Schober H C, Han Z H, Foldes A J, Shih M S, Rao D S, Balena R, Parfitt A M
Division of Internal Medicine, Community Hospital, Wolgast, Germany.
J Am Soc Nephrol. 1998 Jul;9(7):1225-33. doi: 10.1681/ASN.V971225.
To characterize the magnitude and location of mineralized bone loss, 40 patients (20 men, 20 women, 29 white, 11 black) with clinically significant renal osteodystrophy who could be unambiguously classified based on histologic criteria as having osteitis fibrosa (OF; 20 cases) or osteomalacia (OM; 20 cases) were studied; they had been on maintenance hemodialysis for 4.6 +/- 3.0 yr. One hundred forty-two healthy women of similar age and ethnic composition served as control subjects. In all subjects, the proportions of mineralized bone, osteoid, and porosity (nonbone soft tissue) were measured separately in cortical and cancellous bone tissue, from intact full-thickness biopsies of the ilium, representative of the axial skeleton. The results were related to the volumes of cortical and cancellous bone tissue separately and to the volume of the entire biopsy core. Approximately three-quarters of the patients had measurements in the appendicular skeleton by single photon absorptiometry of the radius and morphometry of the metacarpal. Disease effects did not differ significantly between ethnic groups. Mineralized cortical bone volume (per unit of core volume) was reduced by approximately 45% in both patient groups. Mineralized cancellous bone volume was significantly increased by 36% in the patients with OF and nonsignificantly reduced by 9% in the patients with OM; however, the reduction in the latter patients was significant in relation to tissue volume. The combined total deficit for both types of iliac bone was approximately 20% in the patients with OF and approximately 40% in the patients with OM. Significant reductions in appendicular cortical bone were demonstrated in both patient groups at both measurement sites. Regardless of the current histologic classification, the major structural abnormality in the skeleton is generalized thinning of cortical bone due to increased net endocortical resorption, the most characteristic effect on bone of hyperparathyroidism. Protection of the skeleton from the adverse consequences of renal failure will require therapeutic intervention in patients with no symptoms of either renal or bone disease.
为了描述矿化骨丢失的程度和位置，对40例（20名男性，20名女性，29名白人，11名黑人）具有临床显著肾性骨营养不良且可根据组织学标准明确分类为纤维性骨炎（OF；20例）或骨软化症（OM；20例）的患者进行了研究；他们接受维持性血液透析已达4.6±3.0年。142名年龄和种族构成相似的健康女性作为对照。在所有受试者中，从代表中轴骨骼的完整全层髂骨活检中，分别测量皮质骨和松质骨组织中矿化骨、类骨质和孔隙率（非骨软组织）的比例。结果分别与皮质骨和松质骨组织的体积以及整个活检核心的体积相关。大约四分之三的患者通过桡骨单光子吸收法和掌骨形态测量法对四肢骨骼进行了测量。不同种族组之间的疾病影响无显著差异。两组患者的矿化皮质骨体积（每单位核心体积）均减少了约45%。OF患者的矿化松质骨体积显著增加了36%，OM患者的矿化松质骨体积无显著减少，减少了9%；然而，后一组患者的减少相对于组织体积而言是显著的。OF患者两种类型髂骨的总联合缺损约为20%，OM患者约为40%。两组患者在两个测量部位的四肢皮质骨均有显著减少。无论目前的组织学分类如何，骨骼的主要结构异常是由于内皮质净吸收增加导致皮质骨普遍变薄，这是甲状旁腺功能亢进对骨骼最具特征性的影响。要保护骨骼免受肾衰竭的不良后果，需要对无肾脏或骨骼疾病症状的患者进行治疗干预。
