Spontaneous renal artery dissection complicated by renal infarction: description of two cases.

Introduction

Spontaneous renal artery dissection (SRAD) is a rare clinical event that typically presents with acute low back or flank pain, hypertension, fever, hematuria, and acute renal failure. The condition is often misdiagnosed, or the diagnosis is delayed, due to its relative rarity and nonspecific presentation (1,2). The diagnosis can be made by contrasted-enhanced computed tomography (CT) scans, and if a problem is found, vascular reconstruction is performed, which can display the lesion more clearly. Over 300 cases have been reported since the first characterization (3,4) of SRAD. Although different therapeutic strategies are available for SRAD, a consensus has not yet been reached on the most appropriate treatment. Conservative therapy, open surgery, and intravascular intervention have been reported as treatments for SRAD (5,6). Endovascular stent repair is usually applied when prior medical therapy has been ineffective. There are few reports of endovascular therapy in the literature (6-11). In this report, we describe two SRAD cases complicated by renal infarction which were successfully treated by endovascular stenting using the Abbott Absolute Pro self-expanding nitinol stent system.

Case presentation

All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Helsinki Declaration (as revised in 2013). Written informed consent was provided by the patients for publication of these two case reports and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Case 1

A 44-year-old man presented to the Department of Interventional Radiology, Affiliated Jiangyin Hospital, Medical College of Southeast University with a sudden onset of right flank pain of 17 h’ duration. The physical examination showed a blood pressure of 120/71 mmHg and percussion pain over the right flank. The medical laboratory test results showed a lactate dehydrogenase (LDH) level of 469 U/L, mild leukocytosis (18.41×109/L) with 84.5% neutrophils, and slight renal dysfunction (creatinine 119 µmol/L, urea nitrogen 7.32 mmol/L). However, the C-reactive protein (CRP) level was normal. No hematuria or proteinuria was detected in the spot urine, and urinalysis was negative. He had no past medical history and no urinary symptoms. He had been smoking approximately 10 cigarettes a day for 10 years. His bowel sounds were normal. A B-ultrasound examination showed bilateral small renal stones, and after analgesic treatment, no obvious relief of the lower back pain was achieved. Thus, we began to suspect acute renal colic. Computed tomography angiography (CTA) of the aorta and renal arteries showed dissection at the distal end of the main right renal artery, the formation of a dissecting aneurysm, and occlusion of the posterior branch of the right renal artery, including the branches supplying the lower level of the posterior right kidney ().

Figure 1

Axial CTA image shows right renal artery dissection (yellow-brown arrow) and associated renal infarction (blue arrow). CTA, computed tomography angiography.

We decided to perform renal artery stenting after obtaining informed consent. The patient was anticoagulated with low-molecular-weight heparin of 6,000 U every 12 h and administered antibiotics (ceftazidime: 2 g every 12 h; levofloxacin: 0.5 g/day) prior to stenting. We decided to use an Absolute Pro vascular self-expanding stent (Abbott Vascular, Santa Clara, CA, USA) considering lesion length, vessel tortuosity, and the great flexibility and adhesion of this stent. Based on previous surgical experience, we performed stent implantation using the femoral artery approach during the procedure. The 6 F introducer sheath was placed using the Seldinger technique. The 6 F long sheath was delivered through the introducer sheath to the aorta at the level of the renal artery ostium, and a Cobra 5 F catheter (Terumo Corporation, Tokyo, Japan) was sent to the opening of the renal artery, at the best working angle. Then, with the guidance of the road map, the Progreat 2.7 F microcatheter and microwire (Terumo) were coaxially fed through the catheter. The microcatheter and microwire were matched to pass through the lesion and into the distal artery trunk and the V-18 hardened exchange guide wire (Boston Scientific Corp., Natick, MA, USA) (12). A 6 mm × 80 mm Absolute Pro Vascular self-expanding stent (Abbott Vascular) was deployed through the guide wire. A digital subtraction angiography (DSA) review showed that the stent was in a good position and the blood flow was unobstructed ().

Figure 2

Preoperative and postoperative DSA results. (A) Preoperative DSA shows false lumen. (B) Postoperatively, the false lumen essentially disappears. The arrow points to the false lumen. DSA, digital subtraction angiography.

After the procedure, the patient’s right flank pain improved within 1 day. The patient was released from hospital on postoperative day four with anticoagulation and antiplatelet therapy, including low molecular weight heparin 6,000 U every 12 h for 3 days, clopidogrel 75 mg/day, and aspirin 100 mg/day for three months. At discharge, laboratory evaluations revealed that the patient’s blood pressure was 120/70 mmHg, LDH level was 285 U/L, leukocyte count was 5.36×109/L with 64.8% neutrophils, the serum creatinine and urea nitrogen levels were 103 µmol/L and 5.32 mmol/L, respectively. At one month of follow-up, the CTA results showed that the right renal artery stent was unobstructed, the dissecting aneurysm had disappeared, the posterior branch of the right renal artery was recanalized, and the lower level of the right kidney was enhanced. After 10 months, follow-up CTA showed that the lumen of the right renal artery stent was unobstructed and the right kidney was partially atrophied. Moreover, the cortex of the right posterior inferior kidney was thinned and poorly enhanced ().

Figure 3

CTA results at follow-up. (A) 1 month later. (B) 10 months later. CTA, computed tomography angiography.

Case 2

A 44-year-old man developed low back pain without obvious cause 12 h prior to presentation at our hospital with abdominal pain, nausea, and vomiting. The physical examination showed positive percussion pain in the right renal region. Laboratory evaluation revealed a blood pressure of 130/70 mmHg, an LDH level of 1,060 U/L, mild leukocytosis (11.29×109/L) with 88.3% neutrophils, slight renal dysfunction (creatinine 121 µmol/L, urea nitrogen 7.0 mmol/L), and a CRP level of 134 mg/L. Routine testing revealed that urine, coagulation function, procalcitonin, autoantibodies, and other indicators were all normal. The patient had neither past medical history and urinary symptoms nor a history of vascular intervention and recent trauma. However, he did have a history of smoking. Emergency CTA revealed right renal artery dissection with thrombosis and partial right kidney infarction ().

Figure 4

CTA discloses right renal artery dissection with thrombosis and infarction. The arrow points to thrombosis. CTA, computed tomography angiography.

After obtaining the informed consent of the patient and his family, we decided to perform renal artery stenting after thrombolysis. The patient underwent thrombolysis with urokinase 300,000 µ every 12 h, and he was anticoagulated with low molecular weight heparin 8,000 U every 12 h and administered antibiotics (ceftazidime: 2 g every 12 h; levofloxacin: 0.5 g/day) prior to stenting. Given its many advantages (i.e., the ability to reduce complications and better flexibility and bending resistance), we decided to continue using the Absolute Pro vascular self-expanding stent (Abbott Vascular) (13). The same steps were performed to finally deploy the stent. A 6 mm × 80 mm bare stent was deployed through a 6 F long sheath using a 5 F catheter. A DSA review showed that the stent was placed in a good position and blood flow was unobstructed ().

Figure 5

DSA imaging results. (A) Preoperative DSA showing a false lumen. (B) Postoperatively, the false lumen has essentially disappeared. The arrow points to false lumen. DSA, digital subtraction angiography.

The patient’s low back pain improved within half a day after surgery. The patient was released from hospital on postoperative day four with anticoagulation and antiplatelet therapy: low molecular weight heparin 6,000 U every 12 h for three days, clopidogrel 75 mg/day, and aspirin 100 mg/day for three months. At discharge, laboratory evaluations revealed the patient’s LDH level was 396 U/L, leukocyte count was 6.09×109/L with 64.9% neutrophils, and serum creatinine and urea nitrogen levels were 110 µmol/L and 5.14 mmol/L, respectively. After 1 month, follow-up CTA showed no deterioration of renal infarction of the right kidney, the stent was unobstructed, the inner membrane sheet was completely fitted by the stent, and the DSA showed no sign of residual dissection and confirmed the disappearance of the false lumen (). It was suggested that the patient take the medication continuously and return to the clinic every six months for CTA.

Figure 6

Angiography results at follow-up 1 month later. (A) CTA result showing a well-expanded stent without evidence of a residual flap. (B) DSA result showing a well-expanded stent without evidence of a residual tear. CTA, computed tomography angiography; DSA, digital subtraction angiography.

Discussion

The incidence of SRAD accounts for only 1–2% of all arterial dissections, and bilateral involvement occurs in approximately 10–15% of patients (14-16). In a normal healthy individual with no predisposing factors, SRAD is an even rarer phenomenon. Both of the cases we have reported were male patients; SRAD occurs mostly in men between the ages of 40 and 60. The male: female ratio is reported to be in the range of 4:1 to 10:1 (5). The etiology of SRAD is still unclear. Adverse development of the media and alterations of the vasa vasorum, severe atherosclerosis, and blood flow shear stress may be pathogeny. Malignant hypertension, fibromuscular dysplasia (15), strenuous exercise (including sexual) (17), taking medication (18,19), Marfan syndrome (20), and Ehlers-Danlos syndromes (4) are all possible risk factors. In our two case studies, we found that both of the patients had a long history of smoking, which was similar to the reports by other researchers (6,11,21). Therefore, we believe that smoking may be another risk factor for SRAD. However, many cases occur in otherwise healthy individuals (22,23). Furthermore, the nonspecific presentation frequently results in a diagnostic delay. At the same time, the renal artery is located deep in the abdomen, it is relatively slender, and there are many abdominal organs and intestines around it. For patients with obesity or intestinal gas interference, the main renal artery may not be displayed clearly on imaging, and the relatively high requirements for Doppler ultrasound (DUS) instruments make imaging difficult. It is difficult to identify the early stage of SRAD using DUS, with poor sensitivity and low diagnostic rate (24,25). However, when there is a significant renal infarction in the late stage of SRAD, DUS can detect poor renal perfusion, thereby assisting in the diagnosis. A definitive diagnosis requires angiography studies which are able to precisely explain the degree and feature of vascular involvement while identifying potential treatment options. With the progress of science and technology, CTA has replaced conventional angiography owing to its noninvasiveness and accuracy. In these reports, we were without doubt regarding the diagnosis and subsequent follow up of SRAD using CTA. Since the accuracy of CTA is improving, conventional arteriography may be gradually replaced by novel technologies.

The optimal therapeutic approach for SRAD remains unclear. Overall, the treatment of SRAD is divided into two strategies. One is conservative treatment that is often a combination of antihypertensive drugs and systemic anticoagulation. Patients who show neither uncontrollable high blood pressure nor a worsening of serum creatinine levels are frequently treated conservatively. In some cases of conservative treatment, patients have received anticoagulant therapy for a short or long period to avoid thromboembolic events. However, no clinical studies have ever compared anticoagulation therapy with no anticoagulation therapy. Whether thrombolytic therapy should be provided is still controversial. Although thrombolytic therapy can reconstruct the blood flow of true lumen, it will also increase the pressure of false lumen, thereby expanding the dissection and aggravating damage to the intima. In severe cases, it may even lead to deterioration of the dissection and consequences of renal atrophy. When the patient’s drug treatment is ineffective, another method is needed, such as revascularization.

Revascularization includes surgical and endovascular treatment. Some relevant reports have suggested that the surgical effect is poor and can result in acute thrombosis of the renal artery and late anastomotic restenosis (11,15,26,27). Fortunately, owing to the advantages of avoiding clamping and allowing for rapid revascularization, endovascular treatment is emerging as a less aggressive treatment alternative, and, endovascular intervention tends to be the preferred therapeutic method with safer and more effective outcomes (6,11). The indications for vascular intervention are lesions located in the main renal artery with an enlarged false lumen of dissection, uncontrolled hypertension, and deterioration of renal function. Endovascular intervention includes placement of self-expanding stents or stents with coiling and thrombolysis followed by stenting. We chose the Absolute Pro vascular self-expanding stent because it has a thin wall, delivers little stimulation to the intima, and has good flexibility and adherence. Even if the blood vessel were to become twisted, in more severe cases it could completely cover the lesion. These superior features of the stent may significantly reduce the complications associated with arterial puncture points. In both of our cases, the patients’ severe symptoms of pain disappeared after successful revascularization with stent placement, and follow-up CTA in both patients showed that the renal artery stent was unobstructed and renal function was normal.

In conclusion, SRAD is a rare clinical event, and diagnosis is often delayed due to its indistinct and nonspecific clinical symptoms. The accuracy of CTA in diagnosing SRAD has gradually improved, making it the potential replacement for DSA in diagnosis. From the examples reported in this paper, it can be concluded that self-expanding stent implantation for SRAD is associated with favorable clinical results. Hence, the endovascular treatment of SRAD seems to be a safe and effective option that should be considered in the case of bad clinical or radiologic evolution of SRAD.

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