EFFECTS OF RENAL OSTEODYSTROPHY DURING GROWTH

肾性骨营养不良对生长过程的影响

基本信息

  • 批准号:
    7374508
  • 负责人:
  • 金额:
    $ 5.08万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    2005
  • 资助国家:
    美国
  • 起止时间:
    2005-12-01 至 2006-11-30
  • 项目状态:
    已结题

项目摘要

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Renal osteodystrophy (ROD) is a multifactorial disorder of bone metabolism in individuals with renal insufficiency. As renal failure progresses, ensuing abnormal parathyroid hormone (PTH) secretion and calcium metabolism result in sclerosis of trabecular bone and thinning of cortical bone. During childhood and adolescence, skeletal growth is normally characterized by marked expansion of cortical dimensions and increases in trabecular density. Therefore, the growing skeleton may be particularly vulnerable to the structural effects of renal osteodystrophy. Underlying renal disorders associated with elevated systemic levels of inflammatory cytokines and renal therapies, such as glucocorticoids, also may impair bone accretion. Although the impact of these threats to normal bone development among children with renal failure is not fully known, they plausibly may lead to an irreversible failure to develop normal skeletal architecture and peak bone mass. Structural insufficiency may not regress even in the face of kidney transplantation, which reverses many of the metabolic effects of kidney failure that induce renal osteodystrophy. Unlike traditional densitometric measures of bone mass, peripheral quantitative computed tomography (pQCT) permits the discrete assessment of trabecular and cortical bone density and dimensions, and bone strength can be reliably estimated. Therefore, pQCT is an ideal tool to study the structural implications of renal osteodystrophy during growth. Accurate characterization of the structural bone deficits and the risk factors for impaired skeletal development in children with renal disease has not yet been performed and is the focus of this proposed investigation. The hypotheses are that (a) compared to normal controls, expansion of cortical bone volume is significantly impaired in children and adolescents with renal failure, resulting in substantial reduction of bone strength, (b) among children with renal disease, the magnitude and progression of the bone deficit is associated with poor growth and development, and with variability in the renal diseases (e.g., systemic inflammatory renal diseases) and therapies (e.g., glucocorticoids), and (c) the recovery and reconstitution of bone structure following renal transplantation is modulated by skeletal maturation at the time of transplantation, immunosuppressive therapies, rejection episodes, and allograft renal function. AIMS: 1. To perform a cross-sectional study of bone mass (dimensions, density, and strength) comparing children and adolescents with chronic renal failure to healthy controls and subsequently compare subgroups of children with chronic renal failure to identify predictors of decreased bone mass, such as the underlying renal disease, the severity of renal dysfunction, poor growth status, delayed skeletal bone age, decreased muscle strength, prior immunosuppressive therapies (e.g., glucocorticoids, cyclosporine), calcitriol therapy, and serum PTH levels. 2. To perform a longitudinal study of bone mineral accretion velocity (changes in dimensions, density, and strength) comparing healthy controls to each of three groups with renal disease: children with chronic renal failure, children on dialysis, and children following renal transplantation. 3. To compare dual energy x-ray absorptiometry (DXA) and pQCT in the assessment of skeletal structure and bone mineral accretion during childhood renal disease in order to demonstrate that the distinct effects of renal osteodystrophy on bone size and density are not well-characterized by DXA. 4. To determine if baseline levels of serum PTH and biomarkers of bone turnover can predict the subsequent pattern of growth and bone mineral accretion (changes in dimensions, density, and strength) over the follow-up interval among the chronic renal failure, dialysis, and transplantation subjects.
该子项目是利用NIH/NCRR资助的中心赠款提供的资源的许多研究子项目之一。子项目和研究者(PI)可能从另一个NIH来源获得主要资金,因此可以在其他CRISP条目中表示。所列机构为中心,不一定是研究者所在机构。肾性骨营养不良(ROD)是肾功能不全患者的一种多因素骨代谢紊乱。随着肾衰竭的进展,随之而来的异常甲状旁腺激素(PTH)分泌和钙代谢导致骨小梁硬化和皮质骨变薄。在儿童和青少年时期,骨骼生长的特征通常是皮质尺寸显著扩大和骨小梁密度增加。因此,生长中的骨骼可能特别容易受到肾性骨营养不良的结构影响。与炎性细胞因子和肾脏治疗(如糖皮质激素)的全身水平升高相关的潜在肾脏疾病也可能损害骨增生。虽然这些威胁对肾衰竭儿童正常骨骼发育的影响尚不完全清楚,但它们可能导致不可逆的正常骨骼结构和峰值骨量发育失败。结构性功能不全可能不会退化,即使面对肾移植,这逆转了许多肾衰竭的代谢影响,诱导肾性骨营养不良。 与传统的骨密度测量不同,外周定量计算机断层扫描(pQCT)允许对骨小梁和皮质骨密度和尺寸进行离散评估,并且可以可靠地估计骨强度。因此,pQCT是研究生长过程中肾性骨营养不良的结构影响的理想工具。尚未对肾病儿童的结构性骨缺损和骨骼发育受损的风险因素进行准确表征,这是本研究的重点。 假设是:(a)与正常对照组相比,肾衰竭儿童和青少年皮质骨体积的扩张显著受损,导致骨强度显著降低,(B)在肾病儿童中,骨缺损的程度和进展与生长发育不良以及肾病的变异性(例如,全身性炎性肾病)和治疗(例如,糖皮质激素),和(c)肾移植后骨结构的恢复和重建受到移植时骨骼成熟、免疫抑制治疗、排斥发作和同种异体移植肾功能的调节。 目标:1.进行一项骨质的横断面研究,(尺寸、密度和强度)将患有慢性肾衰竭的儿童和青少年与健康对照进行比较,随后比较患有慢性肾衰竭的儿童亚组,以确定骨量减少的预测因素,如基础肾脏疾病、肾功能不全的严重程度、不良生长状态、骨骼骨龄延迟、肌肉强度降低,先前的免疫抑制疗法(例如,糖皮质激素、环孢霉素)、骨化三醇治疗和血清PTH水平。2.进行一项骨矿物质增长速度(尺寸、密度和强度变化)的纵向研究,比较健康对照组与三组肾病患者:慢性肾衰竭儿童、透析儿童和肾移植后儿童。3.比较双能X线吸收测定法(DXA)和pQCT在评估儿童肾病期间骨骼结构和骨矿物质增加方面的作用,以证明DXA不能很好地表征肾性骨营养不良对骨大小和密度的明显影响。4.确定血清PTH和骨转换生物标志物的基线水平是否可以预测慢性肾衰竭、透析和移植受试者在随访期间的后续生长和骨矿物质增加模式(尺寸、密度和强度变化)。

项目成果

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Heidi J Kalkwarf其他文献

Heidi J Kalkwarf的其他文献

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{{ truncateString('Heidi J Kalkwarf', 18)}}的其他基金

Bone Mineral Accretion in Young Children
幼儿骨矿物质沉积
  • 批准号:
    8741982
  • 财政年份:
    2013
  • 资助金额:
    $ 5.08万
  • 项目类别:
Bone Mineral Accretion in Young Children
幼儿骨矿物质沉积
  • 批准号:
    8914657
  • 财政年份:
    2013
  • 资助金额:
    $ 5.08万
  • 项目类别:
Bone Mineral Accretion in Young Children
幼儿骨矿物质沉积
  • 批准号:
    8631290
  • 财政年份:
    2013
  • 资助金额:
    $ 5.08万
  • 项目类别:
EFFECTS OF RENAL OSTEODYSTROPHY DURING GROWTH
肾性骨营养不良对生长过程的影响
  • 批准号:
    7607736
  • 财政年份:
    2007
  • 资助金额:
    $ 5.08万
  • 项目类别:
Clinical-Component
临床成分
  • 批准号:
    10442030
  • 财政年份:
    2007
  • 资助金额:
    $ 5.08万
  • 项目类别:
BONE MINERAL DENSITY IN CHILDHOOD STUDY
儿童时期的骨矿物质密度研究
  • 批准号:
    7607733
  • 财政年份:
    2007
  • 资助金额:
    $ 5.08万
  • 项目类别:
Clinical-Component
临床成分
  • 批准号:
    10620723
  • 财政年份:
    2007
  • 资助金额:
    $ 5.08万
  • 项目类别:
Clinical Component
临床部分
  • 批准号:
    9312951
  • 财政年份:
    2007
  • 资助金额:
    $ 5.08万
  • 项目类别:
REFERENCE VALUES FOR BONE MASS AND DENSITY OF LUMBAR SPINE
腰椎骨量和密度参考值
  • 批准号:
    7607800
  • 财政年份:
    2007
  • 资助金额:
    $ 5.08万
  • 项目类别:
BONE MINERAL DENSITY IN CHILDHOOD STUDY
儿童时期的骨矿物质密度研究
  • 批准号:
    7374504
  • 财政年份:
    2005
  • 资助金额:
    $ 5.08万
  • 项目类别:

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绝经后骨质疏松症对肾性骨营养不良的影响
  • 批准号:
    19K17754
  • 财政年份:
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EFFECTS OF RENAL OSTEODYSTROPHY DURING GROWTH
肾性骨营养不良对生长过程的影响
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肾性骨营养不良对生长过程的影响
  • 批准号:
    7203758
  • 财政年份:
    2004
  • 资助金额:
    $ 5.08万
  • 项目类别:
Structural effects of renal osteodystrophy during growth
肾性骨营养不良对生长过程的结构影响
  • 批准号:
    7041829
  • 财政年份:
    2004
  • 资助金额:
    $ 5.08万
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Effects of Renal Osteodystrophy During Growth
肾性骨营养不良对生长过程的影响
  • 批准号:
    7044198
  • 财政年份:
    2003
  • 资助金额:
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肾性骨营养不良对生长过程的结构影响
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    6621662
  • 财政年份:
    2002
  • 资助金额:
    $ 5.08万
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肾性骨营养不良对生长过程的结构影响
  • 批准号:
    6435602
  • 财政年份:
    2002
  • 资助金额:
    $ 5.08万
  • 项目类别:
STRUCTURAL EFFECTS OF RENAL OSTEODYSTROPHY DURING GROWTH
肾性骨营养不良对生长过程的结构影响
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    7026543
  • 财政年份:
    2002
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  • 批准号:
    6719617
  • 财政年份:
    2002
  • 资助金额:
    $ 5.08万
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STRUCTURAL EFFECTS OF RENAL OSTEODYSTROPHY DURING GROWTH
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    6895172
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