Renal Artery Atheroembolism Mitul Suresh Patel, Alan B. Lumsden and Mark G. Davies Atheroembolic renal disease (AERD) occurs following occlusion of the renal vasculature by cholesterol crystals originating from the aorta or other large arteries spontaneously (primary disease) or following vascular intervention (secondary disease). Cardiac and cerebrovascular cases of atheroembolic disease were the first to be described, with initial reports dating back to the 1870s. Flory, in 1946, was the first to prove that atheromatous aortic plaque is the embolic origin of cholesterol crystals. Despite the work done to date to study and characterize atheroembolization, the diagnosis and correct identification of the disease remains a challenge. Etiology Owing to the variety in clinical presentations, atheroembolic disease remains misdiagnosed or undetected. Studies have reported an incidence of less than 1%, but literature on aortic surgery reports a prevalence as high as 77%. The actual clinical incidence of kidney failure caused by atheroembolism is likely between 3% and 10%. The difficulty in diagnosing atheroembolic disease is also compounded by the multitude of organ systems affected. Although the kidneys are most commonly affected, the skin, gastrointestinal tract, lower extremities, and eyes can also be involved. It has been suggested that the incidence of involved viscera is proportional to its percentage of blood flow. The kidneys receive 20% to 25% of the total cardiac output, correlating with the high incidence of kidney involvement in atheroembolic disease. Studies to localize the embolic source in AERD have shown that almost all patients have atherosclerotic plaque in the thoracic aorta. In addition, 67% of patients were found to have abdominal aortic aneurysms and about 30% were found to have renal artery atherosclerotic disease. Although unlikely, there remains a possibility of patients showering thrombotic emboli from venous thrombosis. A patient foramen ovale (PFO) is often suspected in these patients. The incidence of PFO in the general population is estimated to be between 27% and 35%. Therefore, patients with unexplained kidney failure and normal arterial anatomy should be evaluated for paradoxical embolism from a venous source. Contrast thoracic echocardiography has been shown to detect a PFO in 10% to 15% of the population. As an alternative to thoracic echocardiography, transcranial Doppler provides a safe, noninvasive modality that identifies PFOs and quantifies functionally significant shunts. Sastry and colleagues found transcranial Doppler to be more sensitive than thoracic echocardiography in identifying PFOs and better at quantifying significant shunts. Atheroembolic renal disease occurs most commonly in white men older than 60 years. Additional risk factors are a history of smoking, hypertension, hypercholesterolemia, and diabetes. The incidence of AERD may also be underappreciated in African-American patients owing to the difficulty in identifying its cutaneous manifestations. Primary AERD is the result of spontaneous showering of emboli from eroding plaque. Iatrogenic dislodgement of plaque and destabilization of plaque by either thrombolytic therapy or systemic anticoagulation are secondary causes of AERD. Most cases are the result of iatrogenic causes, with vessel wall trauma following endovascular interventions resulting in most cases of AERD. Scolari and coworkers found that AERD manifested in two forms. The acute or subacute type is the result of a massive shower of emboli or repeated cyclical embolizations caused by abrupt or repeated rupture of unstable plaques. The chronic type is caused by the slow release of emboli from eroding atherosclerotic plaque. The mechanism resulting in AERD also determines its clinical manifestation. Acute and subacute forms of AERD are the result of a massive shower of emboli, often following vascular instrumentation or anticoagulation. In contrast, spontaneous plaque dislodgement is subtle and results in a smoldering and chronic type of kidney failure. Scolari’s group published a report evaluating 354 patients and found that AERD from iatrogenic causes resulted in mostly acute and subacute onset, whereas spontaneous disease was mostly responsible for chronic onset. Twenty percent to 30% of patients with AERD present with kidney failure within 1 week of a high-risk event. In addition to kidney failure, these patients present with massive multiple organ involvement, most often with gastrointestinal and cutaneous emboli. Subacute onset is the most common, and kidney failure occurs weeks or months following the triggering event. Average onset is about 5 weeks following the inciting event, and the delayed presentation suggests a causal role of recurrent showering of emboli along with an endothelial inflammatory reaction. Owing to the slow and progressive form of renal failure associated with chronic AERD, it remains the most challenging to diagnose. There are few symptoms, and renal biopsy is not routinely performed, resulting in missed diagnoses. Persistent or worsening kidney function is thought to be secondary to recurrent debris embolization. Dorros and colleagues report that kidney dysfunction from renal artery stenosis is not a result of ischemia but instead of recurrent atheroemboli causing nonuniform glomerular pathology. Only gold members can continue reading. 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Renal Artery Atheroembolism Mitul Suresh Patel, Alan B. Lumsden and Mark G. Davies Atheroembolic renal disease (AERD) occurs following occlusion of the renal vasculature by cholesterol crystals originating from the aorta or other large arteries spontaneously (primary disease) or following vascular intervention (secondary disease). Cardiac and cerebrovascular cases of atheroembolic disease were the first to be described, with initial reports dating back to the 1870s. Flory, in 1946, was the first to prove that atheromatous aortic plaque is the embolic origin of cholesterol crystals. Despite the work done to date to study and characterize atheroembolization, the diagnosis and correct identification of the disease remains a challenge. Etiology Owing to the variety in clinical presentations, atheroembolic disease remains misdiagnosed or undetected. Studies have reported an incidence of less than 1%, but literature on aortic surgery reports a prevalence as high as 77%. The actual clinical incidence of kidney failure caused by atheroembolism is likely between 3% and 10%. The difficulty in diagnosing atheroembolic disease is also compounded by the multitude of organ systems affected. Although the kidneys are most commonly affected, the skin, gastrointestinal tract, lower extremities, and eyes can also be involved. It has been suggested that the incidence of involved viscera is proportional to its percentage of blood flow. The kidneys receive 20% to 25% of the total cardiac output, correlating with the high incidence of kidney involvement in atheroembolic disease. Studies to localize the embolic source in AERD have shown that almost all patients have atherosclerotic plaque in the thoracic aorta. In addition, 67% of patients were found to have abdominal aortic aneurysms and about 30% were found to have renal artery atherosclerotic disease. Although unlikely, there remains a possibility of patients showering thrombotic emboli from venous thrombosis. A patient foramen ovale (PFO) is often suspected in these patients. The incidence of PFO in the general population is estimated to be between 27% and 35%. Therefore, patients with unexplained kidney failure and normal arterial anatomy should be evaluated for paradoxical embolism from a venous source. Contrast thoracic echocardiography has been shown to detect a PFO in 10% to 15% of the population. As an alternative to thoracic echocardiography, transcranial Doppler provides a safe, noninvasive modality that identifies PFOs and quantifies functionally significant shunts. Sastry and colleagues found transcranial Doppler to be more sensitive than thoracic echocardiography in identifying PFOs and better at quantifying significant shunts. Atheroembolic renal disease occurs most commonly in white men older than 60 years. Additional risk factors are a history of smoking, hypertension, hypercholesterolemia, and diabetes. The incidence of AERD may also be underappreciated in African-American patients owing to the difficulty in identifying its cutaneous manifestations. Primary AERD is the result of spontaneous showering of emboli from eroding plaque. Iatrogenic dislodgement of plaque and destabilization of plaque by either thrombolytic therapy or systemic anticoagulation are secondary causes of AERD. Most cases are the result of iatrogenic causes, with vessel wall trauma following endovascular interventions resulting in most cases of AERD. Scolari and coworkers found that AERD manifested in two forms. The acute or subacute type is the result of a massive shower of emboli or repeated cyclical embolizations caused by abrupt or repeated rupture of unstable plaques. The chronic type is caused by the slow release of emboli from eroding atherosclerotic plaque. The mechanism resulting in AERD also determines its clinical manifestation. Acute and subacute forms of AERD are the result of a massive shower of emboli, often following vascular instrumentation or anticoagulation. In contrast, spontaneous plaque dislodgement is subtle and results in a smoldering and chronic type of kidney failure. Scolari’s group published a report evaluating 354 patients and found that AERD from iatrogenic causes resulted in mostly acute and subacute onset, whereas spontaneous disease was mostly responsible for chronic onset. Twenty percent to 30% of patients with AERD present with kidney failure within 1 week of a high-risk event. In addition to kidney failure, these patients present with massive multiple organ involvement, most often with gastrointestinal and cutaneous emboli. Subacute onset is the most common, and kidney failure occurs weeks or months following the triggering event. Average onset is about 5 weeks following the inciting event, and the delayed presentation suggests a causal role of recurrent showering of emboli along with an endothelial inflammatory reaction. Owing to the slow and progressive form of renal failure associated with chronic AERD, it remains the most challenging to diagnose. There are few symptoms, and renal biopsy is not routinely performed, resulting in missed diagnoses. Persistent or worsening kidney function is thought to be secondary to recurrent debris embolization. Dorros and colleagues report that kidney dysfunction from renal artery stenosis is not a result of ischemia but instead of recurrent atheroemboli causing nonuniform glomerular pathology. Only gold members can continue reading. Log In or Register to continue Share this:Click to share on Twitter (Opens in new window)Click to share on Facebook (Opens in new window) Related Related posts: Technical Aspects of Percutaneous Carotid Angioplasty and Stenting for Arteriosclerotic Disease In-Situ Treatment of Aortic Graft Infection with Prosthetic Grafts and Allografts Treatment of Acute Upper Extremity Venous Occlusion Intraoperative Assessment of the Technical Adequacy of Carotid Endarterectomy Stay updated, free articles. Join our Telegram channel Join
