Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adjuvant therapy may allow patients being treated with epoetin to derive greater clinical benefits. Iron supplementation is currently the most widely used form of adjuvant therapy; intravenous (i.v.) iron is required by the majority of haemodialysis patients receiving epoetin. Measurement of hypochromic red blood cells is the most direct way of assessing iron supply to the bone marrow. During the correction phase, a dose of i.v. iron equivalent to 50 mg/day is recommended, with the total dose not exceeding 3 g. When subclinical vitamin C deficiency is suspected, ascorbic acid may be given orally (1-1.5 g/week) or i.v. (300 mg three times weekly at the end of dialysis). The active vitamin D metabolites alfacalcidol and calcitriol may, under some circumstances, improve anaemia and reduce epoetin dosage requirements. Vitamin B6 requirements are increased during epoetin therapy, and supplementation at a dose of 100-150 mg/week is recommended. Supplementation of vitamin B12 is optional. Folic acid is supplemented routinely in haemodialysis patients, though evidence that it increases the efficacy of epoetin is limited. Low doses (2-3 mg/week) should normally be sufficient to maintain optimal folic acid stores in epoetin-treated patients, although higher doses are necessary for patients with hyperhomocysteinaemia. L-Carnitine supplementation may be appropriate in some patients with anaemia of chronic renal failure (CRF) unresponsive to, or requiring large doses of, epoetin. Androgens potentially could reduce epoetin costs in countries with limited resources, but should only be used in men older than 50 years with a remnant kidney. Recent animal studies indicate that the combination of epoetin and insulin-like growth factor 1 might be beneficial in CRF patients. High doses of angiotensin-converting enzyme (ACE) inhibitors should be reserved for dialysis patients who have hypertension that cannot be controlled by other agents, or who require an ACE inhibitor for treatment of heart failure.
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PMID:Is there a role for adjuvant therapy in patients being treated with epoetin? 1057 78

Endothelins build a peptide family composed of three isoforms, each of them containing 21 amino acids. Endothelin-1 is the isoform mainly responsible for any cardiovascular action and therefore the sole scope of this review. Endothelin-1 is the most potent endogenous vasoconstrictor known; in addition it acts as a potent (co)mitogen. There is a substantial body of experimental evidence that endothelin-1 may contribute not only to sustained vasoconstriction, but also to remodeling within the cardiovascular system. Thus, with the help of endothelin receptor antagonists (available for a few years) the involvement of mainly ETA receptors in structural diseases such as heart failure, pulmonary hypertension, atherosclerosis, restenosis, systemic hypertension, and chronic renal failure has been shown. These data make endothelin receptor antagonists, and especially those selective for the ETA receptor, promising agents for the treatment of chronic cardiovascular diseases associated with remodeling. Currently several chemically distinct, orally available members of this novel class of therapeutic agents are under clinical investigation.
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PMID:Endothelin-1 and endothelin receptor antagonists in cardiovascular remodeling. 1046 Jun 93

We reported a successful operative case of ruptured coronary artery saccular aneurysm associated with bilateral coronary arteries-pulmonary artery fistulas. A 57-year-old woman, had been treated with hemodialysis due to chronic renal failure, suffered from acute heart failure with chest pain suddenly. Echocardiograph showed moderate pericardial effusion. A saccular coronary artery aneurysm with bilateral coronary arteries-pulmonary artery fistulas revealed by coronary angiogram. Ligation of coronary artery fistula, closure of orifice of draining artery to pulmonary artery and aneurysmorrhaphy were performed emergently. Post operative angiogram revealed complete disappearance of the fistulas.
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PMID:[Surgical treatment of a ruptured saccular aneurysm associated with bilateral coronary arteries-pulmonary artery fistulas: a case report]. 1051 58

Malnutrition, inflammation and atherosclerotic cardiovascular disease occur at high prevalence, and often concomitantly, in conjunction with chronic renal failure. Several features of malnutrition (e.g., increased oxidative stress, increased plasma levels of fibrinogen, Lp(a), and inflammation) may all, alone or in concert, increase the risk of cardiovascular disease. Recent findings suggest malnutrition and hypoalbuminaemia in chronic renal failure to be largely the consequence of such factors as heart failure, chronic infection and inflammation, that simultaneously trigger the development of atherosclerotic cardiovascular disease. Central to this scenario is the involvement of proinflammatory cytokines which may cause muscle wasting, hypoalbuminaemia, anorexia, and accelerated atherosclerosis. It is unlikely that the high mortality due to atherosclerotic disease among patients with chronic renal failure can be substantially reduced unless new treatment strategies are developed which address the complex relationships that exist between malnutrition, inflammation and cardiovascular disease.
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PMID:[Strong connection between malnutrition, inflammation and arteriosclerosis. Improved treatment of renal failure if underlying factors are attacked]. 1057 60

The majority of patients with hypertension have one or more additional risk factors for cardiovascular disease. In planning an appropriate treatment program, it is useful to identify and stratify hypertensive patients according to their risk of developing cardiovascular, cerebrovascular, or renal disease. At particular risk are the elderly, patients with diabetes, and those with target-organ damage manifested by impaired renal function. Evidence supports increased risk in these patients, and clinical trial results demonstrate the considerable benefits realized through aggressive blood pressure (BP) control. The number of elderly individuals continues to increase in the United States and other industrialized countries. The prevalence of isolated systolic hypertension (ISH) is higher in the elderly than in younger individuals. ISH is associated with significant morbidity and mortality and should not be considered a physiologic manifestation of the normal aging process. Type 2 diabetes is also increasing in prevalence. Patients with diabetes are at increased risk for coronary heart disease, stroke, renal failure, and other cardiovascular complications. Aggressive treatment of elevated BP can produce dramatic decreases in the cardiovascular complications of diabetes. The incidence of end-stage renal disease has increased 2.5-fold in the past two decades, and poorly controlled BP is a major contributor to the increase. Lowering BP to levels well below the traditional goal of 140/90 mm Hg is needed to slow the progression of renal dysfunction and prevent renal failure in hypertensive patients with renal disease, whether related to diabetes or to another etiology. Aggressive treatment of hypertension in multiple-risk populations (to the goals of JNC VI and the recent WHO-ISH Guidelines for the Management of Hypertension) can be expected to produce significant reductions in the incidence and prevalence of stroke, heart failure, coronary heart disease, chronic renal failure, and total cardiovascular mortality.
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PMID:Treating multiple-risk hypertensive populations. 1059 63

Atherosclerotic renovascular disease (ARVD) continues to challenge the clinician as we enter the third millenium. ARVD frequently complicates patients with other vascular pathological states, and it is an increasingly common cause of end-stage renal failure. Although renovascular interventional procedures are now widely available and are of benefit to some patients with ARVD, a large proportion still progress to dialysis. Recent epidemiological investigations have emphasized the relationship between ARVD and other vascular diseases, and these are notable in patients with coronary artery disease and/or cardiac failure. Increased awareness of the possible coexistence of ARVD in patients with these latter conditions may allow earlier diagnosis and a minimization of complications (eg, angiotensin-converting enzyme inhibitor-related uremia or flash pulmonary edema). Contemporary studies also highlight the importance of intrarenal vascular and parenchymal injury in the cause of chronic renal failure in many patients with ARVD. Severe renal structural damage often coexists with proximal renal arterial narrowing, and this can explain the variability of renal functional outcomes known to accompany revascularization procedures. More appropriate selection of those patients likely to benefit from renovascular revascularization is now required. Large-scale trials that will identify the optimal approach to improving renal functional and survival outcomes in this high-risk group of patients are now long overdue.
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PMID:New insights into the epidemiologic and clinical manifestations of atherosclerotic renovascular disease. 1073 76

The case here described is a young male aged 21 years who met all diagnostic criteria for HES: (1) persistent eosinophilia of over 1500/cubic millimeter (19.904-26.070/cubic millimeter) for longer than 6 month (12 month in our patient); (2) lack of evidence of other known causes of secondary hypereosinophilia (SH); (3) multiple organ involvement. The peculiar aspects found in our case are related to organ involvement: occurrence 2 months after HES onset of chronic myocardial infarction in four locations (apical, anteroseptal and posteroseptal, inferior, left ventricular) demonstrated by electrocardiographic and scintigraphic studies; early global cardiac insufficiency (6 months after the onset); acute renal failure (since HES onset) followed by chronic renal failure. The multiple and severe involvement of the nervous system (up to coma) were not a life threat. It is suggested that a possible explanation for the multiple organ involvement could be the chronic disseminated intravascular coagulation.
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PMID:[The evolutionary characteristics of the hypereosinophilic syndrome]. 1075 16

The obese ZDFxSHHF-fa/fa(cp) model was developed by crossing lean female Zucker Diabetic Fatty (ZDF +/fa) and lean male Spontaneously Hypertensive Heart Failure (SHHF/Mcc-fa(cp), +/fa) rats. The purpose of the present study was to determine renal function and morphology, hemodynamics, and metabolic status in ZDFxSHHF rats. Two sets of experiments were conducted. First, we evaluated heart and kidney function and metabolic status in aged (46 weeks old) male obese ZDFxSHHF and age matched obese SHHF rats, lean Spontaneously Hypertensive (SHR) and lean normotensive Wistar Kyoto (WKY) rats. In the second set of experiments, renal function and structure as well as metabolic and lipid status were determined in lean (LN) and obese (OB) adult (29-weeks of age) ZDFxSHHF rats. At 46 weeks of age ZDFxSHHF rats are hypertensive expressing marked cardiac hypertrophy associated with diastolic dysfunction and preserved contractile function. Fasted hyperglycemia and hyperinsulinemia are accompanied by moderate hypercholesterolemia and hypertriglyceridemia. Obese aged ZDFxSHHF have marked renal hypertrophy, a 3-8 fold decrease in creatinine clearance (compared with SHHF, SHR and WKY), a high percent of segmental + global glomerulosclerosis (59.8%+/-10.8), and severe tubulointerstitial and vascular changes. Obese ZDFxSHHF rats die at an early age (approximately 12 months) from end-stage renal failure. Studies conducted in 29-week animals showed that, although both LN and OB 29-week old animals are hypertensive, OB animals have more severely compromised renal function and structure as compared with lean litter-mates (kidney weight: 2.56+/-0.16 vs. 1.61+/-0.12 g; creatinine clearance: 0.42+/-0.04 vs. 1.24+/-0.13 L/g kid/day; renal vascular resistance 12.39+/-1.4 vs. 6.14+/-0.42 mmHg/mL/min/g kid; protein excretion: 556+/-16 vs. 159+/-9mg/day/g kid, p < 0.05, OB vs. LN, respectively). Obesity is also associated with hyperglycemia (424+/-37 vs. 115+/-11 mg/dL), hyperinsulinemia (117.2+/-8.8 vs. 42.3+/-3.5 microU/mL), hypertriglyceridemia (5200+/-702 vs. 194+/-23 mg/dL), hypercholesterolemia (632+/-39 vs. 109+/-4mg/dL), and presence of segmental + global glomerulosclerosis (20.1+/-3.2% vs. 0.1+/-0.1%) with prominent tubular and interstitial changes (p < 0.05, OB vs. LN, respectively). In summary, the present study indicates that the crossing of rat strains of nephropathy produces hybrids that carry a high risk for severe renal dysfunction. The ZDFxSHHF rats express insulin resistance, hypertension, dislipidemia and obesity and develop severe renal dysfunction. In addition, the hybrids do not develop some of the complications (hydronephrosis or congestive heart failure) common for the parental strains that may compromise studies of renal function and structure. Therefore, the ZDFxSHHF rat may be a useful model fore valuating risk factors and pharmacological interventions in chronic renal failure.
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PMID:Renal function and structure in diabetic, hypertensive, obese ZDFxSHHF-hybrid rats. 1090 Nov 78

The authors report the case of a 28 year old woman with acute left ventricular failure associated with severe hypocalcaemia (1.7 mmol/l) without chronic renal failure or hypoproteinaemia. The echocardiographic appearances were those of dilated and globally hypokinetic cardiomyopathy with a severely depressed left ventricular ejection fraction (23%). Haemodynamic improvement was only obtained by the association of calcium supplements and Vitamin D derivatives (Un-Alfa) to conventional treatment. A low serum calcium associated with hyperphosphotaemia, hypocalciuria, hypophosphaturia and, above all, a high parathormone concentration, provided the diagnosis of a sporadic form of type Ib pseudohypoparathyroidism. Secondary cardiac failure to the hypocalcaemia is mainly observed in children and young adults in the context of chronic renal failure or true hypoparathyroidism. Pseudohypoparathyroidism is a very rare condition and systolic LV dysfunction for which hypocalcaemia is responsible, would seem to be totally reversible after calcium supplementation.
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PMID:[Severe cardiac insufficiency and type Ib pseudohypoparathyroidism]. 1097 40

Despite the improvements in dialysis technology, the cardiovascular mortality rate is still unacceptably high among dialysis patients. It is obvious that traditional risk factors, such as hypertension, chronic heart failure (CHF), dyslipidemia and diabetes mellitus, may account for a large part of the increased cardiovascular mortality rate in these patients. However, based on recent research it could be speculated that other, non-traditional risk factors might also contribute to the high cardiovascular mortality rate in dialysis patients. Chronic inflammation, as evidenced by increased levels of pro-inflammatory cytokines and C-reactive protein (CRP), is a common feature in dialysis patients and is associated with an increased cardiovascular morbidity and mortality. Indeed, elevated levels of pro-inflammatory cytokines (such as TNF-alpha, IL-1 and IL-6) may cause malnutrition and progressive atherosclerotic cardiovascular disease by several pathogenetic mechanisms, which will be discussed in this review. Based on the strong associations observed between malnutrition, inflammation and atherosclerosis in patients with chronic renal failure (CRF) we have proposed that these features constitute a specific syndrome (MIA), which carries a high mortality rate. As elevated levels of pro-inflammatory cytokines may play a central part in the vicious circle of malnutrition, inflammation and atherosclerosis, further research is needed to investigate whether or not different anti-cytokine treatment strategies may improve survival in dialysis patients.
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PMID:Inflammatory and atherosclerotic interactions in the depleted uremic patient. 1111 78


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