Ascites and Kidney Transplantation: Case Report and Critical Appraisal of the Literature

Markov, M.; Thiel, David H. Van; Nadir, Abdul

doi:10.1007/s10620-006-9727-7

Cited by 10 publications

(9 citation statements)

References 30 publications

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“…Abdominal accumulation of fluid after renal transplant in 1 case was felt to be the result of volume expansion during allograft rejection, causing cardiac dysfunction and hepatic congestion in 1 case report. 4 No hepatic, oncologic, or cardiac diseases were present in our patient.…”

Section: Discussionmentioning

confidence: 62%

Surgical Correction of Nephrogenic Ascites in a Renal Transplant Recipient

Jaffers¹,

Narayanan²,

Fasola³

2012

Exp Clin Transplant

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Section: Discussionmentioning

confidence: 62%

Surgical Correction of Nephrogenic Ascites in a Renal Transplant Recipient

Jaffers¹,

Narayanan²,

Fasola³

2012

Exp Clin Transplant

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“…In a post renal transplant patient presenting with ascites, more common causes like chronic liver disease,9 infections like peritoneal tuberculosis will be considered and may result in delay of diagnosis. So a stepwise approach should be employed to establish the diagnosis.…”

Section: Discussionmentioning

confidence: 99%

A rare cause of ascites in a renal transplant recipient

et al. 2018

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Thirty-five-year-old man, underwent renal transplantation 4 years back and was doing well. He now presented with complaints of ascites with engorged neck veins and dyspnoea on exertion for last 6 months. Examination showed elevated jugular venous pressure with two prominent descents, high pitched diastolic heart sound (pericardial knock). Echocardiography showed characteristic features of thickened pericardium, septal bounce, expiratory flow reversal in hepatic veins and phasic variation of mitral inflow, suggestive of constrictive pericarditis. The patient was started on empirical antitubercular therapy and diuretics. The patient symptomatically improved, but in view of persisting constrictive physiology he was planned for pericardiectomy.

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“…3 Ascites can also be classified as associated with portal hypertension (such as liver cirrhosis, heart failure or Budd-Chiari syndrome) or not associated with portal hypertension (peritonitis or peritoneal metastases). 4 Another etiology, uncommon in Western countries, is idiopathic non-cirrhotic portal hypertension, and it is rarely considered in the differential diagnoses. 5 Little is known about the pathophysiology of this entity, which is defined by the presence of clinical signs and symptoms of portal hypertension in the absence of known cirrhosis or liver disease.…”

Section: Introductionmentioning

confidence: 99%

“…2,3 The occurrence of ascites in the post-renal transplantation is rare and may occur with either preserved graft function or in situations of its dysfunction. 4 There are reports of cases associated with problems such as rejection, graft decapsulation, urinary or vascular leakage, lymphocytosis, transudation, or infection. 7,8 In rare cases, ascites and hepatotoxicity is associated with immunosuppressive drugs such as and pathophysiological.…”

Section: Introductionmentioning

confidence: 99%

Refractory ascites and graft dysfunction in early renal transplantation

et al. 2019

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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.

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Ascites and Kidney Transplantation: Case Report and Critical Appraisal of the Literature

Cited by 10 publications

References 30 publications

Surgical Correction of Nephrogenic Ascites in a Renal Transplant Recipient

Surgical Correction of Nephrogenic Ascites in a Renal Transplant Recipient

A rare cause of ascites in a renal transplant recipient

Refractory ascites and graft dysfunction in early renal transplantation

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