Acute unilateral renal embolism: a therapeutic challenge

Abstract

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Acute renal artery embolism (ARAE) is a rare vascular event that precipitates renal infarction (RI) caused by abrupt disruption of renal artery blood flow. RI is frequently misdiagnosed or diagnosed late because of its rarity and frequently ambiguous clinical presentation, potentially leading to irreversible harm to the renal parenchyma or an increased risk of other embolic events affecting other organs. Risk factors for ARAEs include atrial fibrillation, valvular or ischemic heart disease, renal artery embolism/dissection, and coagulopathy, and complete unilateral renal artery embolism is rare. We present the case of one patient with unilateral ARAE caused by atrial fibrillation. We performed percutaneous endovascular therapy (PET) for the renal artery embolism, including catheter-directed thrombolysis (CDT) and aspiration thrombectomy with systemic anticoagulant therapy. At the one-year follow-up, severe atrophy of the affected kidney and compensatory enlargement of the contralateral kidney were observed. We found that procedurally successful revascularization does not necessarily translate to functional recovery of the renal parenchyma. To accurately assess long-term renal functional restoration, we propose incorporating post-thrombectomy anatomical evaluations (e.g., via renal artery angiography or CT angiography [CTA]) combined with functional renal scintigraphy into standardized clinical protocols. This multimodal approach would not only validate the angiographic outcomes but also provide critical insights into the viability of the parenchyma, thereby guiding the development of patient-specific therapeutic strategies. Recommendations for optimal treatment for renal artery embolism are needed. Therefore, we share this case with the aim of providing valuable information for the treatment of renal infarction.

Background

Acute renal artery embolism (ARAE) is a rare but potentially devastating condition that accounts for < 0.01% of emergency admissions. The diagnosis of ARAE is frequently delayed due to its nonspecific symptoms (e.g., flank pain), which are often also observed in renal colic and pyelonephritis. The choice of therapeutic strategy among existing options—including anticoagulation therapy, thrombolysis, and endovascular intervention—remain controversial, particularly in delayed presentations. This case highlights some lessons learned regarding symptom relief and long-term preservation of renal function.

Atrial fibrillation (AF)-induced ARAE is exceptionally rare, and standardized protocols for immediate revascularization are lacking. We herein report a case of AF-related ARAE and propose a new treatment modality involving manual thrombus aspiration combined with renal artery catheter-directed thrombolysis (CDT), followed by 20-month postoperative monitoring to evaluate the patient’s functional outcomes.

Case description

A 65-year-old male presented with a 1-day history of severe pain in the right lower quadrant. The patient had not experienced any episodes of fever, shivers, chest pain, nausea, vomiting, diarrhea, oliguria, or hematuria. As a result of the initial diagnosis of atrial fibrillation, the patient was prescribed anticoagulants, which he only took for 1 year and discontinued shortly thereafter. The patient walked to the clinic and had a blood pressure of 152/88 mmHg and a heart rate of 95 beats per minute. The patient had a 20-year history of tobacco use, cardiac disease, and atrial fibrillation but no history of hypertension. He also denied recently experiencing trauma, alcohol abuse or illicit drug use, and any drug allergies. Examination revealed discomfort upon percussion in the region of the right kidney.

The pain mimicked that of renal colic, leading to an initial misdiagnosis of ureteral stones.

However, a CT scan revealed no urinary tract stones. On the day of admission, the patient’s creatinine (CR) level was 177.5 µmol/L (normal: 58–110 µmol/L), the lactate dehydrogenase (LDH) level was 2729 U/L (normal: 120–246 U/L), and his D-dimer level was 3.29 mg/L (normal: <0.5 mg/L).The patient had an apparent painful consultation and an unknown diagnosis; however, we suspected aortic dissection or thrombosis. Therefore, we performed total aortic CTA and accidentally discovered thrombosis of the distal segment of the right renal artery and its branches, with right renal infarction and right perirenal exudation (Fig. 1). A filling defect was observed in the left heart atrium. The thrombus may have originated from the left atrium (Fig. 2). Immediately following the diagnosis of renal infarction, anticoagulation therapy was initiated with subcutaneous low-molecular-weight heparin (enoxaparin) at 1 mg/kg per dose administered every 12 h (actual dosing should align with drug prescribing information based on renal function). After admission, we discussed and agreed with the patient’s family to perform emergency surgical treatment in an effort to salvage the function of the infarcted kidney.

Fig. 1

CTA images at the time of diagnosis

Contrast-enhanced abdominal computed tomography revealed decreased perfusion of almost the entire right kidney. An intravascular filling defect (arrow) consistent with an embolus

Fig. 2

Enhanced CT revealed a filling defect in the left atrial appendage, and the thrombus may have originated from the left atrial appendage

Renal infarction: a therapeutic challenge

ARAE is an extremely rare cause of renal infarction (RI) that can result in irreversible kidney damage. Studies have indicated that the overall incidence of RI is low, and most cases are associated with cardiac embolism. However, precise epidemiological data on the specific incidence of RI among emergency department admissions remain lacking [1]. The etiologies and biological characteristics of renal infarction can be divided into four major categories: renal infarction of cardiac origin, renal infarction associated with renal artery injury, renal infarction associated with hypercoagulability disorders, and idiopathic renal infarction [2, 3].

Several causes of renal infarction, the most prevalent of which is cardioembolic (90%), have been described in the medical literature. Atrial fibrillation (AF) is the most common cause (in up to 65% of cases), followed by cardiac valvopathies and cardiomyopathies [4]. Arteriosclerosis, vasculitis, trauma, and hypercoagulable conditions are the causes of thrombosis in situ [5].

Nonetheless, the maximum duration of complete renal artery occlusion beyond which thrombolysis would no longer be beneficial is unknown. One study reported little benefit after 90 min, whereas other studies reported some benefit several days later. Delayed therapy is likely to be effective in patients with partial occlusion and in patients with thrombotic occlusion. However, 24 h seems reasonable, and this is a significant area for future research.

For patients undergoing vascular intervention and thrombolysis beyond the conventional time window, the long-term renal function protective benefits remain questionable. Although vascular recanalization during intervention can significantly improve patients’ low back pain symptoms, it does not necessarily result in long-term renal protection. The likelihood of benefiting from revascularization depends on several factors, including the duration of ischemia (determined by the persistence of symptoms and signs), the size of the renal parenchyma at risk of infarction, renal function (eGFR), and the degree of renal vascular occlusion (i.e., complete or partial occlusion), as determined by CTA. An individualized diagnostic and therapeutic approach based on these factors is essential to achieve the best therapeutic outcome.

There are still many questions regarding symptom relief, long-term renal function protection, and the optimal treatment for patients with renal infarction. Specifically, whether more aggressive surgical revascularization is needed, how to evaluate both short-term and long-term benefits for patients, and other related issues require further research and exploration.

Diagnosis

Renal infarction (RI) is relatively uncommon and presents with occasional atypical symptoms; thus, if we do not remain suspicious of its possibility, underdiagnosis and misdiagnosis may occur. Protecting kidney function, therefore, requires immediate diagnosis and treatment [6]. Thus, time is critical. The treatment for this condition is similar to that for myocardial infarction. The clinical manifestations of RI include abdominal or flank pain, nausea, hematuria, oliguria, vomiting, and fever. Severe renin-mediated hypertension or microscopic hematuria occurs in 60% of patients with renal infarction [7].

This condition must be distinguished from urinary stones, urinary colic, pyelonephritis, urinary tumors, and aortic coarctation. Examination of the abdomen at the lumbar region may reveal pressure or discomfort upon percussion. However, laboratory findings are not specific, as the white blood cell count and CRP level can be elevated, slight alterations in kidney function are commonly observed, and elevated markers indicating cell necrosis (LDH) and AKI are observed in most cases (93%)³. As previously reported, the LDH concentration, a common marker of cell necrosis, is frequently elevated (90.5% of the total population) in patients with RIs and often remains above the upper limit of the normal range for a prolonged period (15 days) after the first clinic visit for CT angiography, which remains the gold standard for diagnosing infarction and ruling out alternative diagnoses. Its diagnostic sensitivity exceeds 90% [5, 8].

Pathogenesis

Underlying endothelial injury predisposes a patient to the development of renal artery embolism. Those with a history of atherosclerosis, blunt trauma, or renal artery catheterization should be considered at increased risk [9].

However, the most prevalent cause of renal artery embolism is thromboembolism originating in the heart or massive arteries such as the aorta. Approximately 95% of thromboembolic events originate in the heart [10]. Hypercoagulability is an additional significant risk factor. A cancer diagnosis, regular oral contraceptive use, and systemic inflammatory processes can cause this intravascular condition. In the patient’s medical history, eliciting any genetic conditions that increase the risk of blood clot formation is crucial. Reduced blood flow and increased blood viscosity are factors that may contribute to the development of renal artery thrombosis [4].

Other potential causes include polycythemia vera, nephrotic syndrome, pregnancy, systemic lupus erythematosus, Ehlers–Danlos syndrome, infectious endocarditis, and renovascular hypertension. Some examples include antiphospholipid syndrome, protein C and S deficiency, factor V Leiden, antithrombin III deficiency, hyperhomocysteinemia, and prothrombin gene mutation [3, 7, 11].

Surgical interventions that cause arterial damage can complicate the development of renal thrombosis. This includes procedures such as renal angiography, intra-aortic balloon placement, renal surgery, and renal transplantation. It has also been reported to be secondary to acute pyelonephritis in sporadic cases. Significantly more renal infarctions occurred in patients with hypercoagulable conditions with bilateral kidney involvement. COVID-19 has been linked to thrombotic events and rare thrombotic events after vaccination [12, 13]. As mentioned, it is typically associated with other diseases or causes, and spontaneous cases are extremely uncommon.

Treatment

There is no optimal treatment for ARAE, and the choice of treatment options is still controversial. The treatment for renal infarction varies depending on the underlying cause. Treatment for ARIs primarily includes anticoagulation therapy, thrombolysis, and endovascular interventional procedures, with prompt removal of the infarct and restoration of renal blood flow being of utmost importance [14].

As with patients with conditions affecting other organs, such as myocardial infarction or cerebral artery embolism, patients with renal artery embolism should be treated with anticoagulation therapy immediately after diagnosis. Anticoagulation therapy is the foundation of treatment for RI. A recent retrospective descriptive analysis of patients with acute RI revealed positive early outcomes, with a dialysis-free survival rate of 91% at one year and a decline to 64% at five years. All patients were put on conservative single anticoagulation therapy [15]. However, only 6% of patients had bilateral RIs. Although the value of anticoagulation therapy is undeniable, many unanswered questions remain: What is the effectiveness of novel oral anticoagulants? How long should anticoagulation therapy last? What is the benefit of antiplatelet therapy? When should endovascular procedures be performed?

In much of the literature, researchers recommend conservative systemic anticoagulation therapy, which can result in treatment failure, the abandonment of protective renal function, and failure to relieve the patient’s pain, secondary renal contracture, or even renal hypertension [3]. Thrombolytic treatment consists of systemic intravenous thrombolysis and selective intra-arterial thrombolysis. Systemic thrombolytics increase the likelihood of hemorrhage. With the development of interventional techniques, patients with thromboembolism or protracted embolism of the arterial trunk have access to more aggressive catheter-directed thrombolysis (CDT), pharmacomechanical thrombectomy, and aspiration thrombectomy with possible angioplasty [16]. Endovascular procedures should be reserved for patients without prolonged ischemic times and no cortical atrophy or contraindications to fibrinolysis. CDT is an established alternative to surgery in cases of acute limb ischemia, and the successful use of CDT cases of ARAE have been described [17, 18].

Numerous thrombolysis techniques, such as local injection of guanfacine, tissue fibrinogen activator, and other thrombolytic agents followed by thrombus aspiration or aspiration of the thrombus followed by thrombolysis and possible angioplasty, have been reported [19]. Recent studies revealed that aspiration thrombectomy with or without subsequent local fibrinolysis [20] demonstrated positive outcomes.

Most patients presenting with acute renal artery obstruction are managed conservatively, especially those with unilateral embolisms with limited renal salvage potential. In patients with embolic occlusions, open surgical revascularization has been reported [21].

Protocol for thrombolysis treatment

We performed a two hour renal arteriogram, renal artery thrombus aspiration, and renal artery catheter-directed thrombolysis (CDT) surgery. Multiple filling defects were observed within the secondary branches of the main right renal artery, with interrupted flow localized in the middle segment and partial flow visible at the upper pole of the right kidney. (Fig. 3). After repeated negative pressure aspiration and extraction of small-sized old white thrombi, blood flow was partially restored at the occlusion site in the right kidney, and the occluded branch of the distal renal artery was visualized; however, visualization was significantly delayed, and blood flow stagnated. Initial treatment consisted of a tissue plasminogen activator infusion. (tPA; 50–80 mg). Ten to 15 min after the administration of tPA, imaging was repeated. Urokinase (UK) was continuously infused (1) a significant amount of thrombi was detected on the initial angiogram, and (2) a residual thrombus was detected in the artery after tPA infusion (Fig. 4). In such instances, the multihole catheter was left in the main trunk of the renal artery for 24 h, after which an additional angiogram was performed. An additional dose of UK was infused for 24 h, and a residual thrombus was detected. After surgery, right renal artery catheter-directed thrombolysis (CDT) was achieved with continuous infusion of urokinase, and the patient was treated with heparin, a systemic anticoagulant, and fluid replacement. Approximately 72 h later, we performed an emergency right renal arteriogram, which revealed the renal parenchyma in the middle and upper poles of the right kidney and the medial segment of the lower poles of the right kidney. However, the staining in the middle and lower poles was slightly lighter and more delayed than that in the middle and upper poles (Fig. 5). The patient’s back pain subsided six hours after the procedure, and the LDH level decreased promptly after the procedure and returned to normal levels six days later. Postoperatively, the patient received long-term warfarin anticoagulation therapy (INR 2–3) and demonstrated adequate control (INR 2.5) at the one-year follow-up. The patient returned to the hospital one year after surgery for a checkup. We believe that the previous treatment was quite effective, but the CTA at the time of evaluation revealed prominent atrophy of the right kidney (Fig. 6). The decline in renal function was attributed to irreversible parenchymal necrosis rather than inadequate anticoagulation.

Fig. 3

Vascular interventional renal angiography of the patient

Multiple filling defects within the secondary branches, localized flow interruption in the middle segment and partial flow visible at the upper pole of the right kidney were observed

Fig. 4

After completion of thrombolysis, the site at which the thrombus occluded the right renal artery was considerably more open than it was previously

Fig. 5

Catheter-directed thrombolysis (CDT) in the right renal artery was achieved with urokinase. Three days later, we performed an emergency right renal arteriogram

Fig. 6

A: Contrast-enhanced abdominal computed tomography scan showing decreased perfusion of almost the entire right kidney (coronal plane arrow). B: CTA at the one-year follow-up revealed severe atrophy of the affected kidney despite angiographic patency, highlighting discordance between the anatomical and functional outcomes of the patient

We wondered why, after actively performing renal revascularization for the patient and observing that most of the renal arteries were patent on postoperative renal angiography, the patient’s overall renal function remained within normal limits, with a serum creatinine level of 85 µmol/L (normal range: 58–110 µmol/L). However, the follow-up CT scan revealed severe atrophy of the right kidney, and renal scintigraphy revealed a significantly reduced right kidney glomerular filtration rate (GFR) of 7.53 mL/min (Fig. 7). This raises the following question: did we make a mistake? Despite the percutaneous endovascular treatment (PET) and thrombolysis that successfully recanalized the renal artery after angiography surgery, was our effort futile regarding long-term renal function protection for this patient, given the severe dysfunction observed in the right kidney?

Fig. 7

Postoperative 12-month follow-up renal dynamic imaging and glomerular filtration rate (GFR) measurement (SPECT/CT): TGFR = 47.26 mL/min, R = 7.53 mL/min, L = 39.73 mL/min

Discussion

In the present case, although the patient was treated with CDT, a one-year follow-up examination revealed a significant reduction in the size of the afflicted kidney. There are still many unanswered questions, such as whether a post-CDT intraoperative renal arteriogram can reveal the patency of renal vessels (Fig. 5), indicating the successful recovery of renal function. When should endovascular surgery be performed? Although the kidneys are still atrophied after surgery, is CDT treatment beneficial for controlling renal hypertension? The pain patients experience after CDT is significantly reduced. Is postinfarction pain also an indication for surgery? Of course, early identification and diagnosis of renal infarction is very important.

In this case, in the patient who underwent surgical thrombectomy, thrombectomy effectively relieved hypertension and pain symptoms but was not effective in saving renal function. Although diagnosis and treatment are often delayed, some patients with completely occluded arteries have undergone CDT with satisfactory immediate angiographic results [22]. Despite satisfactory angiographic results, the treated kidney will likely shrink over time, and overall kidney function will likely decline relative to baseline. Furthermore, the decline in renal function stabilizes and does not continue over time. CDT for acute renal artery occlusion (RAO) is a safe therapeutic modality and should be performed for kidney salvage, even in the presence of prolonged ischemia [23].

According to several studies, an ischemic duration of more than 2 h reduces long-term renal recovery to 30–50% of baseline [24]. Others have reported effective hemodialysis after up to 5 weeks of prolonged ischemia. Several factors, such as the duration of ischemia, collateral circulation, and preexisting renal disease, may influence treatment outcomes. Severe pain in patients with renal infarction 72 to 96 h after infarction can be relieved with surgery and revascularization, a study shows [25].

Other vascular diseases, such as stroke and acute coronary syndrome, have a well-established timeline for endovascular therapy [26]. The clinical utility of invasive treatment for ARAE, for which the diagnosis is delayed, remains unclear. Studies on animals revealed substantial renal parenchymal loss after one hour of ischemia [27]. However, these studies do not discuss the capacity for kidney regeneration after acute tubular necrosis or the role of collateral vascular supply. Although the RI is well established after 8 h of ischemia, effective revascularizations have been described after this period [21]. It appears that the renal collateral vascular supply partially sustains renal viability.

The possible mechanism is that successful revascularization prevents complete infarction of partially ischemic renal tissue; analogous to the cortical penumbra band in cases of stroke or renal infarction, which is an incomplete infarction, the body still has a strong ability to repair. In our patient, the upper portion of the kidney that was not completely ischemic was still functional, whereas the completely infarcted kidney tissue had atrophied.

Our follow-up observations revealed that renal tissue atrophy may still occur in partially recanalized vessels, indicating that angiographically successful revascularization does not necessarily equate to functional recovery of the renal parenchyma. For patients with acute total renal artery thromboembolic occlusion and impending renal parenchymal necrosis, the optimal window for restoring patency is limited to 30–40 min. Beyond this critical timeframe, varying degrees of parenchymal necrosis may develop [28]. Notably, the commonly cited 4- to 6-hour intervention window lacks substantial evidence in the literature, with many patients achieving satisfactory outcomes even when treated beyond this timeframe. Regrettably, most studies fail to provide confirmatory renal scintigraphy findings following “successful” revascularization. This necessitates a critical re-evaluation of emergency thrombectomy success rates.

Given the contralateral kidney’s normal function, serum creatinine levels and urine output typically remain unaffected. Notably, patients without a history of chronic kidney disease may maintain normal overall renal function despite partial or complete loss of parenchyma in one kidney. We strongly advocate incorporating renal scintigraphy into standard post-thrombectomy clinical practice. While specific guidelines for the optimal timing of radionuclide imaging are lacking, delaying scintigraphy until after acute tubular necrosis resolution (minimum 3 weeks) is proposed to ensure reliable results [28]. Therefore, we propose a multimodal approach that integrates interventional angiography and renal scintigraphy to holistically assess therapeutic efficacy, encompassing both anatomical revascularization and functional parenchymal recovery.

With advancements in endovascular techniques enhancing procedural safety, we propose adopting more aggressive interventional strategies for managing renal artery thromboembolism. We suggest performing interventional surgery within 24 h with the goal of restoring the patient’s hemodynamics within 24 h after surgery for proximal incomplete obstruction or collateral circulation. This will both alleviate the patient’s symptoms and preserve the patient’s remaining renal function. It is advantageous to prevent renal failure and intractable renal hypertension as much as possible. The recovery potential of the kidney reported in the literature may have been underestimated.

For patients who are generally more likely to benefit from revascularization, we propose development of an individualized diagnosis and treatment plan tailored to achieve the best treatment effect on the basis of the duration of ischemia (determined by the duration of symptoms and signs), the size of the renal parenchyma at risk of infarction, renal function (i.e., eGFR), and the degree of renal vascular occlusion as determined by CTA (i.e., complete or partial occlusion). Within 24 h, we also propose more aggressive treatment for renal infarction involving large vessels, including CDT revascularization and interventional catheter thrombolysis. For patients with complete renal infarction for more than 24 h, surgical revascularization can still benefit patients in terms of symptom relief and renal function protection, but further research is needed to determine whether it is truly optimal for long-term preservation of renal function and control of renal hypertension. While the presented case report provides valuable clinical insights, its inherent limitations—including a single-patient focus, potential retrospective biases, and lack of generalizability—restrict definitive conclusions. Similarly, the accompanying review, though comprehensive, is constrained by heterogeneity among included studies, possible publication bias, and variable methodological rigor across sources. The optimal time window for vascular intervention remains debated in the literature [29]. However, the appropriateness of the 24-hour therapeutic time window remains uncertain. A comprehensive multidisciplinary evaluation and larger-scale studies are warranted to clarify the optimal surgical timing, thereby providing definitive clinical guidance and maximizing patient benefit. Additionally, the single-case design limits the generalizability of our findings.

Conclusion

This case underscores the critical need for early suspicion of acute renal artery embolism (ARAE) in patients with persistent flank pain, atrial fibrillation, elevated LDH, or high thromboembolic risk. Timely intervention within 24 h—particularly thrombus aspiration combined with catheter-directed thrombolysis—may salvage renal function in large-vessel occlusions. For delayed presentations (> 24 h), revascularization still offers symptomatic relief and partial renal preservation, though its long-term benefits on hypertension and renal function require further validation. Treatment decisions should prioritize individualized risk-benefit analysis, emphasizing multidisciplinary evaluation of infarct extent, collateral circulation, and comorbidities. While aggressive revascularization is advocated for acute cases, future studies are warranted to optimize late-intervention strategies and define their role in mitigating chronic sequelae. Notably, successful revascularization does not guarantee functional recovery of the renal parenchyma. To accurately evaluate long-term renal functional restoration, we propose integrating renal scintigraphy into standardized clinical protocols following interventional thrombectomy.