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）术后腹水的发生率较低，可由外科或内科并发症引发。病例报告：患者为61岁男性，有动脉高血压、舌癌病史，日均饮酒12~20g。其慢性肾脏病继发于常染色体显性遗传性多囊肾病（autosomal dominant polycystic kidney disease），无肝多囊病。患者于2017年9月接受尸体供肾肾移植，术后因肾动脉狭窄经手术矫正后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不全，他克莫司血药浓度达标，尿沉渣无异常，伴轻度贫血，无血小板减少。血清白蛋白水平为4.0g/dL，肝生化指标正常。腹腔积液呈漏出液特征，血清白蛋白梯度>1.1。超声检查示肝大、血管轴通畅，无脾大。停用吗替麦考酚酯（mycophenolate mofetil），剩余免疫抑制治疗方案减量。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，亦无心力衰竭。磁共振成像可见符合胆汁囊肿的微小结节。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。行腹腔镜探查术联合肝活检，病理提示不全间隔性肝硬化，病因考虑为血管性，伴部分胆管扩张。患者移植肾功能持续恶化，重新开始血液透析。原计划直接测量门静脉压力，但因腹水消退而延迟实施。后续患者移植肾功能恢复。讨论：不全间隔性肝硬化是一种罕见的非肝硬化性门静脉高压症病因，其定义、形态学及病理生理学特征尚未明确。目前尚无肾移植术后继发于此病理的腹水病例报道，该病变可能与药物、免疫改变、感染、高凝状态及遗传易感性相关。