Calciphylaxis is associated with hyperphosphatemia and increased osteopontin expression by vascular smooth muscle cells
Calciphylaxis is associated with hyperphosphatemia and increased osteopontin expression by vascular smooth muscle cells
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DOI：
10.1053/ajkd.2001.24533
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发表时间：
2001-06-01
影响因子：
13.2
通讯作者：
Moe, SM
中科院分区：
文献类型：
--
作者：
Ahmed, S;O'Neill, KD;Moe, SM
钙化性尿毒症小动脉病（CUA）是透析患者由于皮肤血管钙化而发生的致命性疾病。其发病机制已被归因于甲状旁腺激素（PTH）升高。然而，最近的研究评估血管钙化的非透析患者发现，平滑肌细胞发挥积极的作用，包括生产的骨基质蛋白骨桥蛋白，以检查各种临床参数和平滑肌细胞的CUA的参与，我们进行了病例对照分析比较10 CUA患者与我们目前的透析患者。对可用的组织切片进行骨桥蛋白、平滑肌细胞、内皮细胞和巨噬细胞标记物的免疫染色。CUA患者与我国现有透析人群比较，肥胖、白色、女性患者多见（P < 0.02）。实验室检查结果比较发现，CUA患者血清白蛋白降低，血磷升高，钙磷乘积升高（P < 0.01）。相比之下，两组之间的PTH或钙浓度没有差异。钙化血管的免疫组化显示所有钙化血管骨桥蛋白染色阳性，而所有非钙化血管显示无骨桥蛋白定位。中层平滑肌α-肌动蛋白染色减少伴钙化，细胞脱落，导致血管腔几乎闭塞。我们的病例对照研究表明高磷血症和钙磷乘积升高与CUA相关。组织学检查提示钙化与平滑肌细胞骨桥蛋白表达增加有关。(C)2001年由国家肾脏基金会，公司。
Calciphylaxis or calcific uremic arteriolopathy (CUA) is a fatal disease in dialysis patients due to calcification of cutaneous blood vessels. The pathogenesis has been attributed to elevated parathyroid hormone (PTH). However, recent studies evaluating vascular calcification in nondialysis patients have found that the smooth muscle cells play an active role, including production of the bone matrix protein osteopontin, To examine the involvement of various clinical parameters and smooth muscle cells of CUA, we performed a case-control analysis comparing 10 CUA patients with our current dialysis patients. Available histologic sections were immunostained for osteopontin, markers of smooth muscle cells, endothelial cells, and macrophages. Compared with our current dialysis population, patients with CUA were more likely to be obese, white, and female (P < 0.02), Comparison of laboratory values found CUA patients with lower serum albumin, greater serum phosphorus, and greater calcium X phosphorus product (P < 0.01). In contrast, there was no difference in the concentration of PTH or calcium between the 2 groups. Immunostaining of calcified blood vessels showed that all calcified vessels stained positive for osteopontin, whereas all the noncalcifed vessels showed no osteopontin localization. Staining for smooth muscle alpha -actin decreased in the medial layer with calcification, with cells appearing to be sloughed off, leading to near occlusion of the vessel lumen. Our case control study demonstrates that hyperphosphatemia and an elevated calcium X phosphorus product is associated with CUA. Histologic examination suggests that the calcification is associated with increased expression of osteopontin by smooth muscle cells. (C) 2001 by the National Kidney Foundation, Inc.