Otani Masako, Shimojo Hisashi, Shiozawa Satoshi, Shigematsu Hidekazu
Department of Pathology, Shinshu University School of Medicine, Matsumoto, Japan.
Nephrology (Carlton). 2005 Oct;10(5):530-6. doi: 10.1111/j.1440-1797.2005.00478.x.
Bone marrow transplantation (BMT) is an effective therapeutic strategy for leukaemic malignancies and depressed bone marrow following cancer. However, its side effects on kidneys have been reported. Some drugs and irradiation are also suggested to be nephrotoxic. It is well known that haemolytic uraemic syndrome (HUS) after BMT develops as late-onset BMT nephropathy. Cyclosporine A (CsA) is a possible cause. Radiation nephropathy shows changes that are similar to the histology of HUS. These findings suggest that endothelial damage is closely associated with the pathogenesis of post-BMT nephropathy. Recently, some patients have developed glomerulonephritis accompanied by graft-versus-host disease (GVHD) after BMT. In these patients immune deposits are found mainly in subepithelium and mesangium equal to those of secondary membranous glomerulonephritis. A murine experimental model of GVHD manifests similar symptoms and histological changes to those of actual patients and may suggest the pathogenesis of glomerulonephritis.
骨髓移植（BMT）是治疗白血病恶性肿瘤以及癌症后骨髓抑制的一种有效治疗策略。然而，已有报道称其对肾脏有副作用。一些药物和辐射也被认为具有肾毒性。众所周知，BMT后的溶血性尿毒症综合征（HUS）会发展为迟发性BMT肾病。环孢素A（CsA）可能是其病因。放射性肾病表现出与HUS组织学相似的变化。这些发现表明，内皮损伤与BMT后肾病的发病机制密切相关。最近，一些患者在BMT后出现了伴有移植物抗宿主病（GVHD）的肾小球肾炎。在这些患者中，免疫沉积物主要出现在上皮下和系膜区，与继发性膜性肾小球肾炎的情况相同。GVHD的小鼠实验模型表现出与实际患者相似的症状和组织学变化，可能提示了肾小球肾炎的发病机制。
