Bardin T, Lebail-Darné J L, Zingraff J, Laredo J D, Voisin M C, Kreis H, Kuntz D
Clinique de Rhumatologie, Centre Viggo Petersen, Hôpital Lariboisière, Paris, France.
Am J Med. 1995 Sep;99(3):243-8. doi: 10.1016/s0002-9343(99)80155-7.
Patients treated by long-term maintenance hemodialysis frequently develop a form of chronic arthropathy that is strongly associated with beta 2-microglobulin amyloid deposition and related, at least in part, to beta 2-microglobulin retention. Successful renal transplantation is followed by a rapid fall in serum beta 2-microglobulin levels and might allow dissolution of amyloid deposits. The purpose of this work was to investigate the effects of renal transplantation on dialysis arthropathy.
Fourteen renal transplant recipients were selected on the basis of previous hemodialysis treatment for at least 10 years (mean 16) and a history of chronic joint pain prior to transplantation. They all received 10 to 17.5 mg/d of prednisone. Posttransplant rheumatologic manifestations were studied prospectively and compared to pretransplant rheumatologic manifestations recorded in medical charts and reported during patient interviews. Pretransplant and posttransplant articular roentgenograms were separately analyzed by three observers who were blinded to timing of the films. Beta 2-microglobulin amyloid was identified by Congo red staining and immunohistology.
After a mean posttransplant interval of 54 months (range 12 to 121), the articular condition was improved in 10 patients, unchanged in 1, and worsened in 3, according to patients' assessments. The number of painful joints decreased significantly (P < 0.05) as compared to the pretransplant period. However, the number and size of subchondral bone erosions remained unchanged, destructive arthropathies generally worsened, and articular beta 2-microglobulin amyloid deposits were identified in 2 patients, 2 and 10 years after renal transplantation, respectively.
Renal transplantation appeared to arrest progression of beta 2-microglobulin amyloid in dialysis patients, but it neither led to dissolution of deposits nor prevented progression of destructive arthropathies. Most articular symptoms were improved, probably as a result of corticosteroid therapy.
长期维持性血液透析治疗的患者常发生一种慢性关节病,这种病与β2-微球蛋白淀粉样沉积密切相关,且至少部分与β2-微球蛋白潴留有关。成功的肾移植术后血清β2-微球蛋白水平迅速下降,可能会使淀粉样沉积物溶解。本研究旨在探讨肾移植对透析性关节病的影响。
选择14例肾移植受者,他们此前至少接受了10年(平均16年)的血液透析治疗,且移植前有慢性关节疼痛病史。他们均接受10至17.5mg/d的泼尼松治疗。对移植后的风湿表现进行前瞻性研究,并与病历中记录的移植前风湿表现以及患者访谈中报告的情况进行比较。三位对X线片拍摄时间不知情的观察者分别对移植前和移植后的关节X线片进行分析。通过刚果红染色和免疫组织学鉴定β2-微球蛋白淀粉样物质。
移植后平均间隔54个月(范围12至121个月),根据患者评估,10例患者的关节状况改善,1例不变,3例恶化。与移植前相比,疼痛关节的数量显著减少(P<0.05)。然而,软骨下骨侵蚀的数量和大小保持不变,破坏性关节病总体上恶化,并且在肾移植后2年和10年分别在2例患者中发现关节β2-微球蛋白淀粉样沉积物。
肾移植似乎能阻止透析患者β2-微球蛋白淀粉样变的进展,但既不能使沉积物溶解,也不能阻止破坏性关节病的进展。大多数关节症状得到改善,可能是皮质类固醇治疗的结果。