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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The use of angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) has significantly reduced morbidity and mortality across the continuum of vascular disease. The utilization of these agents, however, remains suboptimal. The drugs are not prescribed in many patients because of concerns regarding their effects on renal function. Despite overwhelming evidence in favor of renoprotection, it is not uncommon for the glomerular filtration rate (GFR) to decrease shortly after starting treatment with an ACE inhibitor or ARB. This response is functional in nature and should be expected based on renal physiology and its dependence on the renin-angiotensin system to maintain GFR. Unfortunately, this phenomenon sometimes is viewed as an adverse effect or an indicator of underlying pathology. Although somewhat counterintuitive, early elevations in serum creatinine concentration are associated with improved long-term renal outcomes in patients with renal insufficiency and thus support, rather than condemn, continued treatment. Clinicians should be aware of the physiologic course associated with blockade of the renin-angiotensin system so that these agents will not be withheld unnecessarily.
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PMID:Elevations in serum creatinine concentration: concerning or reassuring? 1452 53

Renal artery stenosis (RAS) is a common condition associated with hypertension and renal insufficiency. The high prevalence of RAS patients with coronary and lower extremity vascular disease has been well established. Fibromuscular dysplasia in young females and atherosclerosis in patients over the age of 55 are the most common causes. Poorly controlled hypertension refractory to medical therapy, worsening of renal function, and flash pulmonary edema may point to underlying RAS. Duplex ultrasonography and magnetic resonance angiography have largely replaced captopril scanning for RAS screening. However, renal angiography still remains the gold standard to diagnose RAS. Treatment options include medical therapy, angioplasty, and surgery. In general, patients with a stenosis greater than 50%, a translesional systolic pressure gradient greater than 15 mm Hg, and difficult-to-control hypertension and/or worsening renal insufficiency are candidates for renal revascularization. Percutaneous transluminal revascularization has evolved to become the preferred revascularization therapy because it is a less invasive and more cost-effective alternative to surgery and is associated with high technical success, as well as a low complication rate. The natural history of RAS is to progress over time, leading to renal artery occlusion, loss of renal mass, worsening of renal function, and, ultimately, end-stage renal disease. It is therefore important to aggressively screen, recognize, and treat the entity early in its course.
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PMID:Current advances in the diagnosis and treatment of renal artery stenosis. 1558 Jan 59

Renal insufficiency appears clinically to be associated with a bleeding tendency. This has been documented in clinical settings including as a complication of medical interventions such as surgery and also in spontaneous bleeding events at gastrointestinal and intracranial sites. The pathophysiology that underlies this tendency appears to involve platelet dysfunction and an imbalance of mediators of normal endothelial function. It is also may be complicated by the co-morbidities in this population, such as vascular disease, hypertension and anemia, and the medical interventions required to treat such co-morbidities. This article reviews the evidence, the pathophysiology and the risk factors for increased bleeding in patients with chronic renal insufficiency.
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PMID:Uremic bleeding: pathophysiology and clinical risk factors. 1599 29

In old subjects exposed to extreme high temperature during a heat wave, studies have consistently reported an excess of death from cardio- or cerebro-vascular disease. By contrast, dehydration, heat stroke, acute renal insufficiency, and respiratory disease were the main causes of hospital admission in the two studies carried out in elderly during short spells of hot weather. The excess of circulatory disease reported by mortality studies, but not by morbidity studies, could be explained by the hypothesis that deaths from circulatory disease occur rapidly in isolated people before they reach a hospital. Since the contrasting patterns of hospital admission and mortality during heat waves could also be due to chance (random variation over time and space in the spectrum of diseases induced by extreme heat), and bias (poor quality of diagnosis on death certificate and other artifacts), it should be confirmed by a concurrent study of mortality and morbidity. Many heat-related diseases may be preventable with adequate warning and an appropriate response to heat emergencies, but preventive efforts are complicated by the short time interval that may elapse between high temperatures and death. Therefore, prevention programs must be based around rapid identification of high-risk conditions and persons. The effectiveness of the intervention measures must be formally evaluated. If cardio- and cerebro-vascular diseases are rapidly fatal health outcomes with a short time interval between exposure to high temperature and death, deaths from circulatory disease might be an useful indicator in evaluating the effectiveness of a heat watch/warning system.
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PMID:Contrasting patterns of hospital admissions and mortality during heat waves: are deaths from circulatory disease a real excess or an artifact? 1641 37

S-Adenosylhomocysteine (SAH) is the metabolic precursor of all the homocysteine (Hcy) produced in the body. It is formed by the enzyme SAH hydrolase in a reversible reaction. In a previous study we have shown that plasma SAH is a more sensitive indicator of the risk for cardiovascular disease, and in a second study involving patients with renal disease, we also showed that it is a more sensitive indicator of renal insufficiency than plasma Hcy. However, in the latter study, the patients with renal disease were older and had a variety of other diseases such as diabetes and primary hypertension, which are associated with vascular disease and which could reduce renal function by involvement of the kidneys. Our objective was to rule out these complicating factors as the cause of the elevated SAH in renal disease and determine whether renal insufficiency alone was the cause of the elevated SAH. We therefore measured SAH, Hcy, folate, and vitamin B12 in 23 patients between the ages of 1 and 18 years with a wide range of renal function, but who had none of these complicating factors. Glomerular filtration rate (GFR) was calculated using serum creatinine according to the Schwartz formula. None of the children were deficient in folate or vitamin B12. After adjusting for age, folate, and vitamin B12, there was a modest and insignificant decrease of 0.033 micromol/L of Hcy associated with an increase of 1 mL/min of GFR (95% confidence interval, -0.066 to 0.0002). However, there was a strong and statistically significant association between log(SAH) and log(GFR): P < .0005, R2 = 0.76. This result suggests that plasma SAH rather than Hcy is the metabolite primarily affected in renal disease. We suggest that plasma Hcy elevations that have been linked to vascular disease may be due to elevated SAH resulting from renal insufficiency.
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PMID:Relationship between plasma S-adenosylhomocysteine concentration and glomerular filtration rate in children. 1642 34

The United States is currently beleaguered by twin epidemics, heart failure (HF) and renal insufficiency (RI). HF and RI frequently coexist in the same patient, and this conjunction, often called the "cardiorenal syndrome," has important therapeutic and prognostic implications. Approximately 60% to 80% of patients hospitalized for HF have at least stage III renal dysfunction as defined by the National Kidney Foundation (NKF), and this comorbid RI is associated with significantly increased morbidity and mortality risk. Numerous studies have demonstrated that in patients with HF, indices of renal function are the most powerful independent mortality risk predictors. Comorbid RI can result from both intrinsic renal disease and inadequate renal perfusion. Atherosclerosis, renal vascular disease, diabetes mellitus, and hypertension are significant precursors of both HF and RI. Moreover, diminished renal perfusion is frequently a consequence of the hemodynamic changes associated with HF and its treatment. Both HF and RI stimulate neurohormonal activation, increasing both preload and afterload and reducing cardiac output. Inotropic agents augment this neurohormonal activation. In addition, diuretics can produce hypovolemia and intravenous vasodilators can cause hypotension, further diminishing renal perfusion. Management of these patients requires successfully negotiating the delicate balance between adequate volume reduction and worsening renal function. Despite this, few evidence-based data are available to guide management decisions, indicating a compelling need for additional studies in this patient population.
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PMID:The confounding issue of comorbid renal insufficiency. 1711 94

The clinical importance of renovascular disease, atherosclerotic or of other origin, arises from the fact, that renal artery stenosis (RAS), if hemodynamically significant (> 70% diameter reduction), induces arterial hypertension, renal insufficiency or both. The prevalence of RAS rises with increasing age and with the presence of atherosclerosis of the aorta, carotid, coronary and peripheral arteries. Typical clinical symptoms, as uncontrolled hypertension or renal dysfunction in the absence of pathological urinary findings, are helpful to select patients for further screening methods: We see a prominent role of color duplex sonography as a screening procedure. Intra-arterial angiography remains gold standard for the diagnosis of RAS. The major problem in daily clinical practice is the differentiation between patients in which hypertension and kidney function can be improved or normalized by removal of RAS and those with ''fixed'' hypertension and irreversible kidney dysfunction and therefore to decide if it is worth while to perform invasive treatment as angioplasty or surgery. In this setting, the proof of hemodynamic significance is essential and is indicated especially when the stenosis has a diameter reduction of < 50-70% only. Methods proving a critical stenosis are intra-arterial measurement of the pressure gradient, measurement of differential renal vein renin and duplex sonography. In addition, predictors of treatment outcome should be considered. Studies analyzing if patients improve with blood pressure and kidney function after removal of RAS have shown that high grade stenosis and/or very high blood pressure indicate a good outcome. Further prognostic factors are the absence of parenchymal disease and/or positive functional test. In the presence of a critical stenosis in a patient with a clear clinical problem with hypertension and/or renal dysfunction a positive effect of invasive treatment seems warranted despite the risks that must be considered as well in angioplasty as in surgery. The selection for the type of invasive treatment requires a clarification of the treatment goals in the individual patient, the evaluation of the morphology and localization of the stenosis as the presence of other vascular disease (aortic aneurysm, peripheral artery disease etc.) and the assessment of the risk according to the type of intervention.
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PMID:Renovascular disease: a review of diagnostic and therapeutic procedures. 1712 83

In a six-year period from February 1942 to February 1948, 473 patients (185 males and 288 females) were operated upon for essential hypertension and most of them were in advanced stages of hypertensive disease.Patients were selected or rejected for operation on the basis of a set of rules drawn to guide clinical judgment. The total of deaths in and out of the hospital over this period was 79 or a total mortality of 16 per cent. There were 38 inhospital deaths, or a mortality of 8 per cent. The causes of deaths occurring in the hospital were in the following order: cerebral accident, cardiac failure, and renal insufficiency. The out-of-the-hospital deaths were in the following order: cardiac failure, cerebral accident, and renal insufficiency. Operations done early in the series followed the Smithwick procedure from T-9 through L-2, but later the minimal procedure was extended from T-3 through D-3, and in addition about 40 total sympathectomies which included the stellate ganglion were done. Results from the more extensive operation were better than those from the lesser procedure, but the mortality also was greater. Conclusion that complete or nearly complete sympathectomy is preferable to a less extensive procedure must await the collection of more data which can be used in weighing the respective end results against the mortality. Thoracolumbar sympathectomy has a definite place in the treatment of hypertensive vascular disease, but its role in advanced cases is chiefly that of palliation.
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PMID:End results of thoracolumbar sympathectomy for advanced essential hypertension. 1812 23

Reno-vascular disease, along with diabetes mellitus, is the leading cause of dialysis in the elderly population, accounting for 50-66% of cases in patients above 65 years of age. Reno-vascular disease is a broad term, which includes renal artery stenosis, ischemic nephropathy, such as atherosclerotic obstruction, thrombo-embolic phenomenon, nephrosclerosis secondary to hypertension and acute occlusion of renal arteries (either bilateral or unilateral in singlekidney patients). Renal artery stenosis, defined as a 50% or greater occlusion of a renal artery (unilateral or bilateral), is an important cause of secondary hypertension. It often presents as drug refractory hypertension or renal insufficiency. Atherosclerotic renal artery stenosis accounts for 90% of such cases, the remaining 10% being caused by fibro-muscular dysplasia. The incidence of atherosclerotic renal artery stenosis is increasing among the aging population, who are at an increased risk due to cardiovascular complications. This is a review of the emerging trends in the diagnosis and management of renal artery stenosis.
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PMID:Renal artery stenosis: an update on diagnosis and management. 1905 47

Magnesium (Mg) is the main intracellular divalent cation, and under basal conditions the small intestine absorbs 30-50% of its intake. Normal serum Mg ranges between 1.7-2.3 mg/dl (0.75-0.95 mmol/l), at any age. Even though eighty percent of serum Mg is filtered at the glomerulus, only 3% of it is finally excreted in the urine. Altered magnesium balance can be found in diabetes mellitus, chronic renal failure, nephrolithiasis, osteoporosis, aplastic osteopathy, and heart and vascular disease. Three physiopathologic mechanisms can induce Mg deficiency: reduced intestinal absorption, increased urinary losses, or intracellular shift of this cation. Intravenous or oral Mg repletion is the main treatment, and potassium-sparing diuretics may also induce renal Mg saving. Because the kidney has a very large capacity for Mg excretion, hypermagnesemia usually occurs in the setting of renal insufficiency and excessive Mg intake. Body excretion of Mg can be enhanced by use of saline diuresis, furosemide, or dialysis depending on the clinical situation.
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PMID:Magnesium metabolism in health and disease. 1927 87


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