Transient Renal Artery Stenosis in Renal Infarction: A Case Report

Introduction

Renal infarction is a rare and often under-recognized clinical entity, with an incidence estimated at 2.68–3.06 per 100 000 person-years based on recent data from South Korea [1]. It results from acute interruption of renal arterial blood flow, leading to ischemic injury of the renal parenchyma. The condition is frequently misdiagnosed, or diagnosis is delayed due to its nonspecific presentation, which overlaps with more common causes of flank pain, including nephrolithiasis, pyelonephritis, and musculoskeletal disorders. Consequently, a high index of suspicion is required, especially in patients with underlying risk factors.

Renal infarction can be caused by thromboembolism, in-situ thrombosis, arterial dissection or injury, and hypercoagulable states [2,3]. In a large multicenter series, the most common etiology was cardioembolism (55.7%), followed by renal artery injury (7.5%) and hypercoagulability (6.6%), with 30.1% of cases deemed idiopathic [2]. Importantly, both hormone replacement therapy and smoking are established risk factors for thromboembolic events and can contribute to arterial injury or prothrombotic states [4–7]. Despite improved access to advanced imaging modalities, distinguishing between embolic and atherosclerotic etiologies of renal infarction remains a diagnostic challenge, especially when vascular findings are ambiguous or transient.

This case report presents the diagnostic evolution of a patient whose renal infarct was initially attributed to atherosclerotic renal artery stenosis, but whose follow-up imaging revealed complete resolution of the stenosis, prompting reconsideration of the underlying cause. A duplicated renal artery was also noted but was considered a normal anatomical variant with no hemodynamic significance. This case illustrates the critical role of longitudinal imaging and clinical reassessment in accurately identifying the etiology of renal infarction. Beyond its clinical narrative, the case raises important considerations for diagnostic algorithms, particularly in patients with overlapping vascular risk factors but no definitive source of embolism. It also underscores the need for further research into transient vascular phenomena that can masquerade as fixed stenotic disease.

Case Report

INITIAL EVALUATION (DAY 1):

On presentation, her vital signs were within normal limits. She appeared in moderate distress due to pain. A cardiovascular exam revealed normal heart sounds without murmurs, and palpable peripheral pulses without bruits. An abdominal examination revealed moderate left-flank tenderness without rebound tenderness or guarding. Laboratory results were significant for mild hyponatremia of 132 mmol/L and normal anion gap metabolic acidosis with bicarbonate of 18 mmol/L, creatinine 1.19 mg/dL, and lactate 0.90 mmol/L. Urinalysis revealed 1+ protein, 1+ blood, 4 red blood cells, and 13 white blood cells per high-power field. An electrocardiogram was unremarkable. Given her symptoms and risk factors, the initial differential diagnosis included nephrolithiasis, pyelonephritis, musculoskeletal pain, renal infarction, and aortic dissection. CT abdomen/pelvis with contrast (Figures 1, 2) was performed, revealing severe stenosis of the superior left renal artery and extensive left renal infarction. CT angiography (Figure 3) further confirmed these findings and showed a possibly duplicated left renal artery.

INPATIENT COURSE:

Intravenous heparin was initiated for renal infarction. Given the CT scan findings and absence of an overt cardioembolic source at that time, the infarct was initially attributed to atherosclerotic disease. She underwent a transthoracic echocardiogram with bubble study, which showed preserved ejection fraction (65%) and no evidence of a patent foramen ovale. Continuous telemetry showed no arrhythmias. A full thrombophilia panel was negative. By day 3, she was transitioned from heparin to dual antiplatelet therapy (aspirin and clopidogrel) and high-intensity rosuvastatin. The decision to transition from anticoagulation to antiplatelet therapy was based on the working diagnosis of atherosclerotic renal infarction in the context of severe renal artery stenosis and the absence of embolic source on initial workup. Hormone replacement therapy was discontinued, and she received smoking cessation counseling. She was discharged home on a 30-day cardiac event monitor.

FOLLOW-UP (1 MONTH):

At outpatient follow-up, the cardiac event monitor revealed no arrhythmias. A repeat CT angiography of the abdomen demonstrated complete resolution of the prior renal artery stenosis, with no residual narrowing, calcification, or plaque. This unexpected finding prompted diagnostic reassessment, as spontaneous resolution is atypical for fixed atherosclerotic stenosis. The absence of structural atherosclerosis on imaging, combined with the patient’s prothrombotic risk factors, suggested a transient embolic event as the more likely etiology.

This sequence of events underscores the diagnostic complexity of renal infarction and highlights the importance of longitudinal imaging and reassessment in cases with ambiguous or evolving vascular findings.

Discussion

Renal infarction is an uncommon clinical entity, often presenting with nonspecific symptoms such as flank pain, nausea, or fever, which can mimic more prevalent conditions like nephrolithiasis or pyelonephritis fever [8,9]. The major etiologies are cardioembolic disease, in-situ thrombosis, renal artery injury, and hypercoagulable states [2]. In some instances, no definitive cause is identified, adding to the diagnostic complexity [2]. In this case, the diagnostic journey was complicated by the presence of apparent severe renal artery stenosis in a patient with multiple vascular risk factors, leading to initial attribution of the infarct to atherosclerotic disease. What made this case particularly diagnostically challenging was the anchoring bias introduced by the vascular imaging findings in the context of longstanding vascular risk factors such as diabetes, smoking, and hormone replacement therapy. This anchoring overshadowed consideration of other etiologies such as embolism, despite the absence of supporting evidence such as arterial calcification or persistent luminal narrowing.

Notably, the transient nature of the stenosis, confirmed by complete resolution on repeat imaging, was a key diagnostic turning point. The overwhelming consensus in the comparative literature is that spontaneous resolution of atherosclerotic renal artery stenosis is rare and not routinely expected in clinical practice [10,11]. The resolution of the stenosis on imaging prompted a diagnostic reassessment, favoring an embolic mechanism possibly related to multiple prothrombotic risk factors and unrecognized embolic sources. In most reported instances, embolic phenomena were linked to atrial fibrillation or valvular heart disease [2,9]. Unlike those cases, our patient had no identifiable cardioembolic source, pointing to the possible prothrombotic effects of smoking and hormone replacement therapy as contributors. Recent studies have highlighted the thrombogenic risks associated with both these factors, even in the absence of structural cardiac abnormalities [4–6]. This aligns with emerging evidence linking these exposures to increased arterial thrombotic risk and supports the hypothesis of an embolic mechanism in this case.

From a clinical standpoint, the implications are significant. This case underscores the importance of maintaining a broad differential diagnosis and the role of repeat imaging in re-evaluating initial assumptions. It suggests that embolic infarction is under-recognized in patients with concurrent atherosclerotic risk factors, especially when early imaging reveals vascular findings. Clinicians should be particularly vigilant when imaging findings and clinical workup diverge, as this may signal an alternate pathophysiology. In conclusion, this case highlights a rare instance of transient renal artery stenosis mimicking fixed atherosclerotic disease. It contributes to the growing awareness of embolic renal infarction in the absence of typical embolic sources and emphasizes the value of a dynamic diagnostic approach. Follow-up imaging and clinical reassessment are essential tools for accurate diagnosis and appropriate management.

Conclusions

This case underscores the rarity and diagnostic complexity of renal infarction, particularly when vascular imaging suggests atherosclerotic disease. It adds to the limited body of literature on transient or spontaneously resolving renal artery stenosis, which can mimic fixed atherosclerotic lesions and mislead early diagnostic reasoning. Serial imaging and clinical reassessment were pivotal in uncovering the embolic nature of the infarct, despite initial anchoring bias. This case highlights the critical importance of dynamic diagnostic strategies in vascular medicine, especially for uncommon presentations like renal infarction, where timely reassessment can significantly influence patient management and outcomes.