J Korean Med Sci.  2017 Apr;32(4):605-612. 10.3346/jkms.2017.32.4.605.

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

• Yoon K
• Song SY
• Lee CH
• Ko BH
• Lee S
• Kang BK
• Kim MM

• KMID: 2371445
• DOI: http://doi.org/10.3346/jkms.2017.32.4.605

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.

Keyword

Spontaneous Renal Artery Dissection; Renal Infarction; Incidence; Multidetector Computed Tomography

Figure

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  Fig. 1 MDCT images in 85-year-old man with an atrial fibrillation. Axial image (A) shows multiple infarctions in the spleen (white arrows). Coronal image (B) shows multifocal wedge-shaped infarctions in bilateral kidneys (black arrows) and multiple infarctions in the spleen (white arrows). Renal infarction caused by an embolism was diagnosed. MDCT = multidetector computed tomography.

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  Fig. 2 MDCT images in 49-year-old man with new-onset hypertension. (A) Initial. (B) One-month follow-up. (C) 26-month follow-up. Initial curved MPR image (A) shows that the true lumen of a segmental renal artery is compressed by a thrombosed false lumen (black arrow). Curved MPR image at 1-month follow-up (B) shows the aggravated narrowing of the true lumen (white arrow) and the aneurysmal change has developed (white arrow head). The previous infarction area has been atrophied in the cured MPR image at 26-month follow-up (C), even though the dissected renal vessels have been normalized (black arrow heads). Spontaneous renal artery dissection was diagnosed. MDCT = multidetector computed tomography, MPR = multiplanar reconstruction.

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  Fig. 3 Comparison of the eGFR between patients with SRAD (A) and patients with an embolism (B) during the follow-up period. eGFR = estimated glomerular filtration rate, SRAD = spontaneous renal artery dissection.

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  Fig. 4 Comparison of the blood pressure between patients with SRAD (A) and patients with an embolism (B) during the follow-up period. SRAD = spontaneous renal artery dissection.

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