급성신경색의 원인으로서의 자발성 신동맥 박리: 임상적 특징 및 MDCT 소견에 관한 연구

Abstract

Objective The purpose of this study was to assess the incidence of spontaneous renal artery dissection (SRAD) as a cause of acute renal infarction, and to compare the clinical findings and images from and multidetector computed tomography (MDCT) scans from patients with renal infarction caused by SRAD with those from patients with renal infarction caused by an embolism.

Materials and Methods From November 2011 to January 2014, a total of 35 patients (25 men, 10 women; median age 55 years; range 11-85 years) who were diagnosed with acute renal infarction by MDCT were included in this study. We analyzed the 35 MDCT data sets and medical records retrospectively. We also compared clinical and imaging features of patients with renal infarction caused by SRAD with those of patients with renal infarction caused by an embolism, using Fisher’s exact test and Mann-Whitney test.

Results Among the 35 patients included in this study, the most common cause of acute renal infarction was an embolism (n=14, 40.0%), and SRAD was the second most common cause (n=6, 17.1%). Patients with SRAD experienced new-onset hypertension more frequently than patients with an embolism (P=0.018). Patients with an embolism were found to have increased C-reactive protein (CRP) more often than patients with SRAD (P=0.002). Laboratory results, including tests for lactate dehydrogenase (LDH) and blood urea nitrogen (BUN), and the BUN/creatinine ratio (BCR) were significantly higher in the patients with an embolism than in those with SRAD (P=0.012, P=0.009, and P=0.025, respectively). Bilateral renal involvement was detected by MDCT in patients with an embolism (n=9, 64.3%) more often than in patients with SRAD (n=0, 0%) (P=0.014). MDCT images of patients with SRAD showed the cause to be an intimal flap in the renal arterial lumen and stenosis of the true lumen due to compression by a thrombosed false lumen. The arteries involved in SRAD were the main renal to divisional artery (n=2), the divisional to segmental artery (n=2), and the segmental artery (n=2). Clinical follow-up data were available for four patients with SRAD. Hypertension was well-controlled and none of these patients progressed to an estimated glomerular filtration rate < 60 mL/min/1.73 m2 or to end-stage renal disease during the follow-up period.

Conclusion SRAD was the second most common cause of acute renal infarction, and it had a benign clinical course. It should be considered in a differential diagnosis of acute renal infarction, particularly in patients with new-onset hypertension, unilateral renal involvement, and normal ranges of CRP, LDH, BUN, and BCR.