一名系统性红斑狼疮患者因大量血凝块和严重血小板减少导致肾后急性肾损伤并发尿路梗阻:病例报告。

IF 0.9 Q4 RHEUMATOLOGY
Yuya Fujita, Shuzo Sato, Shuhei Yoshida, Tomoyuki Asano, Haruki Matsumoto, Jumpei Temmoku, Naoki Matsuoka, Hiroshi Ohkawara, Norshalena Shakespear, Kiyoshi Migita
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引用次数: 0

摘要

系统性红斑狼疮(SLE)常伴有抗磷脂抗体综合征(APS),这些疾病可能会同时出现严重的免疫性血小板减少症,甚至急性肾损伤(AKI);然而,因出血导致的肾损伤后AKI并不常见。在此,我们描述了一例系统性红斑狼疮和 APS 患者肾后 AKI 和无尿的病例,其原因是继发性免疫血小板减少症引起的大量血凝块导致尿路梗阻。一名50岁的日本女性因无尿、腹部压痛、躯干和双腿紫癜以及严重血小板减少而被送入我院。她在 45 岁之前一直接受 APS 和系统性红斑狼疮的治疗。计算机断层扫描显示,她的双侧尿道都有血凝块,但没有外渗,因此她被诊断为因泌尿系统完全梗阻而导致的肾移植后 AKI。此外,根据她的病史、血小板相关 IgG 水平升高和巨核细胞计数增加,她被诊断为继发性免疫性血小板减少症并发系统性红斑狼疮和 APS。她的 APS 相关自身抗体也升高,包括抗磷脂酰丝氨酸/凝血酶原 IgM 和 IgG。然而,她并没有出现狼疮性肠炎或膀胱炎等并发症。她接受了糖皮质激素、静脉注射免疫球蛋白和持续血液透析/血液滤过的综合治疗,症状和肾功能障碍迅速得到改善。继发性免疫血小板减少症引起的尿路大量出血可导致肾移植后 AKI。要改善这类患者的预后,必须进行适当的诊断和积极的治疗。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Post-renal acute kidney injury complicated by urinary tract obstruction due to massive blood clots and severe thrombocytopenia in a patient with systemic lupus erythematosus: A case report.

Systemic lupus erythematosus (SLE) is often seen with antiphospholipid antibody syndrome (APS), and these conditions may occur concurrently with severe immune thrombocytopenia (ITP) and even acute kidney injury (AKI); however, post-renal AKI due to bleeding is uncommon. Here, we describe a case of post-renal AKI and anuria in a patient with SLE and APS, which were attributable to urinary tract obstruction due to massive blood clots caused by secondary ITP. A 50-year-old Japanese woman was admitted to our hospital with anuria, abdominal tenderness, purpura in the trunk and in both legs, and severe thrombocytopenia. She had been receiving medical treatment for APS and SLE till the age of 45 years. Computed tomography revealed a blood clot without extravasation in both urinary tracts, and she was diagnosed with post-renal AKI due to complete obstruction of the urinary system. Additionally, based on her medical history, elevated platelet-associated Immunoglobulin G (IgG) levels, and increased megakaryocyte count, she was diagnosed with secondary ITP complicated by SLE and APS. She also had elevated APS-related autoantibodies, including antiphosphatidylserine/prothrombin Immunoglobulin M (IgM), and IgG. However, concomitant serositis such as lupus enteritis or cystitis was not seen. She was treated with a combination of glucocorticoids, intravenous immunoglobulin, and continuous haemodialysis/haemofiltration, which resulted in rapid improvement of her symptoms and renal dysfunction. Secondary ITP-induced massive bleeding of urinary tract can cause post-renal AKI. Appropriate diagnosis and aggressive treatment are necessary to improve prognosis in such patients.

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