Return of Renal Function after Endovascular Treatment of Aortic Dissection
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《新英格兰医药杂志》
To the Editor: We report a case of asymptomatic dissection of the descending aorta (type B aortic dissection) with silent renal hypoperfusion. A small, nonfunctioning kidney and a contralateral hypertrophied kidney were identified after symptomatic secondary extension of the aortic dissection occurred. After endovascular treatment, the reperfused kidney returned to a normal size and regained function, and the hypertrophy of the contralateral kidney regressed.
A 44-year-old man was admitted to the hospital for type B aortic dissection. Computed tomographic (CT) scanning showed patency of the celiac, superior mesenteric, and right renal arteries, but hypoperfusion was present from dynamic compression of the true lumen by the false lumen.1 The left renal artery was involved in the dissection but was patent. The right kidney was atrophic (95.8 mm), and scintigraphic studies indicated that there was no function. The left kidney had undergone compensatory hypertrophy (142.5 mm) (Figure 1A). The patient had hypertension of recent onset, but he had not adhered to the recommended medical therapy.
Figure 1. CT Scans of the Patient's Kidneys at Admission (Panel A) and Six Months after the Placement of a Stent–Graft (Panel B).
One week after admission, acute mesenteric ischemia developed. A stent–graft (a stent covered with a Dacron graft) was implanted in the thoracic aorta to close the main entry tear and restore effective flow in the true lumen, after which signs of mesenteric ischemia gradually regressed. The patient was discharged without symptoms on day 19; at the time of discharge, when he was being treated with four oral antihypertensive agents, his systolic blood pressure was 120 mm Hg. Duplex ultrasonographic images showed satisfactory blood flow in the mesenteric and renal arteries. A follow-up CT scan obtained six months later (Figure 1B) showed two normal-size kidneys (right, 113.2 mm; left, 128.4 mm). Scintigraphic studies indicated excellent functional recovery of the right kidney, with symmetric uptake of the tracer.
Silent type B aortic dissections carry a risk of chronic renal hypoperfusion. The case presented here shows the insidious onset of a renovascular hypertension. The recovery of perfusion in the right kidney and its return to a normal size were surprising. Predictive factors for effective renal revascularization are a glomerular pressure of more than 30 mm Hg,2 a peripheral resistance index of less than 0.80,3 and a kidney size of more than 9 cm.4 This case presented all of the necessary conditions that allowed "hibernation" of the right kidney with residual perfusion and recovery after effective reperfusion. The regression of the compensatory hypertrophy of the left kidney is also notable. Renal hypoperfusion in aortic dissection is often missed, because there are few overt symptoms. Systematic screening for renal hypoperfusion, associated with the good results of endovascular techniques,5 can prevent renal atrophy that is still too frequently discovered at a late stage.
Jean-Philippe Verhoye, M.D.
Bertrand De Latour, M.D.
Jean-Fran?ois Heautot, M.D., Ph.D.
University Hospital Pontchaillou
35000 Rennes, France
jverhoye@stanford.edu
References
Williams DM, Lee DY, Hamilton BH, et al. The dissected aorta: part III. Anatomy and radiologic diagnosis of branch-vessel compromise. Radiology 1997;203:37-44.
Mesna L, Delahousse M, Raynaud A, et al. Delayed angioplasty after renal thrombosis. Am J Kidney Dis 2003;41:E9-E12.
Radermacher J, Chavan A, Bleck J, et al. Use of Doppler ultrasonography to predict the outcome of therapy for renal-artery stenosis. N Engl J Med 2001;344:410-417.
Soulez G, Therasse E, Qanadli SD, et al. Prediction of clinical response after renal angioplasty: respective value of renal Doppler sonography and scintigraphy. AJR Am J Roentgenol 2003;181:1029-1035.
Dake MD, Kato N, Mitchell RS, et al. Endovascular stent-graft placement for the treatment of acute aortic dissection. N Engl J Med 1999;340:1546-1552.
A 44-year-old man was admitted to the hospital for type B aortic dissection. Computed tomographic (CT) scanning showed patency of the celiac, superior mesenteric, and right renal arteries, but hypoperfusion was present from dynamic compression of the true lumen by the false lumen.1 The left renal artery was involved in the dissection but was patent. The right kidney was atrophic (95.8 mm), and scintigraphic studies indicated that there was no function. The left kidney had undergone compensatory hypertrophy (142.5 mm) (Figure 1A). The patient had hypertension of recent onset, but he had not adhered to the recommended medical therapy.
Figure 1. CT Scans of the Patient's Kidneys at Admission (Panel A) and Six Months after the Placement of a Stent–Graft (Panel B).
One week after admission, acute mesenteric ischemia developed. A stent–graft (a stent covered with a Dacron graft) was implanted in the thoracic aorta to close the main entry tear and restore effective flow in the true lumen, after which signs of mesenteric ischemia gradually regressed. The patient was discharged without symptoms on day 19; at the time of discharge, when he was being treated with four oral antihypertensive agents, his systolic blood pressure was 120 mm Hg. Duplex ultrasonographic images showed satisfactory blood flow in the mesenteric and renal arteries. A follow-up CT scan obtained six months later (Figure 1B) showed two normal-size kidneys (right, 113.2 mm; left, 128.4 mm). Scintigraphic studies indicated excellent functional recovery of the right kidney, with symmetric uptake of the tracer.
Silent type B aortic dissections carry a risk of chronic renal hypoperfusion. The case presented here shows the insidious onset of a renovascular hypertension. The recovery of perfusion in the right kidney and its return to a normal size were surprising. Predictive factors for effective renal revascularization are a glomerular pressure of more than 30 mm Hg,2 a peripheral resistance index of less than 0.80,3 and a kidney size of more than 9 cm.4 This case presented all of the necessary conditions that allowed "hibernation" of the right kidney with residual perfusion and recovery after effective reperfusion. The regression of the compensatory hypertrophy of the left kidney is also notable. Renal hypoperfusion in aortic dissection is often missed, because there are few overt symptoms. Systematic screening for renal hypoperfusion, associated with the good results of endovascular techniques,5 can prevent renal atrophy that is still too frequently discovered at a late stage.
Jean-Philippe Verhoye, M.D.
Bertrand De Latour, M.D.
Jean-Fran?ois Heautot, M.D., Ph.D.
University Hospital Pontchaillou
35000 Rennes, France
jverhoye@stanford.edu
References
Williams DM, Lee DY, Hamilton BH, et al. The dissected aorta: part III. Anatomy and radiologic diagnosis of branch-vessel compromise. Radiology 1997;203:37-44.
Mesna L, Delahousse M, Raynaud A, et al. Delayed angioplasty after renal thrombosis. Am J Kidney Dis 2003;41:E9-E12.
Radermacher J, Chavan A, Bleck J, et al. Use of Doppler ultrasonography to predict the outcome of therapy for renal-artery stenosis. N Engl J Med 2001;344:410-417.
Soulez G, Therasse E, Qanadli SD, et al. Prediction of clinical response after renal angioplasty: respective value of renal Doppler sonography and scintigraphy. AJR Am J Roentgenol 2003;181:1029-1035.
Dake MD, Kato N, Mitchell RS, et al. Endovascular stent-graft placement for the treatment of acute aortic dissection. N Engl J Med 1999;340:1546-1552.