 Abstract | | |
Gastrointestinal (GI) angiodysplasia is a vascular lesion. It is a common cause of GI bleeding in chronic renal failure (CRF). We report three adult chronic hemodialysis patients with asymptomatic angiodysplasia. Over a period of four years, the hemoglobin level was stable and none of our patients received iron supplementation or erythropoietin (EPO) therapy. Incidence of angiodysplasia may be underestimated in the CRF patients. Further studies may be needed. Keywords: Angiodysplasia, Hemodialysis, Chronic renal failure, Digestive tract.
How to cite this article:
Charfeddine K, Kammoun K, Kharrat M, Yaich S, Mkawar K, Jarraya F, Bahloul H, Hachicha J. Asymptomatic Gastric Angiodysplasia in Chronic Hemodialysis Patients: Case Reports. Saudi J Kidney Dis Transpl 2003;14:57-60 |
How to cite this URL:
Charfeddine K, Kammoun K, Kharrat M, Yaich S, Mkawar K, Jarraya F, Bahloul H, Hachicha J. Asymptomatic Gastric Angiodysplasia in Chronic Hemodialysis Patients: Case Reports. Saudi J Kidney Dis Transpl [serial online] 2003 [cited 2022 Aug 7];14:57-60. Available from: https://www.sjkdt.org/text.asp?2003/14/1/57/33088 |
| Introduction | |  |
Upper gastrointestinal disorders, especially angiodysplasia that manifests as telangiectasia, are recognised with increased frequency in chronic renal failure. [1],[2]
Since the first report about the association of this condition with chronic renal failure in 1981, [3] many studies have confirmed this association and indicated that telangiectasia was a common cause of the initial and recurrent upper gastrointestinal (GI) bleeding in hemodialysis patients.
We report three cases of chronic hemodialysis patients who had angiodysplasia but never presented with gastrointestinal hemorrhage. The clinical characteristics of our three patients are summarised below.
| Case descriptions | | |
Case 1:
A 65-year-old man has been on chronic hemodialysis for four years at the time of this report. He had polycystic kidney disease in the native kidneys. He never had signs of GI hemorrhage or acute anemia. Gastric angiodysplasia was discovered on endoscopy for dyspeptic symptoms.
For at least four years of follow-up after gastric endoscopy, hemoglobin and serum iron level remained stable without iron supplemenation or erythropoietin (EPO) therapy.
Case 2:
A 34-year-old man, with end stage renal failure (ESRF) of undetermined aetiology was maintained well on chronic hemodialysis. He was found to have gastric angiodysplasia on endoscopic examination performed for dyspepsia (?). There was no history of GI bleeding. The surveillance of the hematologic parameters showed stable levels of hemoglobin and serum iron during the follow-up period.
Case 3:
A 43-year-old man was on chronic hemodialysis for ESRF secondary to chronic interstitial nephropathy. Angiodysplasia was discovered on gastric endoscopy. During four years of follow-up, he never presented with either GI symptoms of bleeding or needed any transfusion, iron supplementation and EPO.
In all these cases, endoscopy was systematically performed, and showed only inflammatory gastropathy. The angiodysplasia was diagnosed histologically, [Figure 1] and [Figure 2] In the third case, endoscopy was repeated after the histological results, and showed the typical findings of angiodysplasia.
| Discussion | | |
Angiodysplasia is a vascular lesion of the GI tract that is frequently localised in the right colon, the stomach and the duodenum. [2],[4],[5],[6] Multiple locations of angiodysplasia are frequently observed. [4],[7]
In a retrospective study, angiodysplasia caused 24% of the initial hemorrhage in CRF and 53% of the recurrent GI bleeding. [8] Other studies found that these lesions were an infrequent cause of GI bleeding. [9],[10] Our patients never presented any clinical or biological symptoms of GI hemorrhage during follow-up for four years. Angiodysplasia was fortuitously discovered in our cases due to random screening upper GI endoscopy, while it was diagnosed in the context of GI bleeding in almost all the studies in the literature. The incidence of angiodysplasia may be underestimated in CRF patients in the literature and there may be a need for prospective studies performing systematic screening endoscopy.
The prevalence of angiodysplasia increases with age regardless of renal function. [5],[11],[12],[13] The average age of patients with angiodysplasia in chronic CRF varies from 62 to 73 years, while the age of patients with renal failure and and angiodysplasia are younger [5],[14],[15] The age of our patients was compatible with that reported in the literature.
The diagnosis of angiodysplasia is made by endoscopy [3],[4],[5],[8],[16],[17] It manifests as telangiectasia with a flat or slightly raised lesion and fernlike margins The endoscopic diagnosis of angiodysplasia needs an advanced instrument and experienced physician.
Histopathology can help the diagnosis in atypical cases. In our three cases, the angiodysplasia was confirmed histologically. In one case, endoscopy was repeated, and it showed later typical findings of angiodysplasia.
Although the pathogenesis of angiodysplasia is still unknown, several theories suggested a vascular degenerative process accelerated by the hypoxygenation of the intestinal mucosa secondary to atherosclerotic peripheral vascular disease. [3],[4],[5],[6],[12]
| Conclusion | | |
Angiodysplasia is commonly reported as a cause of GI bleeding in chronic renal failure. Its real prevalence is still unknown. We report three cases of patients on chronic hemodialysis with angiodysplasia, who never had clinically detectable GI haemorrhage and who were accidentally discovered. Our cases raise some questions: Is angiodysplasia more frequent in CRF patients than what is reported in the literature, since it could remain asymptomatic, or is it as frequent as in the general population? Could the difference in frequency be explained only by the high bleeding tendency observed on these patients?
| Acknowledgements | | |
We thank the staff of the department of gastroenterology of the University Hospital, Sfax, Tunisia, for their co-operation in performing this study and also Faiza Mtar and Nabila Frikha for typing the manuscript.
| References | | |
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Correspondence Address:
K Charfeddine
Assistant Professor of Nephrology, Sfax University, P.O. Box 288, 3027 Sfax-Jadida
Tunisia
 Source of Support: None, Conflict of Interest: None  | Check |
PMID: 17657090 
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