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Newlyborn infants with congenital heart disease who develop acute renal failure are particularly difficult to treat. There are often complex associated medical problems and the mortality is high. Continuous arteriovenous haemofiltration (CAVH) provides a slow and gentle removal of fluid, together with the possibility of correcting metabolic abnormalities. We used CAVH in six newlyborn infants all with severe congenital heart disease, who developed acute renal failure early in life. In four patients it was necessary to insert a blood pump into the circuit to maintain adequate blood flow. CAVH alone, with or without a blood pump, was unable to reduce the plasma urea and creatinine, and in three of the infants, dialysis across the filter was required. CAVH was effective in controlling fluid balance. Although mortality remains high we feel CAVH has an important role in selected patients.
Nephrol Dial Transplant 1989
PMID:Continuous arteriovenous haemofiltration in the newlyborn with acute renal failure and congenital heart disease. 251 91

Our objective was to analyze the survival of diabetic patients on renal replacement therapy and to compare their survival on extracorporeal and on peritoneal dialysis. All data regarding diabetic patients admitted to dialysis between 1 January 1983 and 31 December 1993 were collected by means of individual patient questionnaires sent to all of the 44 regional Renal Units (100% answers) of Lombardy, Italy. Cox proportional hazards model, stepwise procedure, was applied in order to select the covariates significantly associated with survival. Age (at baseline), sex, type of diabetes, initial modality of treatment (hemodialysis or peritoneal dialysis), and initial clinical risk factors (malignancies, serious heart disease, vascular disease, cirrhosis of the liver, cachexia) were considered. Descriptive analysis of survival was performed using the Kaplan-Meier technique. The survival of all diabetic patients (895) was 86.5% at one year, 52% at three years, and 34% at five years. The main causes of the 488 deaths of diabetic patients were cardiovascular diseases (56%), cachexia (18%), and infections (11%). The relative death risk of patients on peritoneal dialysis versus those on hemodialysis, after taking into account the main comorbid conditions, did not significantly differ from 1, as estimated by the Cox proportional hazards regression model. Five-year survival of diabetic patients was 34%, and no differences were found between peritoneal dialysis and hemodialysis as far as mortality is concerned.
Perit Dial Int 1996
PMID:Survival of diabetic patients on peritoneal dialysis or hemodialysis. 872 8

Cardiovascular disease is the most common cause of death among dialysis patients. Cardiovascular abnormalities that predispose to mortality include acute myocardial infarction, chronic ischemic heart disease, atherosclerotic peripheral vascular disease, congestive heart failure, left ventricular hypertrophy, dilated cardiomyopathy, hypertrophic hyperkinetic heart disease, prior cardiac arrest, and possibly systemic hypertension. This review explores the influences of cardiovascular disease on survival in patients with end-stage renal disease treated with dialysis.
Adv Perit Dial 1996
PMID:Cardiovascular factors influencing survival in dialysis patients. 886 84

The amount of oxygen delivered to an organ depends on three factors: blood flow and its distribution; the oxygen-carrying capacity of the blood, i.e. haemoglobin concentration; and oxygen extraction. Non-haemodynamic and haemodynamic mechanisms operate to compensate for anaemia. Non-haemodynamic mechanisms include increased erythropoietin production to stimulate erythropoiesis, and increased oxygen extraction (displacement of the haemoglobin oxygen dissociation curve). This decreased affinity of oxygen for haemoglobin is mediated by increased 2,3-diphosphoglycerate concentrations. Increased cardiac output is the main haemodynamic factor, mediated by lower afterload, increased preload, and positive inotropic and chronotropic effects. Decreased afterload is due to vasodilatation and reduced vascular resistance as a consequence of lower blood viscosity, hypoxia-induced vasodilatation, and enhanced nitric oxide activity. Vasodilatation also involves recruitment of microvessels and, in the case of chronic anaemia, stimulation of angiogenesis. With decreased afterload, the venous return (preload) and left ventricular (LV) filling increase, leading to increased LV end-diastolic volume and maintenance of a high stroke volume and high stroke work. High stroke work is also due to enhanced LV contractility attributed to increased concentrations of catecholamines and non-catecholamine inotropic factors. In addition, heart rate is increased in anaemia, due to hypoxia-stimulated chemoreceptors and increased sympathetic activity. In the long term, these haemodynamic alterations lead to gradual development of cardiac enlargement and LV hypertrophy (LVH). The LVH is eccentric, characterized by increased LV internal dimensions and a normal ratio of wall thickness to cavity diameter, as occurs in other forms of volume overload. When anaemia-related LVH develops in an otherwise 'healthy' humoral environment, the lesions are reversible and the type of LVH is primarily physiological and is not associated with impaired diastolic function. In the absence of underlying cardiovascular disorders, severe anaemia (Haemoglobin concentration < 4-5 g/dl) leads to congestive heart failure. In the presence of heart disease, especially coronary artery disease, anaemia intensifies angina and contributes to a high incidence of cardiovascular complications. In end-stage renal disease (ESRD), LVH is influenced by many other factors, leading to intense interstitial fibrosis, to alterations in diastolic function, and usually to poor reversibility. The chronic increase in cardiac output contributes to arterial remodelling of central elastic arteries such as the aorta and common carotid artery. This remodelling consists principally of arterial enlargement and compensatory arterial intima--media thickening. In ESRD, these geometric changes are accompanied by arterial stiffening. The principal consequences of arterial alterations are increased systolic pressure and high inertia due to higher blood mass in the dilated arterial system. These alterations contribute to the development of LVH and abnormal coronary perfusion.
Nephrol Dial Transplant 2000
PMID:Pathophysiology of anaemia: focus on the heart and blood vessels. 1103 52

The prevalence of left ventricular (LV) changes, especially LV hypertrophy (LVH), is high among patients with chronic kidney disease and end-stage renal disease (ESRD). Ventricular enlargement usually is associated with normal systolic function and increased stroke and cardiac index. In the absence of intrinsic heart disease, LV enlargement is most probably attributable to chronic volume/flow overload associated with anaemia, the presence of arteriovenous shunts, and sodium and water retention. In ESRD patients, hypertension is also a leading cause of LVH, but structural LV changes and myocardial fibrosis may also be due to non-haemodynamic factors such as angiotensin II, parathyroid hormone, endothelin, aldosterone, increased sympathetic nerve discharge and increased plasma catecholamines. To improve the clinical outcomes in ESRD, it is essential to prevent LVH and its complications by correcting the factors that contribute to flow and pressure overload, including anaemia.
Nephrol Dial Transplant 2002
PMID:Left ventricular alterations and end-stage renal disease. 1181 9

The number of patients over 65 years of age with chronic renal failure has increased. Peritoneal dialysis (PD) is an effective mode of treatment for such patients. In the present study, we report our experience with automated PD in patients over 65. We recorded the demographic and clinical characteristics of the patients and the exit-site infection rate, the peritonitis rate, and the mortality rate, comparing those parameters with the same parameters in patients under 65. We followed 36 patients (30% of the total study population) who were over 65 years of age (mean: 74.5 +/- 7.3 years). Of the 36 patients, 34 (94.4%) had another chronic disease--arterial hypertension and heart disease being the more common. Eleven of the patients (31%) had diabetes. Duration of PD therapy in the group was 31.5 +/- 20.7 months. Ten of the patients (27.8%) had at least 1 catheter-related complication, including exit-site infection (n = 3), tunnel infection (n = 1), or a noninfectious complication (n = 6). The rate of catheter-related infection was 0.22 episodes/patient-year. Two catheter were lost: 1 in a case of hematoma, and 1 in a case of catheter obstruction. The rate of peritonitis was 0.16 episodes/patient-year, and the most common infectious agent was methicillin-susceptible Staphylococcus aureus. Actuarial survival of our elderly patients was 51.8% at 4 years of follow-up as compared with 81.7% in the younger patients (p = 0.01). All cases of death were related to comorbid conditions, not to PD therapy. Two patients were transferred to hemodialysis. We conclude that PD has proven to be a safe and comfortable therapy for renal replacement in patients over 65 years of age. Results are similar to results in younger patients.
Adv Perit Dial 2004
PMID:Peritoneal dialysis in chronic renal failure patients over 65 years of age. 1538 12

A 71-year-old woman was admitted to the Wakayama Medical University Hospital with dizziness and loss of body balance. She had started hemodialysis at the age of 70. During the 33 days before admission, she received oral tizanidine hydrochloride at 3 mg/day for leg cramps. An admission electrocardiogram (ECG) demonstrated sinus bradycardia of 47 bpm. A 24-h ECG showed a total number of heartbeats of 68,779 and an average heart rate of 48 bpm. The maximum RR interval was 3720 msec. The electrophysiology test demonstrated slight sinus node dysfunction. There was no major organic heart disease. We suspected that tizanidine was the cause of bradycardia and stopped administration of this drug. After discontinuation symptoms gradually disappeared. The serum concentration of the tizanidine showed a higher trough of 1.78 ng/mL. In conclusion, because there was a disappearance of symptoms and a lightening of bradycardia due to the discontinuation of this medication, tizanidine was strongly suspected as the cause of severe bradycardia.
Ther Apher Dial 2005 Feb
PMID:Symptomatic bradycardia probably due to tizanidine hydrochloride in a chronic hemodialysis patient. 1582 11

Vitamin D is taken for granted and is not appreciated for its importance in overall health and well-being. Vitamin D, known as the sunshine vitamin, is appreciated as being important for the prevention of rickets in children. It is now recognized that vitamin D is important for not only the growing skeleton, but for the maintenance of a healthy musculoskeletal system throughout life. Vitamin D deficiency in adults precipitates and exacerbates osteoporosis and causes the painful bone disease osteomalacia. The revelation that vitamin D is biologically inactive and requires sequential hydroxylations in the liver and kidney to form 1,25-dihydroxyvitamin D helps explain why patients with renal failure are often resistant to vitamin D and suffer from secondary hyperparathyroidism and renal osteodystrophy. In addition to its role in maintaining calcium and phosphorus homeostasis, vitamin D is now being recognized as important for maintaining maximum muscle strength and for the prevention of many chronic diseases, including type I diabetes, multiple sclerosis, rheumatoid arthritis, hypertension, cardiovascular heart disease, and many common cancers. Vitamin D status is best determined by the measurement of circulating levels of 25-hydroxyvitamin D. Vigilance for maintaining a 25-hydroxyvitamin D level of at least 20 ng/ml and preferably 30-50 ng/ml has important benefits for both healthy children and adults, as well as children and adults suffering from chronic kidney disease.
Semin Dial
PMID:Vitamin D for health and in chronic kidney disease. 1607 48

There is much symptomatic similarity between acute kidney disease and acute heart disease. Both may present with shortness of breath and chest discomfort, and thus it is not surprising that biomarkers of acute myocardial and renal disease often coexist in many physicians' diagnostic work-up schedules. In this review we explore the similarities and differences between current and future tests of myocardial and renal injury and function, with particular emphasis on the diagnostic utility of currently available biomarkers to assist with the diagnosis of cardiorenal syndromes. Imaging studies have not traditionally been viewed as clinical biomarkers, but as tests of structure and function; they contribute to the diagnostic process, and we believe that they should be considered alongside more traditional biomarkers such as blood and urine measurements of circulating proteins and metabolites. We discuss the place of natriuretic peptides, novel tests of kidney damage as well as kidney function and conclude with a discussion of their place in guiding future research studies whose goals must include better characterization of the degree of dysfunction imposed on one organ system by failure of the other.
Nephrol Dial Transplant 2011 Jan
PMID:Biomarkers in kidney and heart disease. 2097 42

Cardiovascular diseases, in their broad spectrum, are collectively the major cause of death in patients on dialysis. The population of patients treated with peritoneal and hemodialysis are not only subject to the traditional risk factors for heart disease, but also to certain uremia-associated risk factors that are unique in this population. Limited data are available on the effectiveness of routine interventions on cardiovascular outcomes in dialysis patients. Because most dialysis patients are excluded from clinical trials, data from randomized controlled trials regarding outcomes in patients undergoing peritoneal dialysis are almost absent. The present review discusses some of the major cardiovascular problems in the dialysis population, the impact of those problems on survival, and the available therapeutic strategies.
Adv Perit Dial 2010
PMID:Cardiovascular problems in dialysis patients: impact on survival. 2134 79


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