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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2012  |  Volume : 23  |  Issue : 5  |  Page : 925-928
Angiodysplastic lesions as a cause of colonic bleeding in patients with chronic renal disease: Is there an association?

Department of Pharmacology, Medical School, University of Athens; Department of Vascular Surgery, "Iasò General" Hospital, Athens, Greece

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Date of Web Publication13-Sep-2012


Gastrointestinal bleeding due to angiodysplastic lesions of the large bowel is a common problem among patients receiving hemodialysis and may sometimes be life-threatening. Several hypotheses have been advanced in order to explain the increased incidence of these lesions in this cohort of patients, including degenerative, metabolic, circulatory and other systemic factors. In terms of diagnosis, several advances have been made with sophisticated techniques, but endoscopy seems to be the most effective, having a dual role in diagnosis and treatment. Although most bleeds stop spontaneously, conservative treatment may not be enough. Endoscopic treatment, embolization with infusion of vasopressin, surgical resection of the bleeding intestinal segment and hormone administration may be useful therapeutic tools.

How to cite this article:
Galanopoulos G. Angiodysplastic lesions as a cause of colonic bleeding in patients with chronic renal disease: Is there an association?. Saudi J Kidney Dis Transpl 2012;23:925-8

How to cite this URL:
Galanopoulos G. Angiodysplastic lesions as a cause of colonic bleeding in patients with chronic renal disease: Is there an association?. Saudi J Kidney Dis Transpl [serial online] 2012 [cited 2022 Jan 18];23:925-8. Available from: https://www.sjkdt.org/text.asp?2012/23/5/925/100858

   Introduction Top

The term angiodysplasia was first used by Galdabini in 1974. [1] Angiodysplasie are abnormal, dilated and tortuous small vessels with a diameter less than 1 cm within the mucosal and submucosal layer of the large bowel. Their wall is thin and consists of endothelium. Rarely may a thin smooth muscle layer be present circumferentially. [2]

These lesions are frequently multiple and located, in 77% of the cases, in the right colon. [3] Additionally, they are not associated with other cutaneous or visceral lesions. Angiodysplasia of the gastrointestinal tract was an underestimated pathological entity for many decades. The improvement of diagnostic techniques made evident that these vascular malformations were not as rare as it was previously believed. Later, these lesions were recognized as not rare causes of gastrointestinal bleeding, responsible for significant morbidity and mortality, particularly in the elderly and in patients with chronic kidney disease (CKD).

   Epidemiology Top

The prevalence of angiodysplasia of the entire gastrointestinal tract in the general population is 0.82%. [4] Angiodysplasia account for 2-8% of all patients presenting with gastrointes tinal bleeding. [5] Angiodysplastic lesions in the general population are usually detected in patients older than 60 years old, [6] while in patients with CKD they may be detected at a younger age. [7] In this cohort of patients, angiodysplasia is the leading cause of recurrent lower gastrointestinal tract hemorrhage, accounting for 19-32% of all lower gastrointestinal bleedings, while the respective percentage in the general population is 5-6%. [4]

   Etiopathogenesis Top

The etiology of angiodysplastic lesions and their correlation with CKD are not well known. The increased incidence in this cohort of patients indicates that there are some particular conditions that are favorable to developing this kind of lesions.

First of all, angiodysplasia seems to be degenerative in nature, secondary to intermittent obstruction of the submucosal veins and hypoxemia. The intramural components of the colon blood supply are susceptible to chronic, intermittent and partial obstruction due to intestinal motility, especially at the points where they pierce the muscular layers of the colon. Chronic and repeated trauma to the vessel wall with time could cause deformation and, eventually, arteriovenous communications. [8],[9] Hypoxemia and hypoxia at the colonic wall in patients with CKD may be exacerbated due to several comorbidities such as diabetic microangiopathy that can affect the microcirculation of the colon, limiting further blood supply and, subsequently, mucosal oxygenation. Atherosclerotic peripheral vascular disease is another comorbidity that could further damage the intestinal vessel walls, especially in older patients, compromising the microcirculation of the large bowel. [10],[11],[12],[13]

In favor of the theory of the jeopardized blood supply to the colon, as an etiologic factor of angiodysplasia, is the fact that such lesions are often present in patients with aortic stenosis (Heyde's syndrome).

Another hypothesis related to the altered calcium metabolism observed in CKD can be entertained. Hypercalcemia, as a result of hyperparathyroidism, can cause intestinal vascular calcifications that eventually decrease their permeability, compromising the microcirculation of the intestinal mucosa, causing hypoxia, and, in addition, vulnerability of the vessels to repeated trauma caused by intestinal motility.

Another possible correlation between angiodysplastic lesions and functional characteristics of the large bowel in CKD patients is the presence of constipation. The prevalence of constipation in patients on hemodialysis is about 63% versus 10-20% in the general population. [14] This fact depends on several factors such as reduced fiber intake, administration of phosphate-binders and presence of diabetes. [15] Constipation may also be secondary to hyperparathyroidism that causes hypercalcemia. Constipation can increase the intraluminal pressure of the large bowel thus distending it. In accordance with the principle of Laplace, the wall tension is proportional to the intraluminal pressure and the radius. The increased wall tension could exacerbate the above-mentioned occlusion of the intramural vessels of the bowel, causing mucosal hypoxia and, consequently, favoring the alteration of structure and morphology of the small vessels.

Patients with CKD suffer from a bleeding diathesis due to hemostatic disorders. Platelet dysfunction is the main cause of hemorrhagic tendencies in advanced kidney disease. [16] Platelet dysfunction occurs as a result of uremia, including aggregation and adhesion; hemodialysis can partially correct these disturbances. [16]

All the above factors in addition to the frequent use of antiplatelet agents for the cardiovascular comorbidities and heparin and exposure to the artificial hemofilter surfaces during hemodialysis contribute to an important hemorrhagic diathesis and may explain the frequent bleeding from the lower gastrointestinal tract in hemodialysis patients.

   Diagnosis Top

Angiodysplasia can cause acute or chronic bleeding from the gastrointestinal tract. Multiple hemorrhagic episodes are common and mostly occult and intermittent in nature. In a high percentage of about 90%, bleeding stops spontaneously, [12] and patients may present with iron deficiency anemia secondary to recurrent bleeding.

Colonoscopy possesses an eminent position in the diagnostic and also therapeutic armamentarium. Endoscopically, the angiodysplasia appears as flat or slightly raised, bright red-colored lesions with a fern-like pattern of small veins radiating from a central vessel. [17] The diameter of the lesions varies between 2 mm and 10 mm, and they are multiple in 40- 75% of the cases. [4] Colonoscopy has a sensitivity of about 81% in diagnosing angiodysplastic lesions in the large bowel. [17]

Scintigraphy with 99 m Tc may be useful in localizing the source of bleeding, but not the cause of bleeding. It can detect even low-grade bleed of 0.1 mL/min. The sensitivity of this diagnostic tool is poor.

Angiography could be used in cases of active bleeding in order to localize the source of the hemorrhage by visualizing the extravasation of the contrast agent within the intestinal lumen. The bleeding activity must be of at least 1 mL/min. [2] In case of intermittent bleeding, the sensitivity of angiography is low. Another limiting factor in using angiography as a diagnostic method is the need for the use of an intravenous contrast agent.

Emerging data from the use of CT angiography in the diagnosis of gastrointestinal bleeding are promising. It seems to be helpful in the acute setting for visualization of the source of bleeding and its characterization. [18]

   Treatment Top

Conservative treatment must always be considered in hemodynamically stable patients, with fluids and transfusion, because most bleeding episodes stop spontaneously.

Endoscopy can be used as a first-line therapeutic tool. Argon plasma and bipolar coagulation have been used successfully in the treatment of angiodysplasia with a low complication rate. Angiography can be used as a therapeutic option, permitting embolization and infusion of vasopressin. [19] Furthermore, surgery has a role in case of unsuccessful hemostasis by endoscopic or angiographic means, or in case of frequent recurrences. Hormonal therapy must be taken into consideration when a patient cannot be subjected to a surgical operation or when the source of the bleeding cannot be exactly identified due to multiple lesions along the large bowel. Estrogens with or without progesterone have been used in CKD patients with conflicting results. [20] In a small number of patients, oral, intravenous or even transdermal estrogens have been used for long periods; [21] however, controlled trials are lacking. Side-effects of hormonal therapy, such as thrombosis, gynecomastia, gynecologic cancers, stroke and fluid retention, could limit its use. [22] Alternatively, octreotide, a synthetic analogue of somatostatin, can reduce splachnic blood supply, and has been used in the treatment of esophageal varicose veins hemorrhage. In small trials, six-month subcutaneous administration reduced bleeding and its recurrences in patients with advanced chronic renal failure. [23] Accordingly, further trials are needed in order to evaluate the safety and efficacy of the hormonal treatment in patients with CKD.

   References Top

1.Galdabini JJ, Waitman AC, Norellio PA, Greenfield AJ, Ezreleta M. Angiodysplasia of the colon: a cause of rectal bleeding. J Cardiovasc Radiol 1978;1:3-13.  Back to cited text no. 1
2.Poralla T. Angiodysplasia in the renal patient: how to diagnose and how to treat? Nephrol Dial Transplant 1998;13:2188-91.  Back to cited text no. 2
3.Meyer CT, Troncale LJ, Galloway S, Sheahan DG. Arteriovenous malformations of the bowel: an analysis of 22 cases and a review of the literature. Medicine 1981;60:36-48.  Back to cited text no. 3
4.Foutch PG. Angiodysplasia of the gastrointestinal tract. Am J Gasrtoenterol 1993;88: 807-18.  Back to cited text no. 4
5.Hemingway AP. Angiodysplasia: current concepts. Postgrad Med J 1988;64:259-63.  Back to cited text no. 5
6.Dodda G, Trotman BW. Gastrointestinal angiodysplasia. J Assoc Acad Minor Phys 1997;8: 16-9.  Back to cited text no. 6
7.Jesudason SR, Devasia A, Mathen VI, Bhaktaviziam A, Khanduri P. The pattern of angiodysplasia of the gastrointestinal tract in a tropical country. Surg Gynecol Obstet 1985; 161:525-31.  Back to cited text no. 7
8.Boley SJ, Brandt LJ, Frank MS. Severe lower gastrointestinal bleeding: Diagnosis and treatment. Clin Gastroenterol 1981;10:65-91.  Back to cited text no. 8
9.Boley SJ, Sammartano R, Adams A, Dibiase A, Kleinhaus S, Spraynager S. On the nature and aetiology of vascular ectasias of the colon. Gastroenterology 1977;72:650-60.  Back to cited text no. 9
10.Cunningham JT. Gastric telangiectasia in chronic hemodialysis patients: A report of six cases. Gastroenterol 1993;81:1131-3.  Back to cited text no. 10
11.Dave PB, Romeu J, Antonelli A, Eiser AR. Gastrointestinal telangiectasia. A source of bleeding in patients receiving hemodialysis. Arch Intern Med 1984;144:1781-3.  Back to cited text no. 11
12.Clouse RE, Costigan DJ, Mills BA, Zuckerman GR. Angiodysplasia as a cause of upper gastrointestinal bleeding. Arch Intern Med 1985;145:458-61.  Back to cited text no. 12
13.Doherty CC. Gastrointestinal bleeding in dialysis patients. Nephron 1993;63:132-6.  Back to cited text no. 13
14.Yasuda G. Prevalence of constipation in continuous ambulatory peritoneal dialysis patients and comparison with hemodialysis patients. Am J Kidney Dis 2002;39:1292-9.  Back to cited text no. 14
15.Evenepoel P, Meijers BK, Bammens BR, Verbeke K. Uremic toxins originating from colonic microbial metabolism. Kidney Int Suppl2009;76:S12-9.  Back to cited text no. 15
16.Kaw D, Malhotra D. Platelet dysfunction and end-stage renal disease. Semin Dial 2006;19: 317-22.  Back to cited text no. 16
17.Richter JM, Hedberg SE, Athanasoulis CA, Schapiro RH. Angiodysplasia. Clinical presentation and colonoscopic diagnosis. Dig Dis Sci 1984;29:481-5.  Back to cited text no. 17
18.Geffroy Y, Rodallec MH, Boulay-Coletta I, Jullès MC, Ridereau-Zins C, Zins M. Multi-detector CT angiography in acute gastrointestinal bleeding: why, when and how. Radiographics 2011;31:E35-46.  Back to cited text no. 18
19.Uflacker R. Transcatheter embolization for treatment of acute lower gastrointestinal bleeding. Acta Radiol 1987;28:425-30.  Back to cited text no. 19
20.Manzanera MJ, Gutièrrez E, Domínguez-Gil B, García JA, González E, Praga M. Digestive haemorrhage due to angiodysplasia in dialysis patients. Treatment with conjugated estrogens. Nefrologia 2005;25:412-5.  Back to cited text no. 20
21.Sloand JA, Schiff MJ. Beneficial effect of low-dose transdermal estrogen on bleeding time and clinical bleeding in uremia. Am J Kidney Dis 1995;26:22-6.  Back to cited text no. 21
22.Liu YK, Kosfeld RE, Marcum SG. Treatment of uremic bleeding with conjugated oestrogen. Lancet 1984;2:887-90.  Back to cited text no. 22
23.Rivera M, Lucero J, Guerrero A, et al. Octreotide in the treatment of angiodysplasia in patients with advanced chronic renal failure. Nefrologia 2005;25:332-5.  Back to cited text no. 23

Correspondence Address:
Georgios Galanopoulos
Department of Pharmacology, Medical School, University of Athens; Department of Vascular Surgery, "Iasò General" Hospital, Athens
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DOI: 10.4103/1319-2442.100858

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