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A Review of Humoral Rejection in ABO-Incompatible Kidney Transplantation, with Local (Intrarenal) DIC as the Underlying Condition
http://hdl.handle.net/10191/33126
http://hdl.handle.net/10191/33126dc09043c-40ad-407d-87f4-e6d06464ae6c
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
45(3)_95-102.pdf (1.3 MB)
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| Item type | 紀要論文 / Departmental Bulletin Paper(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 2015-08-25 | |||||
| タイトル | ||||||
| タイトル | A Review of Humoral Rejection in ABO-Incompatible Kidney Transplantation, with Local (Intrarenal) DIC as the Underlying Condition | |||||
| タイトル | ||||||
| タイトル | A Review of Humoral Rejection in ABO-Incompatible Kidney Transplantation, with Local (Intrarenal) DIC as the Underlying Condition | |||||
| 言語 | en | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| キーワード | ||||||
| 主題Scheme | Other | |||||
| 主題 | ABO-incompatible kidney transplantation | |||||
| キーワード | ||||||
| 主題Scheme | Other | |||||
| 主題 | anti-A and anti-B antibodies | |||||
| キーワード | ||||||
| 主題Scheme | Other | |||||
| 主題 | humoral rejection | |||||
| キーワード | ||||||
| 主題Scheme | Other | |||||
| 主題 | hyperacute rejection | |||||
| キーワード | ||||||
| 主題Scheme | Other | |||||
| 主題 | local DIC | |||||
| キーワード | ||||||
| 主題Scheme | Other | |||||
| 主題 | intrarenal DIC | |||||
| キーワード | ||||||
| 主題Scheme | Other | |||||
| 主題 | Banff classification | |||||
| 資源タイプ | ||||||
| 資源 | http://purl.org/coar/resource_type/c_6501 | |||||
| タイプ | departmental bulletin paper | |||||
| 著者 |
Takahashi, Kota
× Takahashi, Kota |
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| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | The underlying condition associated with humoral rejection in ABO-incompatible kidney transplantation is local (intrarenal) disseminated intravascular coagulation (DIC). Anti-A and anti-B antibodies adhere to blood group antigens on vascular endothelial cells, triggering antigen-antibody reactions, which cause endothelial cell injury. This, in its turn, induces the production of cytokines, migration factors, and free radicals, which activate platelets and complements, and induce thrombi, the migration of granulocytes and macrophages, and phagocytosis. As lesions progress, interstitial hemorrhage as well as necrosis and infarction due to ischemia are also caused. The degree of renal dysfunction is determined by the amount of antibodies (antibody titer), the degree of vascular endothelial injury, and the site of the lesions in blood vessels (arteries). (Fig. 1). | |||||
| 書誌情報 |
Acta medica et biologica en : Acta medica et biologica 巻 45, 号 3, p. 95-102, 発行日 1997-09 |
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| 出版者 | ||||||
| 出版者 | Niigata University School of Medicine | |||||
| ISSN | ||||||
| 収録物識別子タイプ | ISSN | |||||
| 収録物識別子 | 05677734 | |||||
| 書誌レコードID | ||||||
| 収録物識別子タイプ | NCID | |||||
| 収録物識別子 | AA00508361 | |||||
| 著者版フラグ | ||||||
| 値 | publisher | |||||
