Abstract

Spontaneous renal artery dissection is an uncommon cause of renovascular hypertension, usually associated with fibromuscular dysplasia. Among reported nonautopsy cases (N = 80), arterial reconstruction has seldom been attempted (N = 21) and the outcome has frequently been poor (48% clinical failure rate). This is attributed in part to the frequent involvement of renal artery branches by the dissection. Furthermore, the report of spontaneous reversion to normotension among patients treated medically has also clouded the role of surgery in this disease. Since progress in the technique of renal artery repair now allows successful treatment of anatomically complex lesions, we reviewed our experience with arterial reconstruction in the management of spontaneous renal artery dissection to determine the frequency of and factors correlating with cure after operative repair. Ten patients (eight men, two women; mean age, 39.3 ± 5.9 years) were admitted with severe hypertension (1010), often associated with neurologic symptoms, hematuria, or flank pain (810). Serum creatinine was elevated in only two patients. Angiography demonstrated changes consistent with fibromuscular dysplasia in 7 of 10 patients and evidence of dissection in 6 of 10. Bilateral disease was present in three patients. Only five patients had a single renal artery on the involved side. The dissection extended into the primary branches in 8 of 10 patients and involved both renal arteries in four of the five patients with two arteries. Histologic study confirmed fibromuscular dysplasia in six and intramural dissection in all operative specimens. Five patients underwent revascularization (in one case requiring the ex vivo technique), with use of hypogastric artery as a conduit in four of five or resection and primary reanastomosis in one of five. Three patients became normotensive, and two returned to their previous level of blood pressure control. Follow-up averaged 14.5 years. Two patients underwent nephrectomy after exploration demonstrated nonreconstructible vessels, and two underwent nephrectomy when intraoperative assessment of the kidney showed that revascularization had failed to adequately reverse extensive renal ischemia. After a mean follow-up of 14.6 years these patients remain normotensive, although two require antihypertensive medications. One patient was treated medically and is currently hypertensive off all medications. Nine of 10 patients have maintained a normal serum creatinine during follow-up. We conclude that renal revascularization is frequently successful in spontaneous renal artery dissection (five of seven, 71.4%) and results in sustained relief of hypertension with maximal conservation of renal tissue. This is important because of the young age at onset and the not infrequent occurrence of bilateral fibromuscular dysplasia, and even of dissection. Successful reconstruction is facilitated by early treatment, before the dissection extends into the secondary renal artery branches. Because extension of the dissection is a continued threat and because the hypertension associated with this event is usually severe and difficult to control, we do not think that patients should uniformly be treated medically, waiting to see if spontaneous reversion to normotension will occur.

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