Eusébio Catarina Pereira, Correia Sofia, Silva Filipa, Almeida Manuela, Pedroso Sofia, Martins La Salete, Diais Leonídio, Queirós José, Pessegueiro Helena, Vizcaíno Ramon, Henriques António Castro
Serviço de Nefrologia do Centro Hospitalar de Trás-os-Montes e Alto Douro, Vila Real, Portugal.
Serviço de Nefrologia e Transplantação Renal do Centro Hospitalar do Porto, Porto, Portugal.
J Bras Nefrol. 2019 Oct-Dec;41(4):570-574. doi: 10.1590/2175-8239-JBN-2018-0175.
The occurrence of ascites after Renal Transplant (RT) is infrequent, and may be a consequence of surgical or medical complications. Case report: 61 year-old, male, history of arterial hypertension, tongue carcinoma and alcoholic habits 12-20g/day. He had chronic kidney disease secondary to autosomal dominant polycystic kidney disease, without hepatic polycystic disease. He underwent cadaver donor RT in September 2017. He had delayed graft function by surgically corrected renal artery stenosis. He was admitted in January 2018 for ascites de novo, with no response to diuretics. HE had visible abdominal collateral circulation. Graft dysfunction, adequate tacrolinemia, Innocent urinary sediment, mild anemia, without thrombocytopenia. Serum albumin 4.0g / dL. Normal hepatic biochemistry. Peritoneal fluid with transudate characteristics and serum albumin gradient > 1.1. Ultrasound showed hepatomegaly, permeable vascular axes, without splenomegaly. Mycophenolate mofetil was suspended, with reduced remaining immunosuppression. He maintained refractory ascites: excluded infectious, metabolic, autoimmune and neoplastic etiologies. No nephrotic proteinuria and no heart failure. MRI: micronodules compatible with bile cysts. Upper Digestive Tract Endoscopy did not show gastroesophageal varicose veins. Normal abdominal lymphoscintigraphy. He underwent exploratory laparoscopy with liver biopsy: incomplete septal cirrhosis of probable vascular etiology some dilated bile ducts. He maintained progressive RT dysfunction and restarted hemodialysis. The proposed direct measurement of portal pressure was delayed by ascites resolution. There was further recovery of the graft function. Discussion: Incomplete septal cirrhosis is an uncommon cause of non-cirrhotic portal hypertension. Its definition is not well known, morphological and pathophysiological. We have not found published cases of post-RT ascites secondary to this pathology, described as possibly associated with drugs, immune alterations, infections, hypercoagulability and genetic predisposition.
肾移植（RT）后腹水的发生并不常见，可能是手术或内科并发症的结果。病例报告：一名61岁男性，有动脉高血压、舌癌病史，每日饮酒量为12 - 20克。他患有常染色体显性多囊肾病继发的慢性肾脏病，无肝多囊病。2017年9月接受了尸体供肾肾移植。因手术矫正肾动脉狭窄导致移植肾功能延迟。2018年1月因新发腹水入院，对利尿剂无反应。他可见腹部侧支循环。移植肾功能不全，他克莫司血药浓度正常，尿沉渣无异常，轻度贫血，无血小板减少。血清白蛋白4.0g/dL。肝脏生化指标正常。腹水为漏出液性质，血清白蛋白梯度>1.1。超声显示肝脏肿大，血管轴通透，无脾肿大。停用霉酚酸酯，减少了剩余的免疫抑制。他的腹水持续难治：排除了感染、代谢、自身免疫和肿瘤病因。无肾病性蛋白尿且无心力衰竭。磁共振成像（MRI）：发现与胆管囊肿相符的微小结节。上消化道内镜检查未显示胃食管静脉曲张。腹部淋巴闪烁造影正常。他接受了 exploratory laparoscopy（此处可能有误，推测为“exploratory laparotomy”，即剖腹探查术）并进行了肝活检：可能因血管病因导致的不完全性间隔性肝硬化，一些胆管扩张。他的移植肾功能持续恶化并重新开始血液透析。由于腹水消退，提议的门静脉压力直接测量被推迟。移植肾功能进一步恢复。讨论：不完全性间隔性肝硬化是一种不常见的非肝硬化性门静脉高压病因。其定义在形态学和病理生理学方面尚不明确。我们未发现已发表的关于肾移植后腹水继发于此种病理情况的病例，这种情况可能与药物、免疫改变、感染、高凝状态和遗传易感性有关。
