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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ischemic nephropathy is a long-term cause of hypertension and renal failure. Although its real incidence is unknown, ischemic nephropathy is growing because of the increased mean age of the population and the greater prevalence of hypertensive and diabetic populations. This review describes the clinical profile of afflicted patients. Atherosclerosis in different vascular beds is common in these patients. The evolution of ischemic nephropathy is generally progressive, although some patients present with acute renal failure, either secondary to the administration of angiotensin-converting enzyme inhibitors or caused by thrombosis of the renal arteries. Revascularizing surgery may stabilize or improve renal function, even in patients with nonfunctioning kidneys. The results obtained with intraluminal angioplasty are worse, with a high percentage of restenosis. Placement of an endoprothesis is recommended when the lesions affect the ostium or proximal third of the artery. This complex disease typically affects multiple organs, thus making individual assessment essential.
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PMID:Ischemic nephropathy: clinical characteristics and treatment. 1105 44

An 83-year-old female who had previously (32 years ago) donated a kidney to her husband presented with loin pain, confusion and oliguria. Acute renal failure and pulmonary edema necessitated emergency hemodialysis. The history and findings were thought to be consistent with acute renal artery occlusion on a background of atherosclerosis and severe renal artery stenosis. We present this case, not to imply that renal donation is a hazardous procedure, but rather as an illustration of a complication of donor nephrectomy that in a very large series has proved to be extremely rare. This case illustrates the point that even very rare events become more likely as the period of follow-up increases.
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PMID:A late complication of spousal kidney donation. 1214 8

Approximately 6 million Americans have combined chronic cardiovascular and kidney disease. This clinical intersection presents unique risks to the patient and unique challenges to the clinician. Observational studies have provided quantitative methods for estimating the risk of acute renal failure in patients undergoing percutaneous intervention and bypass surgery procedures. Fortunately, for the general cardiovascular population these risks are small. On the other hand, patients with chronic kidney disease have increased risks of accelerated atherosclerosis, nonfatal myocardial infarction, congestive heart failure, atrial and ventricular arrhythmias, and cardiac death. Chronic kidney disease presents difficult scenarios in using conventional cardioprotective therapy. However, there are increasing bodies of evidence to suggest the kidney and the heart can be targeted with lines of therapy, specifically with renin-angiotensin system antagonism, that benefit both systems with respect to reduction in the progression of disease, and the prevention of hard kidney and cardiac endpoints. This article will focus on the cardiorenal intersection and highlight innovative diagnostic and therapeutic strategies concerning this high-risk patient group.
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PMID:Cardiorenal risk: an important clinical intersection. 1244 50

Approximately 6 million Americans have combined chronic cardiovascular and kidney disease with growing epidemics of heart and kidney failure. This clinical intersection presents unique risks to the patient and unique challenges to the clinician. Observational studies have provided quantitative methods for estimating the risk of acute renal failure in patients undergoing percutaneous intervention and bypass surgery procedures. Fortunately, for the general cardiovascular population, these risks are small. On the other hand, patients with chronic kidney disease have increased risks of accelerated atherosclerosis, nonfatal myocardial infarction, congestive heart failure, atrial and ventricular arrhythmias, and cardiac death. Chronic kidney disease presents difficult scenarios in using conventional cardioprotective therapy. However, there are increasing bodies of evidence to suggest the kidney and the heart can be targeted with lines of therapy, specifically with renin-angiotensin system antagonism, which benefit both systems with respect to reduction in the progression of disease, and the prevention of hard kidney and cardiac endpoints. This paper will address the scope of cardiovascular complications in patients with chronic kidney disease and discuss the rationale for expanded basic and clinical investigation of the cardiorenal patient population.
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PMID:Scope of cardiovascular complications in patients with kidney disease. 1247 54

Heme oxygenase (HO) is a cytoprotective enzyme that degrades heme (a potent oxidant) to generate carbon monoxide (a vasodilatory gas that has anti-inflammatory properties), bilirubin (an antioxidant derived from biliverdin), and iron (sequestered by ferritin). Due to the properties of inducible HO (HO-1) and its products, we hypothesized that HO-1 would play an important role in the regulation of cardiovascular function. In this article we will review the role of HO-1 in cardiovascular function, and highlight our previous studies using gene deletion and gene overexpression transgenic approaches in mice. These studies will include the investigation of HO-1 in the setting of hypertension (renovascular), atherosclerosis and vascular injury (vein graft stenosis), hypotension (endotoxemia), and ischemia/reperfusion injury (heart). In a chronic renovascular hypertension model, blood pressure elevation, cardiac hypertrophy, acute renal failure, and acute mortality induced by one kidney-one clip surgery are more severe in HO-1 null mice. Moreover, absence of HO-1 leads to accelerated atherosclerotic lesion formation and vein graft disease. In addition, HO-1 null mice with endotoxemia have earlier resolution of hypotension, yet the mortality and the incidence of end organ damage are higher in the absence of HO-1. In contrast, mice with cardiac-specific overexpression of HO-1 have an improvement in cardiac function, smaller myocardial infarcts, and reduced inflammatory and oxidative damage after coronary artery ligation and reperfusion. Taken together, these studies suggest that an absence of HO-1 has detrimental consequences, while overexpression of HO-1 plays a protective role in ischemia/reperfusion injury.
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PMID:Role of heme oxygenase-1 in cardiovascular function. 1452 47

Atheromatous disease is particularly common and severe in diabetics with renal failure. The prognosis depends on specific therapeutic measures: in this article, the authors will limit the discussion to the management of coronary artery disease. The cardiovascular risk factors must be treated intensively and corrected. The outlook of these patients also depends on the diagnosis of silent ischaemia with a stress test every two years and the prevention of acute renal failure after coronary angiography. Myocardial revascularisation improves the prognosis of high risk coronary patients. The choice of mode of revascularisation depends on the anatomy of the coronary lesions, the surgical risk and the presence of associated valve disease. The results of coronary angioplasty have been improved by the optimisation of anti-thrombotic treatment and the use of active stents. Despite revascularisation, short and medium-term mortality remains much higher than that of non-diabetics with normal renal function. Non-invasive investigations for residual ischaemia are justified 6 months after angioplasty for diagnosing restenosis and, thereafter, every year to detect progression of the atherosclerosis.
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PMID:[Specificity of the management of atheromatous disease in diabetic renal failure]. 1566 78

Cholesterol crystal embolization (CCE) is a severe systemic disorder caused by vascular migration of cholesterol crystals originating from ulcerative atherosclerotic plaques located in large arteries. We report 2 cases of CCE diagnosed on bladder transurethral resection in 2 men aged 94 and 72 years. Both patients had atherosclerosis disease. One patient had been treated by heparin 1 month before for pulmonary embolism and the other had had a coronary angiography and bypass graft surgery 5 months before for silent myocardial infarction. One patient presented with hematuria and the other with acute renal failure. Cystoscopy showed multiple papillary tumors of the bladder wall. Bladder transurethral resections showed transitional cell carcinoma with cholesterol crystals occluding the lumen of small arterioles in the submucosa. Eight cases of CCE in the bladder wall have been reported in the literature in 3 women and 5 men aged 56 to 79 years. Cholesterol crystal embolization is often discovered in the bladder wall on necropsy specimens. Only 2 cases have been fortuitously discovered on bladder transurethral resection performed for transitional cell carcinoma. Cholesterol crystal embolization in the bladder wall is often a marker of severe disease although the evolution is quite favorable in our patients, still alive 1 and 2 years after diagnosis.
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PMID:Cholesterol crystal embolization diagnosed on bladder transurethral resection. 1608 59

The mechanism behind iodinated radiocontrast nephropathy remains elusive. Direct oxidative damage is the prevailing hypothesis, but the apparent protective effect of iodine against oxidation contradicts this view. We propose that autonomic dysfunction participates in the pathogenesis of radiocontrast nephropathy and may account for other contrast-associated reactions previously attributed to allergy. Iodine, through its effects on thyroid function and chemoreceptor response to metabolic acidosis, may induce hyperadrenergia and consequently diminish renovascular flow and urine output. The renal response to adrenergia likely served an adaptive function during prehistoric evolution when trauma was a dominant source of hypovolemia and adrenergia, but the response may behave maladaptively today as evolutionarily nai ve triggers for adrenergia have emerged. Autonomic dysfunction can further impair renal function by deranging renovascular autoregulation and inducing oxidative reperfusion injury as a secondary phenomenon. Many other causes of acute renal failure such as drug toxicity, surgery, hospitalization, and diabetes may operate through hyperadrenergia, impaired renovascular autoregulation, and oxidative reperfusion injury. Dialysis, a volume reduction therapy for renal failure, can counterintuitively worsen renal dysfunction by exacerbating adrenergia, which may explain its association with accelerated atherosclerosis, inflammation, and cancer. Other examples of vicious cycles that perpetuate renal dysfunction may include renal artery stenosis, carotid stenosis, and atherosclerosis as well as the cardio-renal, hepato-renal, and pulmonary-renal syndromes. The benefits of hydration and bicarbonate in protecting renal function may operate in part through baroreceptor- and chemoreceptor-mediated reduction of sympathovagal ratio, respectively. New treatment paradigms for renal failure including pharmacologic and electro-mechanical therapies are envisioned based on autonomic remodeling, reduced sympathovagal ratio, and neuromodulation of pathways typically associated with trauma such as renin, angiotensin, vasopressin, and aldosterone.
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PMID:Contrast nephropathy may be partly mediated by autonomic dysfunction: renal failure considered as a modern maladaptation of the prehistoric trauma response. 1633 Jan 57

Atheromatous embolization is a multisystem disease complicating advanced atherosclerosis. It occurs most often as a complication of angiography, an endovascular procedure or cardiovascular surgery. Atheromatous embolization can present in a subtle manner where it is often under-recognized, or with catastrophic results including myocardial infarction, strake or acute renal failure. It may mimic other disease processes and often goes underdiagnosed and undertreated. A high clinical suspicion is the key to diagnosis. Atheromatous embolization results in significant morbidity and mortality; therefore, early recognition followed by aggressive management may help to prevent end-organ damage and improve overall clinical outcomes. Management strategies should include risk factor modification, prevention of further insults by discontinuing or avoiding predisposing factors, supportive treatment and interventional or surgical approaches to remove the atheroembolic source. Atheromatous embolization is expected to increase as our population ages and the epidemics of diabetes mellitus and obesity increase.
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PMID:Atheromatous embolization. 1644 59

Systemic cholesterol embolism is a rare complication of atherosclerosis, and has various presentations. Arterial catheterisms are a common cause. However, the association with an aortic dissection has been exceptionally reported. We report the observation of a 70 year-old man, with coronary artery disease, hypertension, diabetes and dyslipidemia. Six months before hospitalization, a coronary angioplasty was performed due to recurrent angina. The association of purpuric lesions on the feet, with acute renal failure confirmed cholesterol embolism syndrome. Transoesophageal echocardiography showed a dissection of the descending thoracic aorta associated with complex atheroma. The evolution was marked by the pulpar necrosis of a toe and by a worsening of the renal failure, requiring definitive hemodialysis. Further echographic control highlighted the rupture of the intimal veil of the dissection. Cholesterol embolism syndrome may reveal an aortic dissection in patients without thoracic symptoms. In such cases, transoesophageal echocardiography is a useful and non-invasive examination.
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PMID:[Thoracic aortic dissection revealed by systemic cholesterol embolism]. 1707 70


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