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.

Ascites development is associated with worse outcome in patients after kidney transplantation

“…Treatment includes increase in frequency of dialysis sessions or changes to dialysate to increase amount of ultrafiltration 14,16 . However, ascites often resolves after kidney transplantation as restoration of fluid balance occurs 1,7,15‐17 . Patients with KT who re‐start or start peritoneal dialysis (PD) after failed renal graft made up 4 (5%) patients with ascites.…”

“…Ascites following kidney transplantation (KT) is believed to be an uncommon but ominous finding that can occur with normal or abnormal kidney function 1‐3 . Ascites can have varying pathophysiology, with the majority of cases in non‐transplanted patients in the United States attributed to hepatic etiologies, most notably cirrhosis (81%) 4‐7 .…”

“…Other causes may include malignancies (10%), heart failure (3%), tuberculosis (2%), besides other etiologies 3,5,8‐10 . Other than limited case reports, no study has characterized the development of ascites in the post‐KT population 1‐3,11 or its effect on overall clinical outcomes.…”