Abstract
Spontaneous renal artery dissection (SRAD) is characterized by an idiopathic intimal separation within the renal artery, representing a rare cause of acute renal infarction. It is often misdiagnosed or overlooked in clinical practice due to infrequent occurrence and non-specific clinical symptoms. In this report, we present a case in which SRAD was definitively diagnosed in our department and subsequently managed through endovascular intervention.
1. Introduction
Spontaneous renal artery dissection (SRAD) is a rare vascular disorder. The clinical presentation of SRAD is often non-specific, varying with the degree of vascular obstruction. Symptoms can range from asymptomatic to severe renal infarction, leading to frequent misdiagnoses or delayed diagnoses. With advances in imaging technology, multislice spiral computed tomography angiography (MSCTA) has emerged as a reliable and widely used modality for the diagnosis of renal artery dissection. Currently, there are no established clinical guidelines specifically for SRAD. Treatment modalities include pharmacotherapy, endovascular interventional procedures, and, in some cases, surgical intervention. In this report, we present a case in which SRAD was definitively diagnosed in our department and subsequently managed through endovascular intervention. By presenting this case, we aim to improve clinicians’ awareness of this rare condition.
2. Clinical data
2.1. Clinical presentation
A 61-year-old male patient was admitted with intermittent chest pain that had been persisting for and progressively worsening over 4 days, with additional upper abdominal pain that had been ongoing for 17 hours. The patient's medical history was notable for coronary artery disease (CAD) treated with percutaneous coronary intervention (PCI), as well as hypertension. Additionally, he had a history of surgery for a gastric stromal tumor, chronic bronchitis, and an allergy to levofloxacin. A physical examination showed a temperature of 36.6 °C, respiratory rate of 20 breaths per minute, pulse of 66 beats per minute, and blood pressure of 163/96 mmHg (1 mm Hg = 0.133 kPa). The patient was conscious, alert, and oriented, presenting in a spontaneous position. No icterus or petechiae were observed on the skin or mucous membranes. No enlarged superficial lymph nodes were palpable, and the lips were non-cyanotic. There was no tenderness upon palpation of the sternum. Lung auscultation revealed clear breathing sounds bilaterally, without dry or wet rales. Cardiac examination revealed no enlargement of the heart borders and a regular heart rate of 68 beats per minute. Heart auscultation revealed no murmurs across all of the valve areas. Abdominal examination revealed a soft abdomen with no tenderness, rebound tenderness, or percussion tenderness in the hepatic and renal areas. No edema was observed in the lower limbs. Comprehensive tests were carried out, including a complete blood count, high-sensitivity C-reactive protein, high-sensitivity troponin T, D-dimer, brain natriuretic peptide, amylase, liver function, renal function, and urinalysis test, the results of which were all within normal limits. A lipid profile showed high-density lipoprotein cholesterol at 0.75 mmol/L, total cholesterol at 1.95 mmol/L, triglycerides at 0.77 mmol/L, and low-density lipoprotein cholesterol at 0.87 mmol/L. An electrocardiogram showed sinus rhythm with ST-T segment changes. Cardiac echocardiography demonstrated no enlargement of the atria or ventricles, no significant pericardial effusion, and a left ventricular ejection fraction of 55% (M-mode), with a left ventricular fractional shortening of 28%. Triple rule-out computed tomography angiography (TRO-CTA) revealed that the thoracic and abdominal aorta trunks and their major branches demonstrated a normal lumen course with adequate contrast filling, and no significant aneurysmal dilation was observed. Mixed-type plaque formation was observed in the walls of the thoracoabdominal aorta and bilateral iliac arteries. A localized double-lumen appearance, approximately 18 mm in length, was identified in the right renal artery (Fig. 1). Coronary artery atherosclerotic heart disease was present, with post-stent implantation changes in the left anterior descending artery. Additionally, a small patchy hypodensity within the stent lumen was discovered, raising the possibility of in-stent lumen loss.
Fig. 1.
Renal artery CTA. (a) Cross-sectional and (b) coronal thin-slice MIP images reveal an intimal plaque in the proximal segment of the right renal artery, resulting in a double-lumen appearance (arrow). CTA, computed tomography angiography; MIP, maximum intensity projection.
2.2. Examination and treatment findings
Selective coronary angiography revealed no significant stenosis in the left main coronary artery. The original stent in the proximal-mid segment of the left anterior descending artery remained patent and displayed mild intimal hyperplasia. The second diagonal branch (D2) showed subtotal occlusion at its origin, and a segmental myocardial bridge was noted in the mid-segment, causing approximately 40%–50% systolic compression with normalization during diastole. No significant stenosis was found in the left circumflex artery. The right coronary artery showed ectasia, with 20%–30% stenosis in the mid-segment and an irregular wall appearance in the distal segment. TIMI grade 3 flow was maintained, and there was no evidence of collateral circulation (Fig. 2). Renal angiography revealed no significant stenosis in the left renal artery. A localized dissection was observed in the proximal right renal artery, and a Palmaz Blue stent (6 × 24 mm) was successfully deployed to obtain complete resolution of the dissection (Fig. 3).
Fig. 2.
Coronary angiography. (a) LM: No significant luminal stenosis is observed. (b) LAD: The previously implanted stent in the proximal segment remains patent, with mild intimal hyperplasia within the stent; subtotal occlusion is observed at the ostium of the D2. (c) RCA: No significant stenosis is observed. LM, left main coronary artery; LAD, left anterior descending artery; D2, second diagonal branch; RCA, right coronary artery.
Fig. 3.
Right renal artery angiography and post-stenting findings. (a) DSA reveals dissection in the proximal segment of the right renal artery. (b) After stent placement, the dissection is resolved with restored unobstructed blood flow and no contrast extravasation on the angiography. DSA, digital subtraction angiography.
Ethical approval was obtained from the authors' affiliated hospital, and written informed consent was provided by the patient.
3. Discussion
Spontaneous renal artery dissection (SRAD) is a condition characterized by an idiopathic intimal separation within the renal artery that occurs in the absence of any prior arterial interventions or trauma. This condition was first described by Rumpus in 1944.1 Most of the existing literature on SRAD, both domestically and internationally, consists of case reports and case series, with fewer than 300 cases reported in the literature. SRAD accounts for approximately 1%–2% of all arterial dissections. It predominantly affects males aged 40–60 years, with a male-to-female ratio ranging from 4:1 to 10:1.2 SRAD typically involves a single renal artery, with bilateral renal artery dissections occurring in approximately 10%–15% of cases.2,3
The exact etiology of SRAD remains unclear, but it is believed to be multifactorial. Research suggests that connective tissue disorders play a significant role in its development; conditions such as fibromuscular dysplasia, Ehlers-Danlos syndrome, Marfan syndrome, and polyarteritis nodosa have been linked to SRAD.3 Other contributing factors include hypertension, atherosclerosis, strenuous physical activity, cocaine abuse, and smoking, and some cases of SRAD have even been observed in otherwise healthy individuals.2,3 Current theories on its pathogenesis include the following: 1) Shear stress injury theory posits that patients with connective tissue disorders, such as Ehlers-Danlos syndrome or Marfan syndrome, possess defective vascular proteins, rendering their blood vessels more susceptible to damage under conditions of high stress such as hypertension or physical trauma.4,5 2) Vascular rupture theory suggests that conditions like fibromuscular dysplasia and polyarteritis nodosa lead to a heightened risk of vascular rupture, potentially precipitating arterial dissection.3,6 3) Segmental arterial mediolysis theory describes a non-inflammatory, non-atherosclerotic process leading to medial dissolution in medium-sized arteries, thereby increasing susceptibility to dissection, hemorrhage, and ischemia.7
The clinical presentation of SRAD is often non-specific, varying with the degree of vascular obstruction. Symptoms can range from asymptomatic to severe renal infarction, leading to frequent misdiagnoses or delayed diagnoses. Symptoms that commonly present include severe hypertension, abdominal pain, fever, hematuria, proteinuria, and acute renal failure.3,8 Abdominal pain is the most frequent symptom, with many patients experiencing renal colic-like discomfort. Early-stage SRAD was historically diagnosed post-mortem. However, advances in imaging technology have given rise to multislice spiral computed tomography angiography (MSCTA) as a rapid, non-invasive, and reliable diagnostic tool. MSCTA clearly visualizes the dissection location, extent, and perfusion status, providing essential guidance for clinical management, treatment evaluation, and follow-up.9 Although renal arteriography remains the diagnostic gold standard, its invasive nature precludes it from being the first investigatory measure taken. Currently, there are no established clinical guidelines specifically for SRAD. Treatment approaches primarily focus on controlling blood pressure, improving renal blood flow, and preserving renal function. Treatment modalities include pharmacotherapy, endovascular interventional procedures, and, in some cases, surgical intervention. Owing to limited long-term follow-up data in many studies, the long-term efficacy of conservative management for SRAD is yet to be fully elucidated. Endovascular interventional procedures are generally considered safe and effective for patients with SRAD.10 However, as these interventions are more frequently applied, concerns have been raised by some scholars regarding the potential for overmedicalization.11
This case involved a 61-year-old male patient with a history of PCI-treated CAD and hypertension. Prior to admission, the patient experienced angina pectoris followed by sudden, persistent abdominal pain. Vigilance is required for conditions such as acute coronary syndrome, aortic dissection, and pulmonary embolism. TRO-CTA revealed a dissection in the right renal artery, located in the main trunk. The lesion was accompanied by refractory hypertension. Although there was no evidence of renal function deterioration or renal infarction, endovascular intervention was ultimately pursued after consulting the patient and his family. A follow-up conducted after 10 months showed effective blood pressure control, stable renal function, and no structural abnormalities in either kidney. For proof of long-term efficacy, further follow-up observations are required.
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CRediT authorship contribution statement
Qingyu Zhao: Writing – original draft, Investigation, Conceptualization. Sanwu Wu: Writing – review & editing, Investigation. Yu Zhan: Validation, Investigation. Zuofeng Qin: Validation, Investigation. Lei Zhang: Validation, Supervision, Investigation. Cui Xie: Supervision, Investigation. Tinglong Wang: Validation, Investigation. Youen Zhang: Writing – review & editing, Visualization, Funding acquisition.
Informed consent statement
The authors have obtained the patient's consent.
Institutional review board statement
Ethical approval was obtained from the Medical Ethics Committee of Shiyan Renmin Hospital (approval number: SYSRMYY-KYXS-2026-001).
Disclosure
All authors report no conflicts of interest in this work.
Funding
The study was supported by Hubei Health and Family Planning Science and Technology Project (WJ2025M027); the College Students’ Innovation and Entrepreneurship Training Program of Hubei University of Medicine (X202310929015).
References
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