FGF23: Is It Ready for Prime Time?
[摘要] Since the identification of fibroblast growth factor 23 (FGF23)2 more than a decade ago, interest in this hormone has grown dramatically among both nephrologists and endocrinologists. FGF23, initially identified in patients with rare forms of hypophosphatemia, is also increased in patients with chronic kidney disease (CKD). A handful of studies have suggested that increased circulating concentrations of FGF23 not only play an important role in the development of secondary hyperparathyroidism but also are associated with adverse systemic effects, including increased mortality and deterioration of renal function—associations that have definitively been confirmed in a new prospective study of 3879 adult patients with CKD (1). Isakova et al. reported that circulating FGF23 concentrations were an independent predictor, over a 5-year period, of both ( a ) progression to end-stage renal disease in patients with a baseline estimated glomerular filtration rate >30 mL · min−1 · (1.73 m2)−1 and ( b ) mortality in patients with predialysis CKD. These findings highlight the systemic importance of FGF23 and raise the question of whether FGF23 measurements should now be considered a clinically useful biomarker for diagnosing and managing CKD mineral and bone disorder (CKD-MBD).Current algorithms for the diagnosis and treatment of CKD-MBD recommend periodic measurement of creatinine, calcium, phosphorus, alkaline phosphatase, parathyroid hormone, and 25-hydroxyvitamin D concentrations in the plasma of patients at all stages of CKD. These biochemical variables are markers of altered mineral, bone, and/or vascular metabolism. FGF23 measurements, however, are not currently recommended by any guidelines, nor are they available in most clinical laboratories. Although the report by Isakova et al.(1) suggests that increased circulating FGF23 concentrations do predict mortality in patients with CKD, several major hurdles …
[发布日期] [发布机构]
[效力级别] [学科分类] 过敏症与临床免疫学
[关键词] [时效性]