|Year : 2007 | Volume
| Issue : 1 | Page : 23-25
Gastric antral vascular ectasia in a renal transplant patient
P George1, G Pawar2, B Pawar3, J Das1
1 Department of Internal Medicine, Christian Medical College and Hospital, Ludhiana, India
2 Department of Gastroenterology, Christian Medical College and Hospital, Ludhiana, India
3 Department of Nephrology, Christian Medical College and Hospital, Ludhiana, India
Department of Internal Medicine, Christian Medical College and Hospital, Brown Road, Ludhiana - 141 008, Punjab
Source of Support: None, Conflict of Interest: None
Gastric antral vascular ectasia syndrome (GAVE) is an uncommon cause of gastrointestinal bleeding. Pharmacotherapeutic and endoscopic intervention in patients with GAVE is a challenge, especially when surgery is a closed option due to an underlying severe hepatic impairment. The clinical presentation and management of a renal allograft recipient with the GAVE syndrome is described.
Keywords: Cirrhosis, endoscopy, gastric antral vascular ectasia, renal transplant
|How to cite this article:|
George P, Pawar G, Pawar B, Das J. Gastric antral vascular ectasia in a renal transplant patient. Indian J Nephrol 2007;17:23-5
| ~ Introduction|| |
Gastric antral vascular ectasia (GAVE) is rare and constitutes a small subset of the vascular causes of gastrointestinal bleeding which, in itself, constitutes only 2-3% of all causes of gastrointestinal bleeding. It has been reported in bone marrow transplant patients but not in renal transplant patients. A renal allograft recipient with the GAVE syndrome and his management is described.
| ~ Case Report|| |
A 42-year-old male who had undergone live, related kidney transplantation elsewhere 15 years ago for chronic glomerulonephritis was admitted with complaints of abdominal distension for a week and fever and altered sensorium for a day. Six months earlier, hepatitis B-related, decompensated cirrhosis with blood loss anemia had been diagnosed. The available records revealed that hepatitis B had been diagnosed 4 years after his kidney transplantation at another hospital, and he had been treated with lamivudine. Details of HBeAg, anti HBc, and HBV DNA at diagnosis were not available. Anti HCV was negative. No records were available with which we could track the disease progression. His upper gastrointestinal endoscopy showed grade 1 esophageal varices and antral erosions. The colonoscopy was normal. Kidney biopsy showed significant glomerular atrophy, mesangial widening with splitting of the basement membrane, and tubular atrophy and fibrosis; these features were consistent with the diagnosis of chronic allograft nephropathy. His immunosupression regimen comprised of prednisolone, cyclosporine, and azathioprine. This was later changed to prednisolone, everolimus, and mycophenolate mofetil.
He did not go for review thereafter but apparently continued to have weight loss, anorexia, and progressive abdominal distension. Intermittent melaena was present for 3 months and blood had been transfused elsewhere during this period.
On examination, he was cachexic, with severe pallor and grade III hepatic encephalopathy. No peripheral edema or icterus was present. He had tachycardia and was normotensive. Abdominal examination revealed a shrunken liver, mild splenomegaly, and moderate ascites. Cardiovascular and respiratory evaluation was normal.
Investigations showed severe anemia (hemoglobin 4 gm/dl), thrombocytopenia (platelet count 78 000/cmm), renal failure (blood urea 248 mg/dl, serum creatinine 4.4 mg/dl), and hypokalemia. He also had hypoalbuminemia (albumin 2.1 gm/dl) and a coagulopathy (prothrombin time: test 27 s and control 12 s). Diagnostic paracentesis showed no evidence of infection. Hypogastrinemia (10 pg/ml) was present. Renal biopsy was not repeated due to his poor fitness for the procedure. Investigations for HBeAg, anti HBc, and HBV DNA were not done because of the severe cirrhosis and the disease progression despite treatment with lamivudine. He was diagnosed as having decompensated postnecrotic cirrhosis (hepatitis B-related) Child-Pugh C with portal hypertension and gastrointestinal bleeding, chronic allograft nephropathy, and blood loss anemia. He was managed on a hepatic coma regime and transfused blood and fresh frozen plasma. Upper gastrointestinal endoscopy showed portal hypertensive gastropathy with gastric antral vascular ectasia [Figure - 1]; endoscopic electrocoagulation with a monopolar electrosurgical hemostasis probe was done (Olympus CD 1U). Seven units of packed cells were transfused. Tranexamic acid, conjugated estrogen, and octreotide infusion were added to his treatment. Daily hemoglobin estimation was done thereafter and the level appeared to be stable at around 9 gm/dl, requiring ten units of packed cell transfusion over the next 17 days. During this period he underwent three further sessions of endoscopic electrocoagulation, at weekly intervals, for GAVE lesions. A gastric antral biopsy was normal. Renal function remained stable. He was referred for argon plasma coagulation on the 24 th day in hospital in view of the persistent GAVE lesions and the persisting need for blood transfusions. An improvement in the endoscopic appearance and his transfusion requirement was observed after argon plasma coagulation [Figure - 2]. However, he succumbed to sepsis 6 weeks after hospitalization.
| ~ Discussion|| |
GAVE is rare and unreported in renal transplant recipients. Management of GAVE in the presence of cirrhosis and allograft nephropathy is a challenge.
Chronic gastrointestinal bleeding occurs in more than half of the patients with GAVE. It is characterized by red patches or spots in either a diffuse or linear array in the antrum of the stomach. Classic biopsy features of the GAVE syndrome include gastric ectasia, gastric dilation, thrombi, increased spindle cell proliferation, and fibrohyalinosis. However, false negative rates are quite high as the lesions are focal, and a negative biopsy does not exclude GAVE. 
Tranexamic acid, a potent antifibrinolytic drug, has been used previously in the treatment of upper gastrointestinal bleeding and in a meta-analysis was found to cause a 20-30% reduction in bleeding, 30-40% reduction in the need for surgery, and a 40% reduction in overall mortality in patients with a variety of causes of upper gastrointestinal bleeding.  It is eliminated mainly in the urine and tends to accumulate in patients with uremia. Appropriate dosage recommendations are given for tranexamic acid therapy in cases of renal failure.  Case reports support the efficacy of estrogen-progesterone treatment, which is particularly effective in patients with renal failure.  It should be the treatment of first choice for multiple, bleeding vascular malformations of the gastrointestinal tract in uremic patients with high transfusion needs, especially when these malformations are inaccessible or refractory to endoscopic therapy and the risk of surgery is unacceptably high or surgical intervention is refused. 
Chronic octreotide injections appeared to have some efficacy in controlling GAVE-associated blood loss in a study of three patients with the GAVE syndrome who were not surgical candidates. 
Endoscopic electrocoagulation with monopolar probe has been reported to be effective and safe for controlling blood loss in patients with GAVE, especially in the presence of cirrhosis. Several sessions have resulted in the eradication of vascular lesions and alleviation of anemia.  It could be the initial modality of therapy for this condition. Argon plasma coagulation (one to four sessions) showed resolution of gastric angiectasia, with no need for postprocedure transfusion, in a study of 17 patients who were followed up over a mean period of 30 months.  This makes it a preferred endoscopic modality of treatment, and gastric antrectomy, which is the curative surgery, is rarely necessary.
Target-of-rapamycin (TOR) inhibitors like everolimus are a promising alternative to calcineurin inhibitor-based immunosuppression in chronic allograft nephropathy patients, but have not been studied in patients with severe hepatic impairment. In patients with moderate hepatic impairment (Child Pugh score 7-9), dose needs to be reduced by half, with monitoring of serum drug levels. 
Initially, our patient responded well to medical management and electrocoagulation, as evidenced by the reduction in transfusion requirement. Argon plasma coagulation was done in view of the persisting vascular lesions and blood transfusion requirement in spite of four sessions of electrocoagulation therapy.
The GAVE syndrome is a rare complication of severe cirrhosis and is treated with argon plasma coagulation with long-term follow-up. It has been used with success in patients with hepatic encephalopathy for intensive management of the mucosal lesions to improve the quality of life.  Management of GAVE in the presence of renal allograft nephropathy requires careful endoscopic and medical management with modification of drug doses. A high index of suspicion is needed for the diagnosis of the GAVE syndrome in renal transplant patients with chronic blood loss and iron deficiency.
| ~ Acknowledgement|| |
Professors Sunita Jacob and Nalini Calton, Department of Pathology, Christian Medical College, Ludhiana.
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[Figure - 1], [Figure - 2]