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Cholesterol embolization syndrome is an increasing but underestimated problem after endovascular intervention or after the start of thrombolytic therapies. Embolies from the aortic wall involves abdominal organs and the skin of the lower extremities or buttocks. In our case a progressive ulceration and necroses occurs spontaneously. Endovascular treatment of the lower extremities was successful for a short period. Due to the progression of necrosis, both legs were amputated. Biopsies were taken from the skin were initially no directions to the diagnosis of Cholesterol embolization syndrome. After a second elliptical excision biopsy the diagnosis of cholesterol embolization syndrome was confirmed. Because the rapid progression of skin necroses despite the treatment of prednisone, patient died due to sepsis and renal failure. This case shows when arterial revascularization is performed and progression in skin necrosis occurs despite optimal arterial vascular status the diagnosis CES should be considered and treated in an early state of disease., Competing Interests: Declaration of Conflicting InterestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Rationale: Cholesterol crystal embolism can be a life-threatening complication of advanced atherosclerosis. Pathophysiology and molecular targets for treatment are largely unknown., Objective: We aimed to develop a new animal model of cholesterol crystal embolism to dissect the molecular mechanisms of cholesterol crystal (CC)-driven arterial occlusion, tissue infarction, and organ failure., Methods and Results: C57BL/6J mice were injected with CC into the left kidney artery. Primary end point was glomerular filtration rate (GFR). CC caused crystal clots occluding intrarenal arteries and a dose-dependent drop in GFR, followed by GFR recovery within 4 weeks, that is, acute kidney disease. In contrast, the extent of kidney infarction was more variable. Blocking necroptosis using mixed lineage kinase domain-like deficient mice or necrostatin-1s treatment protected from kidney infarction but not from GFR loss because arterial obstructions persisted, identifying crystal clots as a primary target to prevent organ failure. CC involved platelets, neutrophils, fibrin, and extracellular DNA. Neutrophil depletion or inhibition of the release of neutrophil extracellular traps had little effects, but platelet P2Y12 receptor antagonism with clopidogrel, fibrinolysis with urokinase, or DNA digestion with recombinant DNase I all prevented arterial occlusions, GFR loss, and kidney infarction. The window-of-opportunity was <3 hours after CC injection. However, combining Nec-1s (necrostatin-1s) prophylaxis given 1 hour before and DNase I 3 hours after CC injection completely prevented kidney failure and infarcts. In vitro, CC did not directly induce plasmatic coagulation but induced neutrophil extracellular trap formation and DNA release mainly from kidney endothelial cells, neutrophils, and few from platelets. CC induced ATP release from aggregating platelets, which increased fibrin formation in a DNase-dependent manner., Conclusions: CC embolism causes arterial obstructions and organ failure via the formation of crystal clots with fibrin, platelets, and extracellular DNA as critical components. Therefore, our model enables to unravel the pathogenesis of the CC embolism syndrome as a basis for both prophylaxis and targeted therapy.

The number of released free cholesterol crystal emboli (fCCE) and their role during percutaneous coronary intervention (PCI) in acute coronary syndrome (ACS) have not been documented yet. Furthermore, fCCE manifesting in the coronary lumen following plaque rupture has been historically overlooked owing to the standard tissue preparation for light microscopy which uses ethanol as a dehydrating agent that can dissolve fCCE, leaving behind empty tissue. In this case report, we evaluated fCCE released during PCI for ACS and their relationship with myocardial injury and coronary artery obstruction on the H&E-stained sections by using polarised light microscopy. To our knowledge, there has been no mention of the visibility of fCCE on H&E-stained frozen polarised sections before., Competing Interests: Competing interests: KK, who is the president of Inter-tec Medicals, Co., developed non-obstructive angioscopy. SK is a technical consultant for Nemoto Kyorin-do Co., (© BMJ Publishing Group Limited 2018. No commercial re-use. See rights and permissions. Published by BMJ.)

Cholesterol crystals embolise when an aortic atherosclerotic lesion ruptures and cholesterol crystals are scattered and obstruct small peripheral arterioles. Risk factors include both iatrogenic factors such as intravascular catheterisation, and spontaneous factors for atherosclerosis such as aging, hypertension, dyslipidaemia, and smoking. We describe the case of an 83-year-old Japanese man who developed unilateral, superficial necrosis of the tongue as a result of spontaneous embolisation of cholesterol crystals., (Copyright © 2018 The British Association of Oral and Maxillofacial Surgeons. Published by Elsevier Ltd. All rights reserved.)

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., Competing Interests: The authors declare no conflict of interest.

Cholesterol-crystal embolization (CE) usually presents as an acute or subacute multisystemic disease. When affecting native kidneys prognosis is poor, often leading to chronic kidney disease. Presentation in renal allografts is a rare condition although probably underdiagnosed. If renal CE originates from the recipient, allograft survival is usually good, whereas if the donor is the origin, graft dysfunction and subsequent graft loss are common. Associated risk factors are common to native and transplanted kidneys. We report 2 renal graft recipients of different cadaveric donors, both male and 68 years old, diagnosed with CE in renal grafts at 19 and 72 months after transplantation, respectively. They presented previous risk factors for CE, including severe atherosclerosis. They presented insidious and asymptomatic impairment of renal function initially. Renal graft biopsy specimens showed CE in the interlobular arteries. Potential triggers for CE were suspended and high doses of steroids were started. However, progressive decline in renal function and requirement of chronic dialysis occurred within the first year after diagnosis in both cases. Herein we discuss the causal or incidental role of CE in the graft failure of these cases, highlighting the serious outcome despite the recipient origin of the CE and the initiation of treatment., (Copyright © 2015 Elsevier Inc. All rights reserved.)

A 79-year-old man with atherosclerosis presented blue toes and livedo reticularis. The patient had eroded aortic atheromatous plaques, and cholesterol embolization syndrome was suspected. An endovascular technique to exclude sources of cholesterol emboli was however performed. The patient immediately presented with severe muscle pain and total functional disability of lower limbs, new ischemic lesions of toes, anal and genital necrosis, and a livedo extended up to the abdomen. A massive rhabdomyolysis occurred associated with acute kidney injury and hyperkaliemia treated by continuous renal replacement therapy with regional citrate anticoagulation. Steroids have been introduced and renal function improved. Cholesterol crystals were also found on a skin biopsy, performed before endovascular procedure., (Copyright © 2013 Société française d’anesthésie et de réanimation (Sfar). Published by Elsevier SAS. All rights reserved.)

Purple toe syndrome is a rare complication of warfarin therapy. It occurs usually after 3 to 8 weeks of therapy and it is caused by cholesterol emboli from atheromatous plaque. Sudden onset of pain in affected area, typically in toes and feet, is the main characteristic of the syndrome. We describe a case of a 65-year-old female with purple toe syndrome after 6 weeks of warfarin. Indication of warfarin was a proximal deep venous thrombosis, which developed after prolonged immobilization. Factor V (FV) Leiden and persistent high FVIII activity were found as additional eliciting factors for venous thromboembolism. After warfarin withdrawal and enoxaparin treatment, symptoms disappeared promptly but a slight discoloration of the toe persists.

Cholesterol crystal embolization (CCE) is one of the many complications of atherosclerosis. CCE is usually an iatrogenic event occurring either after vascular surgery, usually aortic surgery, or invasive angiographic investigations or in the course of anticoagulant or thrombolytic therapy. More rarely, it occurs after trauma or even in the absence of any inciting cause. CCE may manifest with single or multiorgan involvement. Skin involvement is usually seen in the context of a systemic disease, especially affecting the lower extremities and lower trunk. We report on a rare case of isolated spontaneous focal cutaneous involvement of the upper limb, with peculiar mesenchymal and reactive histological changes. A 65-year-old man with a clinical history of atherosclerosis was admitted complaining of a nonhealing painful skin ulceration on his left elbow for 5-month duration. A skin biopsy was taken, and histopathological examination documented an intrarteriolar cholesterol embolus in the dermis along with a peculiar adjacent bizarre fibroblastic reaction, of the type usually seen in atypical decubital fibroplasia of debilitated patients. The ulceration was surgically excised, and the wound was sutured and repaired. At 18-month follow-up, the patient has no evidence of local disease.

Atheroembolic renal disease is caused by foreign-body reaction to cholesterol crystals flushed from the atherosclerotic plaques into the small-vessel system of the kidneys. It is an underdiagnosed entity, mostly related to vascular procedures and/or anticoagulation, and prognosis is considered to be poor. Besides the benefit of aggressive medical prevention of further embolic events, use of steroid therapy has been associated with greater survival. Here we report a case of a patient with a multisystemic presentation of the disease days after performance of percutaneous coronary intervention and anticoagulation initiation due to an episode of myocardial infarction. Renal, cutaneous, ophthalmic, neurological, and possibly muscular and mesenteric involvement was diagnosed. Although medical treatment with corticosteroids and avoidance of further anticoagulation was applied, the patient rapidly progressed to end-stage renal disease requiring hemodialysis and died 6 months after diagnosis. This is a case of catastrophic progression of the disease resistant to therapeutic measures. Focus on diagnosis and more efficient preventive and therapeutic protocols are therefore needed.

Skin ulceration is a major source of morbidity and is often difficult to manage. Ulcers caused by an inflammatory cause or microvascular occlusion are particularly challenging in terms of diagnosis and treatment. The management of such ulcers requires careful assessment of associated systemic conditions and a thorough analysis of the ulcer's clinical and histologic findings. In this article, the authors discuss several examples of inflammatory ulcers and the approach to the diagnosis and treatment of these ulcers., (Copyright © 2010 Elsevier Inc. All rights reserved.)

Atheroembolism is a multisytemic disease which affects many organs, including the kidneys, by the release of cholesterol emboli to tissues from an erosed atherosclerotic plaque, causing vascular obstruction in many tissues. The atheroembolic renal disease (AERD) is histologically represented by cholesterol crystals in renal arterioles with an inflammatory infiltrate around the vessels, and causes acute renal failure that may be severe and prolonged, weeks or even months after the embolic episode. The AERD carries a bad prognosis, with a high mortality. We herein report a case of a patient presenting AERD which was manifested two months after he was submitted to a cardiac catheterism and coronary angioplasty. The prevalence, clinical findings, renal histology, treatment and prognosis of AERD are discussed.

Cholesterol embolism (CE) is characterized by emboli containing cholesterol crystal in the arterioles, most commonly found in the skin and the kidney. The skin presentations of CE include livedo reticularis, blue toe syndrome, ulceration and gangrene. Cutaneous reactive angiomatosis (CRA) is a recently proposed term to describe a group of reactive vascular proliferation in skin caused by various diseases. Its occurrence in association with CE is extremely uncommon. An 82-year-old man with a history of cerebral infarction and on long-term warfarin therapy developed progressive, multiple violaceous papules and nodules on the dorsal feet, soles and toes, simulating Kaposi's sarcoma. Skin biopsy showed marked vascular endothelial cell proliferations characteristic of CRA affecting the full thickness of dermis. In addition, cholesterol crystal emboli were found in dermal arterioles. The skin lesions improved after the warfarin dose was reduced. We emphasize the possible presence of CE in a patient presented with CRA, especially in those with a pre-existing atherosclerotic disease, on anticoagulation therapy, or having a prior history of invasive vascular procedure.

We report on a 55-year-old man who was admitted with increased serum-creatinine (3.4 mg/dl), gross proteinuria (4.6 g/24 h) and arterial hypertension. The medical history included hyperlipidemia, coronary artery disease (CAD) and a recent coronary angiography, but normal serum-creatinine and no proteinuria before coronary intervention. Serology and urinary analysis did not show any signs of a systemic disease. A renal biopsy, however, revealed multiple cholesterol crystal emboli in small vessels along with a typical infiltration of eosinophilic granulocytes. The patient was subsequently treated with an angiotensin-receptor-1 (AT1R) blocker and high-dose statins and was then evaluated for LDL-apheresis. Gross proteinuria was largely unaffected by (AT1R) blockade and renal function further declined necessitating, initiation of hemodialysis. Renal CCE with profound proteinuria is an unusual presentation of acute renal failure, potentially misleading and thereby prolonging correct diagnostics of a rare entity. Identification of high-risk patients is of utmost importance as efficient therapeutic strategies do not exist.

Heparin-induced thrombocytopenia (HIT) is characterized by a reduction in the platelet count and systemic thromboembolism during heparin therapy. Herein is reported a case of HIT with characteristic thrombus formation. A 68-year-old man who had been treated for hypertension for 27 years suffered a brain infarction and was treated with heparin. After this treatment, other new infarctions occurred in multiple organs. Because serum antibodies against heparin/PF4 complex were detected, he was diagnosed as having HIT, and warfarin and argatroban were administered instead of heparin. He died, however, 119 days after the first onset. At autopsy infarction due to organized thrombi with cholesterin deposition in multiple organs were found, similar to usual atherosclerotic emboli, but different to them with regard to clinical course and distribution of thrombi. This case in which organization and frequent cholesterin deposition were found in thromboembolized lesions of multiple organs after relatively long-term follow up, is unusual. The findings suggest that HIT accompanied by marked hypercholesterolemia of long duration contributes to a characteristic form of thromboembolism that needs careful management.

Introduction: Modifiable vascular risk factors (MVRF) for atherotrombotic or lacunar cerebral infarction have been clearly established, even though only a few population studies have been conducted and we do not know the risk of glycemic status prior to the diabetes mellitus (DM). This study has aimed to determine the relationship between impaired fasting glucose (IFG) and others MVRF with atherothrombotic or lacunar cerebral infarctions., Methods: A population based case-control study was conducted in two urban health care centers., Cases: 236 patients with atherothrombotic or lacunar CI, diagnosed by computed tomography scan magnetic resonance imaging. Unusual, indeterminate and cardioembolic cerebral infarction and cerebral hemorrhage were excluded., Controls: 441 patients without cerebral infarction, matched by age and gender, selected by means of simple random sampling. The odds ratios (OR) of IFG, DM, smoking, high blood pressure, hypercholesterolemia, hypertriglyceridemia, and obesity were measured with logistic regression., Results: Mean age was 71.1 years old, 62 % being male. Prevalence in cases of MVRF was: IFG, 32.9%; DM, 49.6 %; smoking, 26.3%; high blood pressure, 78.8%; hypercholesterolemia, 29.3%; hypertriglyceridemia, 18.2%, and obesity, 63.5%. All MVRFs were associated in the crude analysis with increased risk of cerebral infarction. In the multivariate analysis, significant associations were found for IFG (OR: 3.2; 95 % confidence interval [CI]:1.1-7.9), DM (OR: 4.5; 95 % CI: 1.4-14.9), high blood pressure (OR: 2.6; 95 % CI: 1.5-4.5), hypercholesterolemia (OR: 2.3; 95 % CI: 1.4-3.9), and obesity (OR: 1.7; 95% CI: 1.0-2.9)., Conclusions: Alterations of the glucose metabolism IFG and DM are important MVRF for atherothrombotic or lacunar cerebral infarction as seen by the high rate of OR and high prevalence in the population with cerebral infarction.

Segmental infarction of the testis represents a rare entity in that there have been fewer than 40 cases documented in the literature. Like global infarction, segmental infarction of the testis can masquerade as a mass lesion or torsion of the testis. Reported herein is a very rare case of segmental testicular infarction due to atheroembolism in a 58-year-old man. The patient presented with severe left testicular pain and underwent left high orchiectomy on the clinical diagnosis of testicular torsion. The testis had a segmental hemorrhagic necrosis around which many cholesterol emboli were observed. This is the first report to describe cholesterol embolism-associated segmental testicular infarction.

Cholesterol embolization into native kidneys has a dim prognosis for renal function and frequently leads to irreversible renal failure. Although uncommon, cholesterol embolization may also occur in renal allografts, particularly if either the recipient or the donor has prominent atherosclerosis. We report here on a case of a 65-yr-old man with cholesterol emboli in the renal allograft and delayed graft function. The recipient's arteria iliaca externa was a potential source because of heavy atherosclerosis. The patient was dialysis-dependent for two wk after transplantation. However, renal function improved, no cholesterol emboli were found in a second biopsy of the graft and serum creatinine is 260 micromol/L six months after the transplantation. In the case of primary renal non-function or dysfunction, cholesterol embolization must be considered in the differential diagnosis. If renal cholesterol embolization originates from the recipient, allograft survival is usually good. In contrast, if cholesterol embolization is of donor origin, graft dysfunction and subsequent graft loss are common. The reason for this difference may be the more extensive embolization developing in an atherosclerotic cadaver donor occurring during the organ procurement or the severe trauma leading to death.

A 65-year-old man who received a deceased renal allograft in September 2001. The donor of the allograft was a 54-year-old hypertensive man who expired from intracerebral hemorrhage. Atheroma with hard plaques was present in both renal arteries and aortic patches. After vascular anastomosis and clamp release, the allograft recoloration was inadequate, and the patient remained anuric. Computerized tomography scan demonstrated disseminated infarction areas, suggesting cholesterol emboli, which was confirmed later by a graft biopsy. As approximately 50% of the renal parenchyma was perfused, graft nephrectomy was not indicated and dialysis was restarted. Diuresis was over 3000 ml/day and serum creatinine decreased and stabilized at 360 micromol/L by the 32nd postoperative day. The allograft supported the patient for only two years, and he eventually was successfully retransplanted in June 2003. We believe that delayed graft function due to cholesterol emboli disease may be reversible if areas of infarction are not too large.

Objective: To investigate the effects of granulocyte colony stimulating factor (G-CSF) on myocardial apoptosis following coronary microembolization (CME) and possible role of Janus kinase/singnal transducer and activator of transcription (JAK/STAT) pathway in this process., Methods: A total of 92 male Sprague Dawley rats were randomized into CME (n = 24), G-CSF (100 microg x kg(-1) x d(-1) i.p. 2 hours post CME for 5 days, n = 24), JAK2 inhibitor AG490 (G-CSF plus AG490, 5 mg x kg(-1) x d(-1) i.p. 2 hours post CME for 5 days, n = 24), all rats received left ventricular injection of homologous microthrombotic particle suspension post clamping the ascending aorta. Sham-operated group (n = 20) served as control. The rats were sacrificed at day 3, 7, 14 and 28 after operation. The myocardial mRNA expressions of Bcl-2, Bax, Fas, FasL and GAPDH which was used as the intercomparison, were evaluated by real time PCR. The ratio of Bcl-2/Bax was compared. The protein expression of Caspase-3, cleaved PARP, t-JAK2, p-JAK2, t-STAT3 and p-STAT3 were detected by western blot. Myocardial apoptosis were examined by TUNEL staining., Results: Compared with Sham rats, the mRNA of Bcl-2, Bax, Fas and FasL significantly increased whereas the ratio of Bcl-2/Bax (0.28 +/- 0.04 vs. 2.98 +/- 0.49) significantly decreased and the protein expression of Caspase-3 (0.762 +/- 0.129 vs. 0.133 +/- 0.027), PARP (0.992 +/- 0.146 vs. 0.386 +/- 0.074) and the myocardial apoptosis index (17.2 +/- 1.9 vs. 1.2 +/- 0.6) significantly increased in CME hearts (all P < 0.05). rhG-CSF significantly attenuated CME induced changes and cotreatment with JAK2 inhibitor AG490 abolished the effects of rhG-CSF. The protein expressions of t-JAK2 and t-STAT3 among the groups were similar. P-JAK2 and p-STAT3 protein expressions were significantly increased in G-CSF group compared to other groups (P < 0.05)., Conclusion: G-CSF attenuated myocardial apoptosis induced by CME via JAK2/STAT3 pathway.

Objective: Ocular symptoms and signs often herald hemispheric neurological events associated with extracranial cerebrovascular disease. However, the presence of a Hollenhorst plaque (HP) or retinal artery occlusion (RAO) and the risk of stroke is unclear. The purpose of this study was to review the outcomes of all patients who presented with a HP or RAO at a single institution., Methods: Between 2000 and 2005, the management and outcome of 130 consecutive patients with a diagnosis of HP, central RAO, or branch RAO (ICD-9 codes 362.30 to 362.33) were reviewed. Patients with transient monocular visual loss (amaurosis fugax), retinal venous occlusion, and other ocular pathologies were excluded. Electronic and hardcopy medical records were reviewed for demographic data, clinical variables, radiological, and noninvasive vascular lab testing. Duplex and magnetic resonance angiography (MRA) of the carotid arteries were reviewed to confirm the presence of a lesion and quantify the degree of stenosis., Results: During the study interval, 70 males and 60 females, with a mean age of 68 +/- 16 (+/-SD) years underwent ophthalmologic evaluation. Symptoms were present in 61% of patients and included eye pain, blurred vision, or atypical visual symptoms, while 39% were asymptomatic. Atherosclerotic risk factors in this population included the presence of hypertension (73%), diabetes (33%), hyperlipidemia (75%), and tobacco use (38%). A majority of patients underwent carotid interrogation via Duplex imaging (68%). Carotid bifurcation stenoses ipsilateral to the ocular findings were <30% in 68% of the patients, between 30 and 60% in 22% and >60% in only 8% of patients. Six patients with lesions greater than 60% went on to have either a carotid endarterectomy or carotid stenting. Follow-up data on this group ranged from 1 to 49 months (median, 22 months), with no stroke or transient ischemic attack identified. There were five deaths during follow-up; none related to stroke. Serial carotid Duplex examinations failed to identify progression of carotid stenoses in this group of patients. Overall survival was 94% at 36 months for this cohort., Conclusion: The presence of a HP or RAO is associated with a low prevalence of extracranial cerebrovascular disease that requires intervention. Furthermore, in contradistinction to amaurosis fugax, these ocular findings are not associated with a high risk for hemispheric neurological events.

We present a case of true spontaneous cholesterol embolisation causing acute renal failure. There was no history of vascular procedural interventions or thrombolytic therapy prior to her presentation, but the patient did have a history of difficult hypercholesterolemia and atherosclerosis. This case highlights the importance of remembering cholesterol embolisation as a potential cause of acute renal failure despite no apparent precipitant, especially with the presence of unexplained eosinophilia.

Background: Atheroembolic renal disease (AERD) is caused by showers of cholesterol crystals released by eroded atherosclerotic plaques. Embolization may occur spontaneously or after angiographic/surgical procedures. We sought to determine clinical features and prognostic factors of AERD., Methods and Results: Incident cases of AERD were enrolled at multiple sites and followed up from diagnosis until dialysis and death. Diagnosis was based on clinical suspicion, confirmed by histology or ophthalmoscopy for all spontaneous forms and for most iatrogenic cases. Cox regression was used to model time to dialysis and death as a function of baseline characteristics, AERD presentation (acute/subacute versus chronic renal function decline), and extrarenal manifestations. Three hundred fifty-four subjects were followed up for an average of 2 years. They tended to be male (83%) and elderly (60% >70 years) and to have cardiovascular diseases (90%) and abnormal renal function at baseline (83%). AERD occurred spontaneously in 23.5% of the cases. During the study, 116 patients required dialysis, and 102 died. Baseline comorbidities, ie, reduced renal function, presence of diabetes, history of heart failure, acute/subacute presentation, and gastrointestinal tract involvement, were significant predictors of event occurrence. The risk of dialysis and death was 50% lower among those receiving statins., Conclusions: Clinical features of AERD are identifiable. These make diagnosis possible in most cases. Prognosis is influenced by disease type and severity.

Introduction: Atheroembolization during renal artery angioplasty and stenting (RA-PTAS) has been postulated as a cause for the inferior renal function results observed when compared with those with surgical revascularization. To further characterize procedure-associated atheroembolism, we analyzed recovered atheroembolic debris and clinical data from patients undergoing RA-PTAS with distal embolic protection (DEP)., Methods: RA-PTAS procedures were performed with DEP using a commercially available temporary balloon occlusion and aspiration catheter system between July 2005 and December 2006. Following RA-PTAS but prior to deflation of the distal occlusion balloon, the static column of blood proximal to the balloon was aspirated and submitted for embolic particle analysis. Angiograms, demographics, and laboratory data were reviewed. Glomerular filtration rate (eGFR) was estimated before RA-PTAS and at 4 to 8 weeks postintervention using the abbreviated Modification of Diet in Renal Disease formula. Associations between clinical factors, captured particle counts, and changes in renal function were examined using univariate techniques and multiple linear regression., Results: Twenty-eight RA-PTAS procedures were performed with DEP. Mean total number of embolic particles counted per procedure was 2033 +/- 1553 for particles 20-60 microm and 265 +/- 132 for particles >60 microm. Significant positive associations with quantity of captured particles 20 to 60 microm were observed for African American race (P = .002), predilation (P = .005), and stent diameter (P < .001); a significant negative association was observed for preoperative aspirin use (P =.016). Quantity of captured particles >60 microm was positively associated with ratio of stent to renal artery diameter (P =.009). Change in eGFR was positively associated with preoperative aspirin use (P = .006) and preoperative eGFR (P < .001), while a negative association was observed for captured particle counts >60 microm (P = .015)., Conclusion: These results demonstrate the liberation of thousands of atheroembolic particles during RA-PTAS. Clinical, anatomic, and device-related factors may be predictive of procedural embolization, and increasing captured particle counts >60 microm were associated with inferior renal function results. Further investigation is warranted to establish relationships between atheroembolism, end organ functional impairment, and clinical responses.

Cholesterol embolization (CE) in renal allografts is a rare occurrence, the natural history and prognostic significance of which is poorly characterized. We studied the clinicopathologic features and outcome of the largest known series of CE in renal allografts and combined our cases with those in the literature. We identified renal allograft biopsies with CE from 1997 to September 2004 at University of Pittsburgh Medical Center (UPMC). All pathology material related to such biopsies were examined and correlated with clinical information to determine the most probable CE source. Among 5435 RAB, 19 from 12 cadaveric transplant recipients comprising 7 males and 5 females (median age=63 y) had CE. Donors consisted of 9 males and 2 females (median age=47 y). One donor's age and sex was unknown. The most probable CE source was recipient in 9 cases and donor in 3 cases. Five had acute renal failure without acute cellular rejection and 2 had CE-specific failed allografts. Of 19 RAB, the most frequent coexisting diagnosis was chronic allograft nephropathy (63%). The median follow-up time was 661 days. Combining UPMC and non-UPMC cases (n=37) revealed a statistically significant loss of grafts with donor-derived (P value=0.00459) and early CE (P value=0.00938). In renal allografts, CE most often correlated with recipient and donor atherosclerosis. It may present with acute renal failure, but usually not acute graft loss. Graft failure is significantly associated with donor-derived and early CE. Although its prognosis may be poor in the setting of primary nonfunction, prolonged graft survival may be seen.