Refractory ascites and graft dysfunction in early renal transplantation

Abstract 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.

摘要：肾移植（Renal Transplant, RT）术后腹水的发生较为罕见，其诱因多为手术或内科并发症。
病例报告：患者为61岁男性，有动脉高血压病史、舌癌病史，日均饮酒12~20g。患者因常染色体显性遗传性多囊肾病继发慢性肾脏病，未合并肝多囊病。于2017年9月接受尸体供肾肾移植手术，术后因肾动脉狭窄接受手术矫正，出现移植肾功能延迟恢复。2018年1月因新发腹水入院，利尿剂治疗无效，查体可见腹部侧支循环。患者存在移植肾功能异常，他克莫司血药浓度达标，尿常规无异常，伴轻度贫血，无血小板减少症；血清白蛋白水平为4.0g/dL，肝生化指标正常。腹水呈漏出液特征，血清-腹水白蛋白梯度＞1.1g/dL。超声检查提示肝脏肿大，血管轴通畅，无脾大。临床暂停使用吗替麦考酚酯，剩余免疫抑制治疗方案减量，但患者仍存在难治性腹水，已排除感染性、代谢性、自身免疫性及肿瘤性病因，无肾病性蛋白尿，未出现心力衰竭。磁共振成像（MRI）提示存在与胆管囊肿相符的微小结节；上消化道内镜检查未发现胃食管静脉曲张，腹部淋巴显像结果正常。行腹腔镜探查联合肝活检术，病理提示为可能由血管病因导致的不完全间隔性肝硬化，伴部分胆管扩张。患者移植肾功能进行性恶化，重新开始血液透析治疗，原计划实施的门静脉压力直接测量术因腹水消退而暂缓。后续患者移植肾功能有所恢复。
讨论：不完全间隔性肝硬化是一种少见的非肝硬化性门静脉高压病因，目前对其定义、形态学及病理生理机制尚未完全明确。目前尚未检索到因该病理类型导致肾移植术后腹水的已发表病例，现有研究认为该病症可能与药物、免疫改变、感染、高凝状态及遗传易感性相关。