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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient with the hungry bone syndrome following parathyroidectomy for hyperparathyroidism developed congestive heart failure, probably due to the myocardial depressant effects of hypocalcemia and hypomagnesmia. Calcium and magnesium alone were instrumental in relieving his symptoms, decreasing his heart size, and clearing the pulmonary congestion. A mechanism for the pathogenesis of hypocalcemia and hypomagnesemia induced heart failure is proposed.
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PMID:Case report. Congestive heart failure complicating the hungry bone syndrome. 13 Aug 1

Plasma levels of atrial natriuretic peptide (ANP), renin activity (PRA), and endothelin (ET) are often elevated in uremic patients on hemodialysis treatment. The profile of these vasoactive hormones and their relationships with hemodynamic indices in patients on continuous ambulatory peritoneal dialysis (CAPD), however, are not clear. We therefore measured plasma concentrations of ANP, PRA, ET, together with parathyroid hormone (PTH) in 17 patients (mean age 38.5 years) on maintenance CAPD over a period of 12 weeks. Baseline ANP, PRA, and ET levels were significantly higher than those of healthy subjects, and no significant changes in these indices were observed over the 12 week period. There was a significant positive correlation between levels of plasma ANP and PRA [rank correlation coefficient, R(s) = 0.496, p less than 0.05] as has been reported in cardiac failure. Despite the absence of clinically overt heart failure, a significant proportion (approximately 50%) of our patients demonstrated evidence of myocardial dysfunction on echocardiography. Furthermore, a significant positive correlation was demonstrated between plasma ANP and left atrial size [R(s) = 0.61, p less than 0.01] and an inverse correlation existed between plasma ANP and the left ventricular ejection fraction [R(s) = 0.51, p less than 0.05]. Twelve patients (71%) had biochemical evidence of hyperparathyroidism with raised levels of serum PTH. Our study demonstrates increased levels of plasma ANP, PRA, and ET in uremic patients on long-term CAPD. A positive correlation exists between plasma ANP and PRA suggesting their myocardial function may be compromised and this was confirmed on echocardiography. The possibility that high circulating PTH concentrations contribute to impaired cardiac function in such patients, deserves further study.
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PMID:Vasoactive hormones in uremic patients on continuous ambulatory peritoneal dialysis. 183 Feb 51

Among dialysis patients, only 23% have a normal echocardiogram, about 10% have recurrent or chronic congestive heart failure, and 17% have asymptomatic ischemic heart disease. The predisposing factors for congestive heart failure are dilated cardiomyopathy, hypertrophic hyperkinetic disease, and ischemic heart disease. Dilated cardiomyopathy, a disorder of systolic function, includes among its risk factors age, hyperparathyroidism, and smoking. Hypertrophic disease results in diastolic dysfunction, and its predictors include age, hypertension, aluminum accumulation, anemia, and, perhaps, hyperparathyroidism. Ischemic heart disease is due to the presence of coronary artery disease and also to nonatherosclerotic disease caused by the reduction in coronary vasodilator reserve and altered myocardial oxygen delivery and use. The clinical outcome of congestive heart failure is comparable to that of nonrenal patients with medically refractory heart failure. Left ventricular hypertrophy is an important independent determinant of survival. A subset have hyperkinetic disease with severe hypertrophy and have a bad survival, as low as 43% have a 2-yr survival after the first admission to hospital with cardiac failure. The prognosis for those with dilated cardiomyopathy is less severe but is worse than those with normal echocardiogram. The survival of patients with symptomatic ischemic heart disease was little different from that of patients without symptoms, suggesting that the underlying cardiomyopathies had an adverse impact on survival independent of ischemic disease. Much research needs to be undertaken on the risk factors, natural history, and therapy of the various types of cardiac disease prevalent in dialysis patients.
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PMID:The natural history of myocardial disease in dialysis patients. 183 84

The numerous metabolic abnormalities encountered in chronic purgative abusers were investigated and the new concept of autonomous pseudo-Bartter's syndrome documented. Detailed metabolic screening tests were performed in 9 women aged 17-54 years. Two patients underwent further studies, including serum renin and aldosterone, blood volume, total body potassium, urinary chloride and prostaglandin determinations, and each underwent renal biopsy on admission and after 1 year free from laxative abuse. Clinical complications included confusion, convulsions, coma, skeletal muscle weakness with or without paralysis or rhabdomyolysis, cardiac failure, urinary tract infections and bone disease (osteomalacia, secondary hyperparathyroidism and osteoporosis). Hypokalaemia, hypomagnesaemia, hypocalcaemia and hypophosphataemia were frequent findings. Serum creatine kinase correlated inversely with the product of the potassium and serum phosphate (r = -0.86; P less than 0.03), suggesting that hypokalaemia and hypophosphataemia act synergistically to produce muscle damage. After laxative withdrawal, oedema and weight gain, followed by diuresis, ensued in 7 patients. In the other 2, ongoing chloruresis, kaliuresis, hyper-reninaemia and raised urinary prostaglandin secretion persisted. Renal biopsies in these 2 patients showed the features of juxtaglomerular apparatus hyperplasia as well as medullary interstitial cell hyperplasia. In conclusion, pseudo-Bartter's syndrome was documented in 9 chronic laxative abusers. Because patients often indulged in more than one aberrant habit, e.g. laxative and/or diuretic abuse or bulimia, the clinical syndrome produced a myriad of confounding metabolic derangements, which we termed 'metabolic madness'. Laxative withdrawal was complicated by temporary pseudo-idiopathic oedema, which persisted in 2 patients. Further studies in these 2 women strongly supported the concept of 'autonomous pseudo-Bartter's syndrome'.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chronic laxative abusers with pseudo-idiopathic oedema and autonomous pseudo-Bartter's syndrome. A spectrum of metabolic madness, or new lights on an old disease? 225 4

Autopsy of a twenty year old girl dying from complications of renal and cardiac failure demonstrated severe hepatocellular calcification, a rare finding. The pathogenesis is thought to be a combination of dystrophic calcification caused by severe centrilobular necrosis and metastatic calcification due to secondary hyperparathyroidism.
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PMID:Hepatocellular calcification. 310 28

This paper discusses the possible pathogenesis of the cerebral atrophy (CA) observed in a large percentage of uraemic patients, taking the form of prevalently cortical damage (cortical atrophy) and/or subcortical enlargement of ventricular cavities (subcortical atrophy). This central nervous system pathology seems to share very little either with the better known 'dialysis encephalopathy' or with the 'acute encephalopathy syndrome', even though sporadic cases of both these forms have shown concomitant CA. Histopathologically it offers the picture of loss of neurons and nerve fibres and can thus be compared with uraemic peripheral nervous system damage. CA is unquestionably important because of its implications in terms of impairment of superior cortical functions, just as in CA of non-uraemic aetiology. A first aetiopathogenic hypothesis might include endogenous uraemic intoxication to the nerve tissue, believed responsible for peripheral uraemic neuropathy, but other possibilities merit consideration: vascular calcification secondary to hyperparathyroidism, blood lipid disorders, and systemic hypertension--factors that contribute to impairing the brain vasculature, with cascade effects on brain tissue oxygenation, neuronal metabolism, and energy exchanges. Tissue oxygenation is already jeopardized in the uraemic patient by the concomitant chronic anaemia and by cardiac insufficiency in cases with hypertensive heart disease. In dialysis patients with volume-dependent hypertension the brain may be further damaged by abrupt pressure changes produced by dialytic ultrafiltration; these constitute a severe challenge to cerebral blood flow autoregulation. Cyclic variations of brain tissue hydration connected with regular dialysis treatment may have adverse effects on neurotransmitter functions, particularly those mediated by neuropeptidergic systems. Chronic intoxication may result from oral Al(OH)3 of phosphorus-chelating agents: in animal studies and clinical observations in non-uraemic populations the neurotoxic potential of Al is indicated by a significant correlation between histological neuronal damage, impaired function, and Al concentration in brain tissues. In addition, a concausal role of malnutrition in central nervous system damage in the uraemic patient cannot be overlooked, since malnutrition is known to give rise to functional and structural alterations in non-uraemic human pathology. In the light of these clinical observations and experimental findings, it would appear that the prevention of CA in uraemia is today feasible.
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PMID:Pathogenesis of cerebral atrophy in uraemia. State of the art. 328 91

Echocardiography and radionuclide ventriculography were performed in 37 uremic patients on maintenance hemodialysis with no apparent coronary artery disease, pericardial effusion, valvular heart disease or heart failure. These non-invasive studies were performed during the interdialytic period (about 18 hours after a dialysis). Sixty-two percent of our patients had abnormal left ventricular function with one or more abnormal echocardiographic parameters. The significant abnormalities were enlargement of the left ventricular cavity, a reduction of myocardial contractility, and thickening of the left ventricular posterior wall. Similar findings were found in 10 undialyzed uremic patients. Measurement of cardiac index and ejection fraction were found to be inadequate for a full assessment of left ventricular function and other parameters such as the mean velocity of circumferential fiber shortening and mean normalized posterior wall velocity should be included. There is a significant number of hemodialysis patients (7/37) with congestive cardiomyopathic features on the echocardiogram. Their clinical features are no different from the other patients in this study, except they have a significantly higher prevalence of uremic hyperparathyroidism. Our findings support that the existence of a specific uremic cardiomyopathy and uremic hyperparathyroidism may play an important role in the pathogenesis.
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PMID:Left ventricular function in uremia: echocardiographic and radionuclide assessment in patients on maintenance hemodialysis. 398 3

Nephrogenic ascites is a clinical diagnosis defined as persistent ascites in an uremic patient without evidence for a causative (specific) underlying disease. The incidence is not known. Contributing mechanisms may include peritoneal membrane changes, fluid overload, hyperparathyroidism, reduced lymphatic drainage, heart failure and hypoproteinemia. Rigid fluid control, intensive hemodialysis, high-protein diet, intravenous albumin infusion, intraperitoneal steroid injections and paracenteses as well as implantation of a peritoneatrial pump have all been found ineffective as treatment. Peritoneal dialysis has been shown to resolve ascites, however, the only effective treatment is so far renal transplantation. The development of nephrogenic ascites is associated with a poor prognosis. Thus, one year after the development of nephrogenic ascites 1/3 had died.
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PMID:Nephrogenic ascites. Case report and review of the literature. 781 79

Nephrogenic ascites is a clinical diagnosis defined as persistent ascites in a uraemic patient without evidence of a causative specific underlying disease. Contributing mechanisms may include peritoneal membrane changes, fluid overload, hyperparathyroidism, reduced lymphatic drainage, heart failure and hypoproteinemia. A specific treatment has not yet been found. Rigid fluid control, intensive haemodialysis, high-protein diet, intravenous albumin infusion, intraperitoneal steroid injections and paracenteses as well as implantation of a peritoneoatrial pump were all found to be ineffective. Use of peritoneal dialysis has been shown to resolve ascites, but the only effective treatment is renal transplantation, as demonstrated in the case-report.
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PMID:[Nephrogenic ascites]. 831 65

Cardiomyopathy in chronic uremia results from pressure and volume overload. The former causes concentric left ventricular [LV] hypertrophy, results from hypertension and aortic stenosis, and is also associated with diabetes mellitus and anemia. Volume overload causes LV dilatation, results from arteriovenous shunting, salt and water overload, and anemia, and is also associated with ischemic heart disease, hypertension, and hypoalbuminemia. Decreased major arterial compliance and an early return of arterial wave reflections are also associated with the extent of LV hypertrophy. Cardiomyopathy predisposes to diastolic and systolic dysfunction. The latter results from myocyte death, and predisposing factors include ischemic heart disease and the uremic environment. Ischemic heart disease may be atherosclerotic or nonatherosclerotic in origin. Multiple factors contribute to the vascular pathology of chronic uremia, including injury to the vessel wall, dyslipidemia, prothrombotic factors, increased oxidant stress, and hyperhomocysteinemia. Ischemic risk factors include hypertension, LV hypertrophy, hypoalbuminemia, and perhaps hyperparathyroidism. The clinical consequences of cardiomyopathy include heart failure, ischemic heart disease, dialysis hypotension, and arrhythmias. The adverse impact of ischemic heart disease is probably mediated through the development of cardiac failure.
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PMID:Cardiac disease in chronic uremia: pathogenesis. 923 25


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