Abstract
Renal disease caused by cholesterol crystal embolism (CCE) occurs when cholesterol crystals become lodged in small renal arteries after small pieces of atheromatous plaques break off from the aorta or renal arteries and shower the downstream vascular bed. CCE is a multisystemic disease but kidneys are particularly vulnerable to atheroembolic disease, which can cause an acute, subacute, or chronic decline in renal function. This life-threatening disease may be underdiagnosed and overlooked as a cause of chronic kidney disease (CKD) among patients with advanced atherosclerosis. CCE can result from vascular surgery, angiography, or administration of anticoagulants. Atheroembolic renal disease has various clinical features that resemble those found in other kidney disorders and systemic diseases. It is commonly misdiagnosed in clinic, but confirmed by characteristic renal biopsy findings. Therapeutic options are limited, and prognosis is considered to be poor. Expanding knowledge of atheroembolic renal disease due to CCE opens perspectives for recognition, diagnosis, and treatment of this cause of progressive renal insufficiency.
Highlights
Cholesterol crystal embolism (CCE) occurs when small pieces of atheromatous plaques from the aorta or other major arteries break off and shower small arteries cholesterol crystal emboli
One proposed explanation for anticoagulant and thrombolytic agents related CCE is that anticoagulants and thrombolytic treatment agents may initiate the rupture of plaques by causing internal hemorrhage or dissolution of fibrous caps, exposing the underlying low-density lipoprotein-derived cholesterol crystals (CCs) to the systemic circulation
A recent study reported that low-density lipoprotein apheresis (LDL-A) decreased the risk of maintenance dialysis in 49 CCE patients with renal dysfunction after 24 weeks [58]
Summary
Cholesterol crystal embolism (CCE) occurs when small pieces of atheromatous plaques from the aorta or other major arteries break off and shower small arteries cholesterol crystal emboli. CCE is becoming a common cause of renal insufficiency in adults over the age of 60 with advanced atherosclerosis [2,3]. The clinical presentation of CCE is diverse, with limited therapeutic options and poor long-term outcomes for resulting atheroembolic renal disease [4]. This life-threatening disease may be underestimated and overlooked as a cause of chronic kidney disease (CKD) in patients with diffuse atherosclerosis and/or undergoing interventional cardiac catheterization, and its diagnosis and management still remain unresolved. We discuss the recent advances in the clinical and pathological findings in CCE
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