Spontaneous Renal Artery Dissection as a Cause of Acute Renal Infarction: Clinical and MDCT Findings

Abstract

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 evaluate the clinical and multidetector computed tomography (MDCT) findings of SRAD. From November 2011 to January 2014, 35 patients who were diagnosed with acute renal infarction by MDCT were included. We analyzed the 35 MDCT data sets and medical records retrospectively, and compared clinical and imaging features of SRAD with an embolism, using Fisher's exact test and the Mann-Whitney test. The most common cause of acute renal infarction was an embolism, and SRAD was the second most common cause. SRAD patients had new-onset hypertension more frequently than embolic patients. Embolic patients were found to have increased C-reactive protein (CRP) more often than SRAD patients. Laboratory results, including tests for lactate dehydrogenase (LDH) and blood urea nitrogen (BUN), and the BUN/creatinine ratio (BCR) were significantly higher in embolic patients than SRAD patients. Bilateral renal involvement was detected in embolic patients more often than in SRAD patients. MDCT images of SRAD patients showed the stenosis of the true lumen, due to compression by a thrombosed false lumen. None of SRAD 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. SRAD is not a rare cause of acute renal infarction, and it has 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.