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Query: UMLS:C0007222 (cardiovascular disease)
 65,817 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

End-stage renal disease (ESRD) patients have a high cardiovascular mortality rate. Precise estimates of the prevalence, risk factors and prognosis of different manifestations of cardiac disease are unavailable. In this study a prospective cohort of 433 ESRD patients was followed from the start of ESRD therapy for a mean of 41 months. Baseline clinical assessment and echocardiography were performed on all patients. The major outcome measure was death while on dialysis therapy. Clinical manifestations of cardiovascular disease were highly prevalent at the start of ESRD therapy: 14% had coronary artery disease, 19% angina pectoris, 31% cardiac failure, 7% dysrhythmia and 8% peripheral vascular disease. On echocardiography 15% had systolic dysfunction, 32% left ventricular dilatation and 74% left ventricular hypertrophy. The overall median survival time was 50 months. Age, diabetes mellitus, cardiac failure, peripheral vascular disease and systolic dysfunction independently predicted death in all time frames. Coronary artery disease was associated with a worse prognosis in patients with cardiac failure at baseline. High left ventricular cavity volume and mass index were independently associated with death after two years. The independent associations of the different echocardiographic abnormalities were: systolic dysfunction-older age and coronary artery disease; left ventricular dilatation-male gender, anemia, hypocalcemia and hyperphosphatemia; left ventricular hypertrophy-older age, female gender, wide arterial pulse pressure, low blood urea and hypoalbuminemia. We conclude that clinical and echocardiographic cardiovascular disease are already present in a very high proportion of patients starting ESRD therapy and are independent mortality factors.
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PMID:Clinical and echocardiographic disease in patients starting end-stage renal disease therapy. 773 Nov 45

Control of serum phosphorus (P) levels is a central goal of managing patients with chronic renal failure (CRF). Hyperphosphatemia develops invariably with kidney failure, and inadequate control of serum P leads to an elevated calcium-phosphorus (Ca x P) product. Further contributing to an elevated Ca x P product is the fact that hemodialysis patients are generally in a net positive calcium balance-dietary intake of calcium, ingestion of calcium-based phosphate binders, calcium absorption from dialysate, and abnormalities in bone buffering and turnover all contribute to the calcium burden in hemodialysis patients. In addition, treatment with calcitriol to manage secondary hyperparathyroidism increases intestinal absorption of both calcium and P. These abnormalities in divalent ion metabolism can result in a number of harmful conditions in CRF patients, including vascular calcification, cardiovascular disease, calciphylaxis, and death. We are now beginning to realize that our current therapeutic approaches to CRF management may not only be ineffective in controlling P and Ca x P product, but may actually contribute to serious calcific and cardiovascular hazards in these patients. Elevated P and Ca x P product are both significant predictors of cardiovascular mortality in hemodialysis patients. These effects are observed at P and Ca x P product levels that were considered safe until recently. Based on current national studies, we now recommend that serum P levels and Ca x P product of patients with CRF be maintained between 3.0-5.0 mg/dl and less than 55 mg2/dl2, respectively. Achieving these more rigorous treatment goals will require a shift in our therapeutic management strategies to incorporate aggressive use of calcium-free phosphate binders and, when necessary, use of less calcemic vitamin D analogs.
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PMID:Prevalence and clinical consequences of elevated Ca x P product in hemodialysis patients. 1107 8

Cardiovascular disease is the leading cause of death in dialysis patients, accounting for nearly half of all deaths among end-stage renal disease (ESRD) patients. Even young dialysis patients are at risk. Cardiovascular disease in chronic renal failure patients has been associated with elevated serum phosphorus levels and elevated calcium-phosphorus (Ca x P) product, and mismanagement of calcium and phosphorus metabolism has been implicated as a major factor in the development of soft tissue calcification and cardiovascular disease. ESRD patients frequently face hyperphosphatemia as well as excess calcium load, which elevate the Ca x P product, thereby contributing to the development of calcific complications. Electron beam computed tomography (EBCT) can be used to detect different calcification stages in a variety of tissues, and is a sensitive tool for detecting calcified coronary artery plaques as well as cardiac and valvular calcifications. Hemodialysis patients have high calcium scores on EBCT imaging, and these are associated with elevations in Ca x P product. In a recent study, patients with calcification were found to have had twice the daily calcium intake from calcium-based phosphate binders than patients without calcification. Strategies to reduce cardiac risk in hemodialysis patients include use of a dialysate low in calcium, use of vitamin D analogs that are less calcemic, and use of calcium-free phosphate binders. EBCT can be a useful adjunct to these therapies, since it permits sensitive and quantitative initial assessment, as well as ongoing monitoring of disease progression.
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PMID:Detection and quantification of cardiovascular calcifications with electron beam tomography to estimate risk in hemodialysis patients. 1107 9

Cardiovascular disease is the major cause of death in patients with end-stage renal disease (ESRD). ESRD patients are almost invariably hypertensive. They all have acquired combined hyperlipidemia and increased Lp(a), hyperhomocysteinemia, decreased physical activity, psychosocial stress, insulin resistance, procoagulant factors, left ventricular hypertrophy, and increased oxidative stress. Diabetes mellitus, a major risk factor for both cardiovascular disease and ESRD, has become the commonest cause of ESRD. If ESRD patients choose to smoke, the additive risk is profound. Moreover, ESRD patients are becoming older and are often menopausal if female. Finally, ESRD patients have a dramatic tendency for vascular and cardiac calcification, probably related to hyperphosphatemia and hyperparathyroidism. Cardiovascular disease is also a major risk in patients with decreased renal function of nearly any degree. Data from the HDFP study showed that patients with a serum creatinine concentration > 1.5 mg/dl had a profoundly higher risk of cardiovascular disease than patients with creatinine values below this value. These data were recently corroborated in the HOPE study. Microalbuminuria (MAU), with or without diabetes mellitus, indicates increased cardiovascular disease risk even without decreases in glomerular filtration rate. We found earlier that nondiabetic hypertensive patients with MAU had much higher rates of myocardial infarction, stroke, and peripheral vascular disease, than similar hypertensive patients without MAU. In conclusion, the presence of decreased renal function or MAU is a major cardiovascular risk factor. ESRD can be regarded as a catastrophic risk factor. Prophylactic measures known to be effective in reducing the risk from cardiovascular disease are grossly underused. Unfortunately, they are less effective in patients with renal disease, and new strategies are needed.
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PMID:Renal disease as a risk factor for cardiovascular disease. 1119 57

The interlinking of CVD with CKD is undeniable. CVD accounts for more than 50% of all morbidity and mortality in patients with kidney disease who have undergone renal replacement therapy, and CVD is also prevalent in patients with mild and moderately severe kidney disease. To help address the elevated risks of these patients, primary care physicians need to maintain vigilance in (1) identifying patients who have CKD and (2) implementing strategies for reducing the prevalence of CVD in this population. It is essential that patients be screened for relatively mild kidney disease by measurement of serum creatinine and urine microalbumin and by calculation of the glomerular filtration rate in mL/min/1.73 m2 using equations based on serum creatinine. Rigorous assessment of conventional risk factors, including dyslipidemia, hypertension, and diabetes, is also necessary to prevent the poor outcomes currently observed in persons with CKD. Routine use of ACE inhibitors and aspirin is encouraged in all patients with CKD, and strict glycemic and blood pressure control is recommended for optimal outcomes. In addition, patients should be screened and treated for risk factors particularly associated with kidney disease and CVD morbidity and mortality, including anemia, hyperphosphatemia, and hyperparathyroidism. Finally, physicians should be careful to avoid therapeutic nihilism in patients with kidney disease; those at highest risk of CVD are likely to receive the greatest benefit from cardiovascular therapies.
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PMID:Cardiovascular disease and the kidney. Tracking a killer in chronic kidney disease. 1198 33

The mortality risk from cardiovascular disease is increased in patients with end-stage renal disease (ESRD). This is due to both traditional and dialysis-specific factors. Recently, a number of the dialysis-specific risk factors have been implicated in the pathogenesis of cardiovascular calcification. These include: hyperphosphatemia, high calcium-phosphate (Ca x P) product, elevated parathyroid hormone levels, duration of dialysis, and treatment with calcium-containing phosphate binders and vitamin D analogs. The recent availability of electron beam computed tomography (EBCT) has triggered increased awareness of the occurrence of cardiovascular calcification in ESRD patients. Given the development of transient hypercalcemia with calcium-containing binders, a link between calcium load from use of calcium-containing phosphate binders and development coronary calcification has been proposed. However, a causal relationship between use of these agents and cardiovascular calcification has not been established. Moreover, this phenomenon had been recognized over a century ago, long before these phosphate binders became available. Although its pathogenesis is likely to be multifactorial, available data strongly implicate elevated serum phosphorus as the primary culprit. Furthermore, the risk of calcification may be aggravated by vitamin D therapy, particularly in patients with severe secondary hyperparathyroidism. Therefore, achieving vigorous control of serum phosphorus, Ca x P product and parathyroid hormone level might decrease cardiovascular calcification and improve survival of patients on maintenance hemodialysis. Since calcium acetate is the most cost-effective phosphate binder available, we recommend that it should remain the first line treatment of hyperphosphatemia in patients with ESRD.
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PMID:Cardiovascular calcification in patients with end-stage renal disease: a century-old phenomenon. 1241 Aug 60

Cardiovascular disease is a major cause of morbidity and mortality in adult patients with end-stage renal disease receiving maintenance dialysis. Coronary artery calcifications (CAC) contribute to the high prevalence of cardiac disease and are associated with hyperphosphatemia, an elevated calcium-phosphorus product (CaxP), and prolonged time on dialysis. Chronic inflammation and malnutrition are also associated with an increased risk for development of cardiac calcifications. Young adults receiving maintenance dialysis develop cardiac calcifications at a degree out of proportion to healthy adults of the same age and gender. Many of these young adults initiated dialysis as children or teenagers. Risk factors associated with the development of CAC are also seen in the pediatric dialysis population. To date, reports of cardiac calcifications in pediatric patients receiving maintenance dialysis are limited to post-mortem studies. We present two pediatric patients with ANCA-positive vasculitis diagnosed with cardiac calcifications while receiving maintenance dialysis. Hyperphosphatemia and an elevated CaxP product were seen in both patients and probably contributed to the development of extraskeletal calcifications. In addition, both patients had an underlying systemic inflammatory disease and significant weight loss/malnutrition that may have contributed to the early and rapid onset of cardiac calcifications.
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PMID:Cardiovascular calcifications in pediatric patients receiving maintenance dialysis. 1277 20

Hyperphosphatemia and dyslipidemia are common clinically significant conditions in end-stage renal disease (ESRD). Hyperphosphatemia management is essential; however, use of calcium-based phosphate binder has been associated with elevated risk of cardiac calcification in ESRD, increasing risks for cardiovascular disease and death. An alternative to calcium-based phosphate binders is sevelamer hydrochloride, a calcium-free, metal-free, nonabsorbed polymer that binds phosphate effectively. We conducted a meta-analysis on the effects of sevelamer hydrochloride on parameters of mineral metabolism (serum phosphorous, calcium, Ca x P, and iPTH) and the lipid profile (total, LDL, HDL, and non-HDL cholesterol, and triglycerides) in dialysis patients. After application of inclusion/exclusion criteria, 17 core studies were statistically analyzed to determine the sevelamer treatment effect on the study parameters as demonstrated by simple, n-weighted, and inverse variance-weighted mean changes. Analysis of inverse variance-weighted mean changes indicated that sevelamer treatment was associated with a 2.14 mg/dL drop in serum phosphorus (P <.001), no significant overall effect on calcium (0.09 mg/dL, P =.364), significant decline in Ca x P product (15.91 mg(2)/dL(2), P <.001), 35.99 pg/mL reduction in iPTH (P =.026), significant reduction in total cholesterol (30.58 mg/dL, P <.001), 31.38 mg/dL drop in LDL cholesterol (P <.001), significant increase in HDL cholesterol (4.09 mg/dL, P =.008), and a significant reduction in triglycerides (22.04 mg/dL, P x.001). This meta-analysis suggests that sevelamer offers a dual therapeutic benefit in dialysis patients-a population at high risk for cardiovascular disease-by improving phosphorus control and the lipid profile, without altering serum calcium.
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PMID:Meta-analysis of the effect of sevelamer on phosphorus, calcium, PTH, and serum lipids in dialysis patients. 1287 74

Despite rapid improvement in dialysis technology during the last 20 years the mortality rate is still very high in patients with end-stage renal disease (ESRD), and is in fact comparable to that of many cancer patients with metastases. The main cause of mortality in ESRD is cardiovascular disease (CVD), and cardiac mortality for dialysis patients aged 45 years or younger is more than 100-fold greater than in the general population. Recent evidence suggests that the high cardiovascular mortality rate in this patient population is associated with extensive vascular and valvular calcification. Although hyperphosphatemia may be the major cause of vascular calcification in this patient group it has been suggested that chronic inflammation also contributes to this process. Indeed, recent evidence suggests that inflammatory mediators, such as pro-inflammatory cytokines and adipocytokines, may promote vascular calcification in vitro. Moreover, a2-Heremans Schmid glycoprotein (fetuin), an intrinsic inhibitor of the calcification process, is down-regulated during chronic inflammation. Lower levels of fetuin have recently been found to predict mortality in ESRD. Thus, further studies are needed to elucidate the roles of calcium-free phosphate binders as well as focused anti-inflammatory treatment strategies in the prevention of vascular and valvular calcification in ESRD.
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PMID:[Why do patients with kidney diseases end up with a heart of stone? Disturbances in calcium-phosphate balance and chronic inflammation important causes]. 1471 5

Mortality rates in ESRD are unacceptably high. Disorders of mineral metabolism (hyperphosphatemia, hypercalcemia, and secondary hyperparathyroidism) are potentially modifiable. For determining associations among disorders of mineral metabolism, mortality, and morbidity in hemodialysis patients, data on 40,538 hemodialysis patients with at least one determination of serum phosphorus and calcium during the last 3 mo of 1997 were analyzed. Unadjusted, case mix-adjusted, and multivariable-adjusted relative risks of death were calculated for categories of serum phosphorus, calcium, calcium x phosphorus product, and intact parathyroid hormone (PTH) using proportional hazards regression. Also determined was whether disorders of mineral metabolism were associated with all-cause, cardiovascular, infection-related, fracture-related, and vascular access-related hospitalization. After adjustment for case mix and laboratory variables, serum phosphorus concentrations >5.0 mg/dl were associated with an increased relative risk of death (1.07, 1.25, 1.43, 1.67, and 2.02 for serum phosphorus 5.0 to 6.0, 6.0 to 7.0, 7.0 to 8.0, 8.0 to 9.0, and >/=9.0 mg/dl). Higher adjusted serum calcium concentrations were also associated with an increased risk of death, even when examined within narrow ranges of serum phosphorus. Moderate to severe hyperparathyroidism (PTH concentrations >/=600 pg/ml) was associated with an increase in the relative risk of death, whereas more modest increases in PTH were not. When examined collectively, the population attributable risk percentage for disorders of mineral metabolism was 17.5%, owing largely to the high prevalence of hyperphosphatemia. Hyperphosphatemia and hyperparathyroidism were significantly associated with all-cause, cardiovascular, and fracture-related hospitalization. Disorders of mineral metabolism are independently associated with mortality and morbidity associated with cardiovascular disease and fracture in hemodialysis patients.
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PMID:Mineral metabolism, mortality, and morbidity in maintenance hemodialysis. 1528 7


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