 serum levels in pediatric chronic kidney disease. , 2010, The Journal of clinical endocrinology and metabolism.
[32] D. Leaf,et al. Elevated FGF-23 in a patient with rhabdomyolysis-induced acute kidney injury. , 2010, Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association.
[33] C. Cohen,et al. Role of CX3C-chemokine CX3C-L/fractalkine expression in a model of slowly progressive renal failure. , 2010, Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association.
[34] M. Wolf,et al. Circulating fibroblast growth factor 23 in patients with end-stage renal disease treated by peritoneal dialysis is intact and biologically active. , 2010, The Journal of clinical endocrinology and metabolism.
[35] Jean-Philippe Lafrance,et al. Acute kidney injury associates with increased long-term mortality. , 2010, Journal of the American Society of Nephrology : JASN.
[36] C. Ronco,et al. NGAL: a biomarker of acute kidney injury and other systemic conditions , 2010, International Urology and Nephrology.
[37] R. Takagi,et al. FGF23 is mainly synthesized by osteocytes in the regularly distributed osteocytic lacunar canalicular system established after physiological bone remodeling. , 2009, Journal of electron microscopy.
[38] R. Pereira,et al. Patterns of FGF-23, DMP1, and MEPE expression in patients with chronic kidney disease. , 2009, Bone.
[39] Hang Lee,et al. Effects of hPTH(1‐34) Infusion on Circulating Serum Phosphate, 1,25‐Dihydroxyvitamin D, and FGF23 Levels in Healthy Men , 2009, Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research.
[40] C. Chazot,et al. High levels of serum fibroblast growth factor (FGF)-23 are associated with increased mortality in long haemodialysis patients. , 2009, Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association.
[41] R. Elashoff,et al. Relationship between plasma fibroblast growth factor-23 concentration and bone mineralization in children with renal failure on peritoneal dialysis. , 2009, The Journal of clinical endocrinology and metabolism.
[42] S. Mundra,et al. Fibroblast Growth Factor 23 and Mortality among Patients Undergoing Hemodialysis , 2009 .
[43] Jonathan Himmelfarb,et al. Acute kidney injury increases risk of ESRD among elderly. , 2009, Journal of the American Society of Nephrology : JASN.
[44] G. Yancopoulos,et al. Angiopoietin-1 therapy enhances fibrosis and inflammation following folic acid-induced acute renal injury. , 2008, Kidney international.
[45] I. Heilberg,et al. Usefulness of a quick decalcification of bone sections embedded in methyl methacrylate[corrected]: an improved method for immunohistochemistry. , 2008, Journal of bone and mineral metabolism.
[46] I. Heilberg,et al. Usefulness of a quick decalcification of bone sections embedded in methyl metacrylate: an improved method for immunohistochemistry , 2008, Journal of Bone and Mineral Metabolism.
[47] S. Takeda,et al. Effect of acute changes of serum phosphate on fibroblast growth factor (FGF)23 levels in humans , 2007, Journal of Bone and Mineral Metabolism.
[48] A. Arnold,et al. Parathyroid hormone regulates fibroblast growth factor-23 in a mouse model of primary hyperparathyroidism. , 2007, Journal of the American Society of Nephrology : JASN.
[49] J. Aubin,et al. Mineralized tissue cells are a principal source of FGF23. , 2007, Bone.
[50] I. Day. Cardiac Surgery and Inflammation: The Inflammatory Response and Strategies to Reduce the Systemic Inflammatory Response Syndrome , 2007 .
[51] T. Yamashita,et al. Dietary phosphorus regulates serum fibroblast growth factor-23 concentrations in healthy men. , 2006, The Journal of clinical endocrinology and metabolism.
[52] Hang Lee,et al. Regulation of C‐Terminal and Intact FGF‐23 by Dietary Phosphate in Men and Women , 2006, Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research.
[53] Jason R. Stubbs,et al. Fibroblast growth factor 23 is a counter-regulatory phosphaturic hormone for vitamin D. , 2006, Journal of the American Society of Nephrology : JASN.
[54] Jonathan Himmelfarb,et al. Incidence and mortality of acute renal failure in Medicare beneficiaries, 1992 to 2001. , 2006, Journal of the American Society of Nephrology : JASN.
[55] Joseph V Bonventre,et al. Acute kidney injury, mortality, length of stay, and costs in hospitalized patients. , 2005, Journal of the American Society of Nephrology : JASN.
[56] M. Wolf,et al. Fibroblast growth factor-23 mitigates hyperphosphatemia but accentuates calcitriol deficiency in chronic kidney disease. , 2005, Journal of the American Society of Nephrology : JASN.
[57] K. White,et al. Genetic dissection of phosphate- and vitamin D-mediated regulation of circulating Fgf23 concentrations. , 2005, Bone.
[58] Y. Takeuchi,et al. Targeted ablation of Fgf23 demonstrates an essential physiological role of FGF23 in phosphate and vitamin D metabolism. , 2004, The Journal of clinical investigation.
[59] Y. Takeuchi,et al. FGF‐23 Is a Potent Regulator of Vitamin D Metabolism and Phosphate Homeostasis , 2003, Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research.
[60] H. Jüppner,et al. Circulating concentration of FGF-23 increases as renal function declines in patients with chronic kidney disease, but does not change in response to variation in phosphate intake in healthy volunteers. , 2003, Kidney international.
[61] Hideaki Takahashi,et al. Changes of bone remodeling immediately after parathyroidectomy for secondary hyperparathyroidism. , 2003, American journal of kidney diseases : the official journal of the National Kidney Foundation.
[62] D. Miao,et al. Parathyroid hormone is essential for normal fetal bone formation. , 2002, The Journal of clinical investigation.
[63] A. Tamori,et al. Severely reduced production of klotho in human chronic renal failure kidney. , 2001, Biochemical and biophysical research communications.
[64] R. Baron,et al. Normalization of mineral ion homeostasis by dietary means prevents hyperparathyroidism, rickets, and osteomalacia, but not alopecia in vitamin D receptor-ablated mice. , 1998, Endocrinology.