Teaching Case

A 50-year-old male smoker with a history of cocaine use and thalassemia came to the emergency department due to left flank pain. BP 163/112 mmHg, HR 84 bpm. Blood test: 18,000 leukocytes/µL. Urinalysis: negative.

With initial suspicion of renal colic, an ultrasound scan showed unremarkable findings. Subsequently, to rule out renal infarction, CT angiography was performed (Figures 1a, 1b and 1c), which identified a dissection of the left renal artery with extension towards the anterosuperior and anteroinferior segmental branches, with a pseudoaneurysm dependent on the anterosuperior branch. A digital subtraction angiography (DSA) was performed (Figures 2, 3, 4 and 5), identifying the pseudoaneurysm and confirming the origin in the anterosuperior segmental artery. A risk-benefit assessment was performed, with a pseudoaneurysm rupture risk greater than that of thrombosis progression, so covered stents were placed in the anterosuperior segmental branch with medical management of the rest of the dissection. At the first 5-day follow-up CT (Figure 6), no bleeding was identified. At the 3-month follow-up CT (Figure 7), with optimisation of medical treatment, the area of renal infarction decreased markedly with hypertrophy of normal parenchyma and no pseudoaneurysm patency.

Background

Isolated renal artery dissection (IRAD) accounts for 1%–2% of all arterial dissections. In many IRAD cases, the aetiology is unknown and are therefore classified as spontaneous (SRAD). The incidence of SRAD is 0.05%, with a 4:1 male predominance [1–5].

Factors that increase the likelihood of spontaneous renal artery dissection (SRAD) encompass severe hypertension, fibromuscular dysplasia, cocaine consumption, intense physical activity, and collagen-related vasculitides. Three potential mechanisms suggested for the development of IRAD include shear forces, rupture of the vasa vasorum, and segmental arterial mediolysis (SAM). A potential complication associated with SRAD is the formation of a pseudoaneurysm or rupture of the vessel [2,3].

Clinical Perspective

The most prevalent symptom at presentation is intense flank pain, while the most common clinical sign is uncontrolled hypertension. Other non-specific symptoms might include nausea, vomiting, headache, and fever. Leukocytosis and increased serum LDH levels may also be observed, suggesting a loss of renal parenchyma. Urinalysis frequently shows no abnormalities [2,3].

Imaging Perspective

The preferred diagnostic test is CT angiography. CT angiography and magnetic resonance angiography (MRA) offer higher sensitivity, at 91% and 93%, respectively, compared to Doppler ultrasound, which has a sensitivity of 27% [2].

The findings on CT may include an intimal flap, causing a double lumen, or irregular luminal stenosis due to thrombosis or lack of repletion of a false lumen, with or without widening of the renal artery itself [6,7].

Renal angiography can evaluate luminal narrowing. However, it may not offer a precise evaluation of the arterial wall. Its application is typically limited to therapeutic interventions [7].

Outcome

The initial approach to managing SRAD depends on factors such as the duration of total renal ischemia, the severity of renal injury, associated hypertension, complications like bleeding, and the viability of the contralateral kidney. There are no specific guidelines for managing this condition. Medical treatment is typically the primary approach, focusing on antihypertensive therapy, pain control, and optimizing cardiovascular risk factors. Immediate surgical intervention—either endovascular procedures or open arterial reconstruction, and in rare cases, nephrectomy—is considered for cases of uncontrolled hypertension, worsening dissection, renal impairment, or other complications such as bleeding, as seen in our case [6–8].

The technical success rate of endovascular treatment is reported to be between 93.3% and 100%. This approach avoids the need for laparotomy and eliminates the requirement to clamp the renal artery. Coil embolisation can be employed to prevent rupture of the dissection, while stents may be used to ensure continued renal blood flow. Currently, there are no specialised devices designed specifically for treating SRAD, so the choice of equipment is left to the discretion of the treating radiologist [4,6–8].

Written informed patient consent for publication has been obtained.