Renal artery embolism and thrombosis can both lead to acute occlusion of the main renal artery or its branches, resulting in corresponding clinical manifestations.
Epidemiology and Pathophysiology
Renal artery embolism typically occurs unilaterally, though 15%–30% of patients may experience bilateral renal artery embolism. Segmental renal infarction is more common than infarction of the entire kidney. Emboli in renal artery embolism are primarily cardiogenic (accounting for approximately 90%). The most common source is atrial thrombi in patients with atrial fibrillation. Other sources include left ventricular thrombi, valvular heart disease, bacterial or non-bacterial endocarditis, and atrial myxomas. Non-cardiogenic sources of emboli include aortic plaques, mural thrombi, and paradoxical emboli passing through atrial septal defects or patent foramen ovale.
Renal artery thrombosis is relatively rare and may occur as a complication of progressive atherosclerosis or in association with prothrombotic conditions, such as antiphospholipid syndrome. It may also result from inflammatory diseases, including Takayasu arteritis, syphilis, thromboangiitis obliterans, and systemic vasculitis. Structural abnormalities of the renal artery, such as aneurysms or fibromuscular dysplasia, can lead to in situ thrombosis. Acute thrombosis may also result from arterial intimal tears, contusions, or retroperitoneal hematoma caused by blunt trauma or deceleration injuries. Iatrogenic thrombosis can occur following procedures such as percutaneous transluminal renal artery angioplasty.
Clinical Manifestations
The clinical presentation varies depending on the degree and extent of renal artery occlusion, as well as the presence of comorbid conditions. These symptoms can be easily confused with common urinary system disorders, such as renal colic or pyelonephritis.
In kidneys with pre-existing renal artery disease and established collateral circulation, renal artery occlusion may not result in renal infarction or may only cause small-scale infarction, with mild clinical symptoms.
Acute occlusion of the main renal artery or major branches can lead to renal infarction, presenting as severe ipsilateral flank or costovertebral pain, nausea, emesis, and hematuria. Pain may also be located in the abdomen, back, or chest, and up to half of patients may not experience any pain. Anuria suggests bilateral renal involvement or occlusion of the main renal artery in a solitary kidney. Urinalysis often shows hematuria and mild proteinuria. Blood tests typically reveal non-specific findings, such as elevated white blood cell counts, as well as increased serum aspartate aminotransferase (AST), lactate dehydrogenase (LDH), and alkaline phosphatase (ALP). Elevated urinary LDH levels are relatively specific for diagnosing renal artery occlusion. In cases of unilateral renal infarction, serum creatinine and blood urea nitrogen levels may show transient elevations. However, bilateral renal infarction or infarction in a solitary kidney can lead to more severe and prolonged renal dysfunction.
Diagnosis
Non-contrast and contrast-enhanced CT scans are reliable diagnostic tools for renal artery occlusion, offering rapid and accurate detection while also identifying potential associated trauma. Contrast-enhanced CT can reveal filling defects in the main renal artery or its branches and a lack of enhancement in the renal tissue supplied by the affected artery. In patients with an eGFR <30 mL/min, the risk of contrast-induced nephropathy is high, and the use of iodinated contrast agents is generally avoided. Contrast-enhanced MR imaging provides high diagnostic accuracy and can serve as an alternative to CT. However, in patients with CKD stage 3b or higher, gadolinium-based contrast agents are contraindicated. Radionuclide renography, which can demonstrate segmental or extensive renal perfusion defects, was once widely used for diagnosing renal artery occlusion but has largely been replaced by CT and MR imaging. Ultrasound has low sensitivity and is not recommended for diagnosis. Interventional angiography, while invasive and associated with some risks, can be used when the diagnosis is uncertain or when percutaneous revascularization is being considered.
In addition, echocardiography is necessary to evaluate for intracardiac thrombi in patients suspected of thrombotic renal artery occlusion. For cases of non-traumatic thrombosis leading to renal artery occlusion, it is important to assess for the presence of prothrombotic conditions, vasculitis, or progressive atherosclerosis.
Treatment
Restoring vascular patency as quickly as possible is the primary focus of treatment for acute renal artery embolism or thrombosis.
Treatment for non-traumatic renal artery thrombosis includes systemic anticoagulation with heparin or low-molecular-weight heparin for 7–10 days. Oral warfarin is typically initiated on the third day of anticoagulation and continued for one year, maintaining an INR between 2.0 and 3.0. The efficacy and safety of other novel direct oral anticoagulants have not yet been fully established. In addition, percutaneous renal artery interventions, including thrombolysis, thrombectomy, and stent placement, can successfully treat acute renal artery occlusion, although there is a lack of randomized controlled trials (RCTs) comparing these interventions with medical therapy. Surgical vascular reconstruction carries a higher mortality rate compared to medical therapy and does not improve the success rate of renal function recovery. Therefore, it is not recommended as a first-line treatment and is only considered in cases of bilateral renal artery embolism or embolism involving a solitary kidney.
For traumatic renal artery thrombosis, surgical intervention is the preferred treatment, and early intervention is critical for preserving renal function.
Blood pressure should be managed through appropriate pharmacological therapy in cases of renal artery embolism or thrombosis. Adequate fluid hydration is also necessary.