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FGF-23 Regulation in Chronic Kidney Disease

FGF-23 对慢性肾脏病的调节

基本信息

批准号：
8522274
负责人：
KATHERINE WESSELING-PERRY
金额：
$ 17.45万
依托单位：
UNIVERSITY OF CALIFORNIA LOS ANGELES
依托单位国家：
美国
项目类别：
财政年份：
2009
资助国家：
美国
起止时间：
2009-09-15 至 2015-07-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/8522274
关键词：
Address Adult Affinity Animals Back Binding Biopsy Blood Vessels Bone Diseases Bone Pain Calcium Cardiovascular Diseases Cause of Death Child Childhood Chronic Kidney Failure Data Defect Development Dialysis patients Diet Disease Early Intervention Early treatment Effectiveness End stage renal failure Enteral Evaluation Event Excretory function Fibroblast Growth Factor Receptors Fracture Functional disorder Growth Histology Homeostasis Hormones Hypocalcemia result In Vitro Individual Instruction Intake Ions Kidney Kidney Failure Lead Lesion Link Metabolism Minerals Mixed Function Oxygenases Modeling Monitor Morbidity - disease rate Oral Parathyroid gland Pathology Patients Phosphorus Population Production Proteins Recommendation Regimen Regulation Renal Osteodystrophy Renal function Resistance Secondary Hyperparathyroidism Serum Staging Sterols Therapeutic Time Treatment Protocols Up-Regulation Vitamin D adverse outcome bone bone metabolism cofactor cohort demineralization falls feeding fibroblast growth factor 23 human data inorganic phosphate mineralization mortality prevent response skeletal young adult

项目摘要

Bone disease is prevalent in pediatric patients with chronic kidney disease (CKD) and leads to adverse outcomes such as poor growth, bone pain, and fractures. Furthermore, cardiovascular disease is the leading cause of death in children and adults with CKD while bone and cardiovascular disease appear to be linked in this population. Currently, calcium, phosphorus, PTH, and vitamin D metabolism are used to monitor bone disease and guide its treatment. However, correction of these factors ameliorates, but does not cure, bone and vascular lesions in CKD. A newly described protein, fibroblast growth factor 23 (FGF- 23), has been identified in individuals and animals with normal kidney function who have bone disease and disordered mineral ion homeostasis. High levels of the protein are also found in individuals with CKD and these high levels have been linked to an increased mortality rate. FGF-23 is made in bone and levels rise as CKD progresses; the regulation of FGF-23 in individuals with CKD is, however, unknown. Thus, this study will evaluate: 1) The response of FGF-23 to phosphate binder therapy in CKD stages 2-4 CKD 2) The bone expression of FGF-23 and other factors involved in skeletal mineralization in patients with CKD stages 2-4 These specific aims will be investigated by evaluating changes in FGF-23 to oral phosphate load in a cohort of patients with CKD stages 2-4 who are treated with phosphate binding agents. The relationship between FGF-23 and skeletal mineralization will be assessed by immunohistochemical evaluation of bone in patients with CKD who undergo bone biopsy.

骨病在患有慢性肾病 (CKD) 的儿科患者中普遍存在，并会导致不良后果生长不良、骨痛和骨折等后果。此外，心血管疾病是慢性肾病儿童和成人死亡的主要原因，而骨骼和心血管疾病似乎是与这个人群有联系。目前，钙、磷、PTH、维生素D代谢被用来监测骨病并指导其治疗。然而，纠正这些因素会改善情况，但不会无法治愈 CKD 中的骨骼和血管病变。一种新描述的蛋白质，成纤维细胞生长因子 23 (FGF- 23），已在患有骨病和肾功能正常的个体和动物中发现矿物质离子稳态紊乱。在患有 CKD 和这些高水平与死亡率上升有关。 FGF-23 在骨骼中生成，其水平随 CKD 进展；然而，FGF-23 在 CKD 患者中的调节尚不清楚。因此，本研究将评估： 1) CKD 2-4 期中 FGF-23 对磷酸盐结合剂治疗的反应 2) CKD患者骨中FGF-23及其他骨骼矿化相关因子的表达第2-4阶段这些具体目标将通过评估队列中 FGF-23 与口服磷酸盐负荷的变化来研究接受磷酸盐结合剂治疗的 CKD 2-4 期患者的比例。之间的关系 FGF-23 和骨骼矿化将通过患者骨骼的免疫组织化学评估进行评估患有 CKD 并接受骨活检的人。