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Patients with chronic uremia have a substantially elevated risk of death from cardiovascular disease than do the general population. Although uremic and nonuremic groups share some of the risk factors for cardiovascular mortality, such as older age, diabetes, and inflammation, other factors appear to affect cardiovascular mortality in the opposite direction. For example, being overweight and having hyperlipidemia are established risk factors in the general population, whereas lower body mass index and lower plasma cholesterol have been shown to be risk factors for cardiovascular mortality in end-stage renal disease (ESRD). This paradoxical phenomenon is explained by two facts: (1) that malnutrition is a strong predictor of cardiovascular mortality in ESRD and (2) that plasma lipid levels are lowered in malnutrition. However, it is not known whether atherosclerosis is promoted by malnutrition or by low cholesterol level. Because the cardiovascular mortality rate is theoretically the product of event rate and fatality rate after an event, risk factors for cardiovascular mortality could fall into two categories: those raising the event rate and those affecting the fatality rate. Some factors could work both ways. Patients with ESRD show a significant increase in both event rate and fatality rate. Dyslipidemia is an independent factor affecting atherosclerotic arterial wall changes and cardiovascular events in ESRD. Other factors affecting the cardiovascular event rate in ESRD include diabetes and an elevated homocysteine level. In contrast, factors associated with poor survival after an event include diabetes and anemia. Malnutrition could be a factor causing the fatality rate to rise, although there is no direct evidence supporting this possibility. Further studies are needed to show the differential effects of a risk factor on event rate and fatality rate. Patients with ESRD would have a better chance of living longer by better management of the two categories of risk factors.
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PMID:Paradox of risk factors for cardiovascular mortality in uremia: is a higher cholesterol level better for atherosclerosis in uremia? 1157 13

Cardiovascular disease is the leading cause of morbidity and mortality in end-stage renal disease. Causes include those usually found in the general population, those related to the uremic status, and those related to dialytic treatment. Hypertension, hypotension, anemia, hypoalbuminemia, malnutrition, dyslipidemia, reactive C protein, calcium-phosphate product, dialysis modalities, and hyperhomocysteinemia are discussed extensively. Special emphasis is put on hyperparathyroidism as a traditional toxin. The emergent role of sleep apnea has been confirmed in animal models as well as in humans studied using polysomnography. There are difficulties in diagnosing coronary disease, because angiography is not risk-free, is expensive, and should be reserved for patients having symptoms of heart failure and/or patients having diabetes mellitus, and/or patients entering a transplantation list. This allows patients with coronary disease to undergo coronary artery bypass (preferably) or percutaneous transluminal angioplasty. Patients for whom surgery is not appropriate should be treated using more traditional medical procedures.
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PMID:The heart in uremia: role of hypertension, hypotension, and sleep apnea. 1157 20

The HIV infection leads to many nutritional problems. For a long time, the Wasting Syndrome was one of the most frequent inaugural features of AIDS and still concerns many patients. The weight loss worsens the prognosis of the disease. The reduced dietary intakes, the increased digestive losses and energetic expenditure result in severe malnutrition. Therefore, the nutritional support and its association with orexigenes, anabolic agents and physical activity has to be carefully selected. The adverse events of new antiretroviral drugs influence the nutritional state and the patient's compliance towards their treatments. For lipodystrophy, whose etiology is still unknown, no treatment has yet been found. Metabolic disorders (dyslipidemia, glucose intolerance, diabetes, etc.) in this presently chronic disease require particular attention since they increase cardiovascular risks. In general they are sensitive to a dietary approach.
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PMID:[Nutrition and HIV infection]. 1172 3

Optimization of the management of chronic renal failure (CRF) is aimed at decreasing morbidity and mortality risks of CRF patients, due to the progression of CRF toward end-stage renal disease (ESRD), and to CRF-related complications with functional or life-threatening consequences. The so-called spontaneous progression of CRF toward ESRD depends on factors related to the primary renal disease, and on non-specific factors mainly related to hypertension and renal functional adaptations to nephron loss. Secondary prevention of CRF needs: early identification of primary renal disease, in order to start specific therapies; the treatment of hypertension; dietary advice on protein intake; prevention of events and drug toxicity potentially harmful to renal function. Clinical events appear late in the course of CRF, following several disorders often present for a long time: hypertension, dyslipidemia, phosphocalcic disorders, anaemia, malnutrition). These disorders should be screened for, and treated, as a part of tertiary prevention measures. When dialysis becomes unavoidable, early information and medical preparation of the patient are mandatory, giving the best chances of success to the applied dialysis method. Unfortunately, most CRF patients are referred at a late stage of the disease, when the effects of therapeutic interventions are limited; this results in increased length of hospital stays, increased risk of early dialysis complications, and decreased capacity to be treated at home.
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PMID:[How do we optimize the management of chronic renal failure?]. 1180 90

Dyslipidemia increases the risk of cardiovascular events among individuals with renal disease, and there is a growing body of evidence that it hastens the progression of renal disease itself. Children with nephrotic syndrome or renal transplants have easily recognized hyperlipidemia. Among those with chronic renal insufficiency or end-stage renal disease, detection of dyslipidemia requires more careful analysis and knowledge of normal pediatric ranges. Disordered lipoprotein metabolism results from complex interactions among many factors, including the primary disease process, use of medications such as corticosteroids, the presence of malnutrition or obesity, and diet. The systematic treatment of dyslipidemia in children with chronic renal disease is controversial because conclusive data regarding the risks and benefits are lacking. Hepatic 3-methylglutaryl coenzyme A reductase inhibitors (statins), fibrates, plant stanols, bile acid-binding resins, and dietary manipulation are options for individualized treatment. Prospective investigations are required to guide clinical management.
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PMID:Dyslipidemia in pediatric renal disease: epidemiology, pathophysiology, and management. 1198 Dec 90

This thesis is based on clinical studies including virtually all patients treated with peritoneal dialysis in Gothenburg during the 1990s. The patients had a fundamentally altered body composition compared to healthy subjects, characterised by a reduction in body cell mass and body fat already at start of dialysis. During PD treatment. a further decrease in body cell mass was observed. Energy stores tended to normalise during the first years of treatment and remained constant thereafter, or declined subsequently. Extracellular water, calculated from the four-compartment model, was increased when patients started PD treatment and increased further, in parallel to the reduction in body cell mass. These alterations were seen in combination with a normal. or slightly reduced, body weight. Standard methods of assessing nutritional status may therefore not be valid in the dialysis population. Prediction equations to estimate total body water, used in measurements of dialysis adequacy, give erroneous results in PD patients, as shown in a study on our PD population. This may have important clinical consequences, especially in wasted patients. Reduced muscle mass is a marker of protein-energy malnutrition, and therefore simple and reliable methods to measure muscle mass are warranted. When lean body mass was calculated from creatinine generation rate and compared to lean body mass estimated from measurements of total body potassium. the agreement between the two methods was low. Furthermore, when repeated measurements of creatinine generation rate were performed, the variation coefficient was unacceptably high. Thus. creatinine generation rate cannot be recommended as a method to evaluate somatic protein status in PD patients. The lipoprotein metabolic derangements are pronounced in PD patients. in which a further increase in cholesterol and cholesterol-rich apoB-containing lipoproteins are added to the already pre-existing renal dyslipidemia. characterised by increased concentration of triglycerides and triglyceride-rich complex lipoproteins. There are indications that dialytic variables may influence this development. When peritoneal function was assessed by the Peritoneal Dialysis Capacity test at start of dialysis, it was observed that peritoneal function reflected patient characteristics and co-morbidity. Patients with systemic disease had enhanced diffusion capacity compared to patients with primary renal disorders. Furthermore, in patients with more severe co-morbidity. peritoneal protein losses were increased. Finally, elderly patients had ultrafiltration conditions that were different from those of younger patients. Peritoneal function remained essentially stable during medium-long term follow up. Body composition features in dialysis patients are similar to those seen in severe disease in general. Thus, it is difficult to separate the effects of malnutrition from the effects of the underlying disease. Specific standards for nutritional status adapted for patients with renal failure are required.
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PMID:Nutritional status in peritoneal dialysis: studies in body composition, lipoprotein metabolism and peritoneal function. 1205 16

Patients with end-stage renal disease have markedly increased risk for death from cardiovascular disease. Renal failure is associated with multiple metabolic and endocrinologic abnormalities, and these alterations are involved in advanced atherosclerosis and high cardiovascular risk. Increased insulin resistance index by homeostasis model assessment (HOMA-IR), a simple index of insulin resistance, was an independent predictor of cardiovascular mortality in nondiabetic patients on maintenance hemodialysis. Renal failure impairs lipoprotein metabolism leading to the atherogenic lipoprotein profile characterized by increased triglyceride-rich remnant lipoproteins such as intermediate-density lipoprotein, an independent factor of increased aortic stiffness. Non-high-density lipoprotein cholesterol, the sum of cholesterol of intermediate-density lipoprotein and other apoB-containing lipoproteins, is an independent factor associated with increased arterial thickness and a predictor of cardiovascular death in hemodialysis patients. The risk for cardiovascular death in hemodialysis patients is associated closely with hypertension and malnutrition, but not with obesity. The constellation of insulin resistance, dyslipidemia, hypertension, and malnutrition in renal failure suggests the presence of another type of metabolic syndrome promoting cardiovascular disease. In addition, vitamin D deficiency and abnormalities in calcium, phosphate, and parathyroid hormone levels increase the death risk from cardiovascular disease in renal failure. It is expected that treatment of these metabolic and endocrinologic alterations would improve the survival of patients with renal failure.
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PMID:Roles of metabolic and endocrinological alterations in atherosclerosis and cardiovascular disease in renal failure: another form of metabolic syndrome. 1549 Apr 3

The metabolic syndrome has several similarities with Cushing's syndrome (impaired glucose tolerance, hypertension, dyslipidemia, central obesity) suggesting that abnormalities in the regulation of the hypothalamic-pituitary-adrenal axis may have a link with the metabolic syndrome. Several studies suggested an association between the clinical signs of the metabolic syndrome and the increased hypothalamic-pituitary-adrenal axis activity based on increased cortisol concentration at 09.00 a.m. and increased cortisol response to corticotropin. According to the Barker hypothesis the fetal malnutrition could determine adult cardiovascular diseases (coronary heart disease, hypertension), some endocrine and metabolic disorders (obesity, type 2 diabetes and hyperlipidemia). The suggested mechanism of the phenomenon is that the suboptimal fetal nutrition results in glucocorticoid overproduction. The 11beta-hydroxysteroid dehydrogenase (converts biological inactive cortisone to cortisol and vice versa) is an important enzyme in cortisol metabolism. The increased expression of 11beta-hydroxysteroid dehydrogenase type 1 in fat tissue could lead to central obesity and impaired glucose tolerance. The hypothesis that increased corticotropin-releasing hormone production drives the overactive hypothalamo-pituitary-adrenal axis was not proven. Further investigations are needed to identify additional pathogenetic factors and to find new therapeutic possibilities.
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PMID:[Correlations between the hypothalamo-pituitary-adrenal axis and the metabolic syndrome]. 1572 52

Cardiovascular disease (CVD) remains the main cause of morbidity and mortality in patients with end-stage renal disease (ESRD). Although traditional risk factors, such as diabetes mellitus, hypertension, dyslipidemia and advanced age, are prevalent in ESRD patients they may not be sufficient by themselves to account for the high prevalence of CVD in patients with this condition. Thus, the search for other, non-traditional, risk factors that may be involved in the pathogenesis of uremic CVD has been an area of intense study. Data suggest that the accelerated atherosclerotic process of ESRD may involve several interrelated processes, such as oxidative stress, endothelial dysfunction and vascular calcification, in a milieu of constant low-grade inflammation. The cause(s) of inflammation in ESRD are multifactorial and, while it may reflect underlying CVD, an acute-phase reaction may also be a direct cause of vascular injury via several pathogenetic mechanisms. Available data suggest that pro-inflammatory cytokines play a central role in the genesis of both malnutrition and CVD in ESRD. Thus, it could be speculated that suppression of the vicious cycle of malnutrition, inflammation and atherosclerosis (MIA syndrome) would improve survival in dialysis patients. Recent evidence has demonstrated strong associations between inflammation and both increased oxidative stress and endothelial dysfunction in ESRD patients. As there is not yet any recognized, or even proposed, treatment for ESRD patients with chronic inflammation it would be of obvious interest to study the long-term effect of various anti-inflammatory treatment strategies on the nutritional and cardiovascular status as well as outcome of these patients.
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PMID:Traditional and non-traditional risk factors as contributors to atherosclerotic cardiovascular disease in end-stage renal disease. 1576 53

Cardiovascular risk is dramatically increased in patients with end-stage renal disease (ESRD). However, even minor dys-functions such as microalbuminuria or a mild increase in serum creatinine (Cr) have a major impact on cardiovascular risk. Increased cardiovascular risk is present in multiple populations, including general populations, patients with moderate risk such as hypertensives, and high-risk patients including patients with heart failure and myocardial necrosis. There are many mechanisms underpinning the increased cardiovascular risk. Regarding atherosclerosis, the kidney can be victim or villain. On the one hand, both kidney disease per se and renal insufficiency can induce vascular damage, thereby increasing cardiovascular risk. Kidney disease without renal insufficiency can cause an increased prevalence in hypertension, dyslipidemia (nephrotic syndrome), sympathetic system hyperactivity, and in renin angiotensin system hyperactivity. A moderate-severe renal insufficiency can induce an increase in many vasculotoxic substances such as ADMA, lipoprotein(a), homocysteine, disturbances in calcium and phosphate metabolism, anemia and left ventricular hypertrophy. A more severe renal insufficiency can induce the ominous malnutrition-inflammation-atherosclerosis (MIA) syndrome. On the other hand, the kidney can be the victim of atherosclerosis. Ischemic nephropathy, caused by atherosclerotic renal artery disease and atheroembolism from abdominal aorta are two examples. Finally, it is important to consider that the kidney, being an organ with a wide vasculature, could be a sophisticated sensor of subclinical cardiovascular damage.
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PMID:[Hypertension, atherosclerosis and kidney]. 1578 9


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