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Case Report |
1 Department of Radiology, Leyenburg Hospital, Leyweg 275, 2545 CH The Hague,
The Netherlands.
2 Department of Surgery, Leyenburg Hospital, 2545 CH The Hague, The
Netherlands.
3 Department of Urology, Leyenburg Hospital, 2545 CH The Hague, The
Netherlands.
4 Department of Pathology, Leyenburg Hospital, 2545 CH The Hague, The
Netherlands.
Received July 25, 2001;
accepted after revision January 8, 2002.
Address correspondence to P. C. G. Simons.
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Seventeen months after stent-graft placement, the patient presented to his urologist because of left-sided abdominal pain. The patient had no fever. Serum creatinine level and leukocyte counts were normal. Erythrocyte sedimentation rate was slightly elevated at 21 mm/hr.
Abdominal sonography and excretory urography showed dilatation of the left pelvicaliceal system and obstruction of the left ureter at the level of the fourth lumbar vertebral body (Fig. 1D). CT showed the diameter of the aneurysm as unchanged. The aortic wall became thickened and enhanced after IV administration of contrast medium. The left ureter was obstructed at the level of the thickened aortic wall (Figs. 1E and 1F). The position of the stent-graft was unchanged, and no endoleak was found. Nuclear renal scanning performed before and after the administration of furosemide showed an obstructed left kidney with 18% of total renal function.
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Because the patient had persistent pain in the left abdominal area and poor left renal function, a nephrectomy was performed. Findings at surgery were consistent with those on CT; the left renal pelvis and proximal ureter were obstructed. More distally, the left ureter was surrounded by inflammatory tissue that was continuous with the aortic wall. The springs of the stent-graft seemed to be palpable through the aortic wall.
Histopathologic examination showed a diffuse infiltrate of lymphocytes and plasma cells in the renal parenchyma in association with atrophic changes of the tubules and focal glomerulosclerosis. No signs of a primary glomerulonephritis were seen. The mucosa of the ureter showed edema and a focal aggregate of lymphocytes. Only the proximal part of the ureter had been resected, and around this structure, small lymphoplasmacytic infiltrates were found in the connective tissue surrounding the muscular layers.
To rule out allergies as the cause of the complication, we had the patient undergo skin sensitivity testing for various component materials (including nickel) of the stent-graft. The results of these tests were all negative. Five months after nephrectomy, the patient was doing well. Continuing CT follow-up has shown the position of the stent-graft and the diameter of the aneurysm to be unchanged, no evidence of endoleaks, and a normal appearance of the right kidney and other abdominal organs. However, a proximal progression of aortic wall thickening was observed. Therefore, in light of the reported success in treating retroperitoneal fibrosis with tamoxifen [3], we prescribed tamoxifen (10 mg twice daily) for the patient in an effort to stop progression of the periaortitis and to prevent further complications.
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In our patient, an unusual complication occurred. One year after the stent-graft placement, the aortic wall thickened, resulting in a radiologic appearance that suggested periaortitis. Clinically, the thickening caused ureteral obstruction, which eventually led to the left kidney and proximal ureter having to be resected. Histologically, the changes were compatible with hydronephrosis due to a lower urinary tract obstruction. No signs or symptoms of active glomerulonephritis or infection were found.
Atherosclerotic aortic aneurysm is a recognized cause of periaortitis and retroperitoneal fibrosis; these diseases in turn may cause ureteral obstruction and adhesions of adjacent abdominal organs. This triad of entities is also known as "inflammatory aortic aneurysm." The treatment of choice for an inflammatory aneurysm is surgical repair. Once the aneurysm is excluded from the blood circulation, the pressure on the aortic wall diminishes, and the periaortitis typically resolves spontaneously, resulting in the subsequent release of the ureters. The exact pathogenesis of inflammatory aortic aneurysm is not known [4]. An inflammatory response to leakage of atheromatous material and subsequent fibrosis have been suggested as the cause [5]. We carefully reviewed the patient's medical history and findings of CT and sonography but found no signs of inflammatory aortic aneurysm in our patient before or immediately after stent-graft placement. After 1 year, the stent-graft caused a macroscopic inflammatory response that affected the aortic wall. The microscopic inflammatory process is likely to have started earlier. Whether placement of the stent-graft may have induced release of atheromatous material into the deeper layers of the aortic wall remains unknown.
The literature includes reports of inflammatory reactions to polyester-covered endoluminal stents that caused reduced patency and perivascular thickening in animals [6]. Sapoval et al. [7] reported a stent-graft—related wall thickening in a patient who received a polyester-covered stent for an iliac artery dissection (after an angioplasty); the wall thickening resolved spontaneously after 11 months. These observations indicate that the polyester on the stent might be responsible for inflammatory reactions, although the exact mechanism of causation is unknown. The case of our patient differs from these reported cases in three regards. First, reports of polyester-related inflammatory reaction have never described the reaction as being so severe that it caused hydronephrosis. Second, Sapoval et al. [7] observed a transient reaction that decreased within 1 year, whereas the reaction in our patient showed progression after 1 year. Third, although Blum et al. [8] described a postimplantation syndrome with signs and symptoms such as fever, the elevation of the C-reactive protein level, and leukocytosis, to our knowledge reactions such as wall thickening and subsequent hydronephrosis have never before been reported in humans who have undergone stent-graft placement for aneurysms. The possibility that the reactions occur more commonly but remain undetected is unlikely because thorough follow-up of patients with the stents is performed with CT, and most patients are registered in databases like the EUROSTAR registry [2].
Alternatively, the small amounts of nickel in the metal meshwork of the stent-graft could have caused an allergic reaction in the patient. However, findings of skin tests performed to confirm this allergy were negative. A concomitant bacterial infection might have caused the periaortitis. However, the patient did not report any physical discomfort during the period immediately after stent placement, nor did he have a fever, leukocytosis, or a highly elevated erythrocyte sedimentation rate.
The exact mechanism of this patient's secondary periaortitis unfortunately remains unknown. This unexpected complication of stent-graft implantation in our patient emphasizes the need for long-term follow-up care and continuing critical evaluation of endovascular repair therapy.
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