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)

From the group of 66 patients (pts) treated with in-hospital haemodialysis (HD), 30 pts were selected for 48 hrs monitoring of heart rhythm to register arrhythmias using Holter method. Cardiovascular complications were observed in 24 pts (80%) of the studied group; ischemic heart disease in 10 pts (33%), chronic cardiac failure in 8 pts (27%), left ventricular hypertrophy in 16 pts (53%) and hypertension in 24 pts. During 48 hrs of heart rhythm monitoring ventricular heart arrhythmias (VHA) were registered in 23 pts. 8 pts of this group had more then 100 additional ventricular beats for 24 hrs. VHA were registered before HD in 14 pts, during HD in 15 pts and after in 15 pts. The frequency of VHA pt/one hour of monitoring increased during and immediately after HD. There were no statistically significant differences between 23 pts with VHA and 7 pts without VHA with respect to the following parameters measured before HD: blood pressure, urea, calcium, kalium and magnesium blood concentrations. We found statistically significant difference between both groups of pts for creatinine values (p < 0.02); respectively 899.7 mmol/l SD 152 mmol/l versus 767 mmol/l SD 95.3 mmol/l and for interdialytic body weight increase (p < 0.012); respectively 2.65 kg SD 0.8 kg versus 2.04 kg SD 0.46 kg. Our initial results indicate that VHA appears in the majority of hemodialysed pts and that HD intensifies arrhythmogenic influence of irreversible renal failure on heart. It is also possible that non-adequate HD might be responsible for induction of ventricular heart arrhythmias during and after dialysis.
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PMID:[Ventricular arrhythmia in patients with chronic renal failure treated with hemodialysis]. 1139 59

Urea transporters have been cloned from kidney medulla (UT-A) and erythrocytes (UT-B). We determined whether UT-A proteins could be detected in heart and whether their abundance was altered by uremia or hypertension or in human heart failure. In normal rat heart, bands were detected at 56, 51, and 39 kDa. In uremic rats, the abundance of the 56-kDa protein increased 1.9-fold compared with pair-fed, sham-operated rats, whereas the 51- and 39-kDa proteins were unchanged. We also detected UT-A2 mRNA in hearts from control and uremic rats. Because uremia is accompanied by hypertension, the effects of hypertension per se were studied in uninephrectomized deoxycorticosterone acetate salt-treated rats, where the abundance of the 56-kDa protein increased 2-fold versus controls, and in angiotensin II-infused rats, where the abundance of the 56 kDa protein increased 1.8-fold versus controls. The 51- and 39-kDa proteins were unchanged in both hypertensive models. In human left ventricle myocardium, UT-A proteins were detected at 97, 56, and 51 kDa. In failing left ventricle (taken at transplant, New York Heart Association class IV), the abundance of the 56-kDa protein increased 1.4-fold, and the 51-kDa protein increased 4.3-fold versus nonfailing left ventricle (donor hearts). We conclude that (1) multiple UT-A proteins are detected in rat and human heart; (2) the 56-kDa protein is upregulated in rat heart in uremia or models of hypertension; and (3) the rat results can be extended to human heart, where 56- and 51-kDa proteins are increased during heart failure.
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PMID:UT-A urea transporter protein in heart: increased abundance during uremia, hypertension, and heart failure. 1146 20

Patients on maintenance hemodialysis therapy for end-stage renal disease have reduced exercise tolerance. Multiple processes related to uremia and hemodialysis have been implicated in the pathophysiology of this impairment. However, limited data are available to identify the separate and combined effects of clinical factors on the degree of impairment for individuals within this population. For this purpose, data from 193 patients who had undergone exercise testing for two clinical trials were retrospectively analyzed. Univariate and multiple linear regression analyses were used to identify demographic and clinical correlates of peak exercise oxygen uptake (VO2). Peak VO2 averaged 18.5 +/- 6.4 mL/min/kg. On univariate analysis, peak VO2 correlated positively with male sex and hemoglobin, serum albumin, and serum creatinine concentrations and correlated negatively with dialytic age and diagnosis of diabetes or chronic heart failure. In a multiple linear regression model, sex, hemoglobin concentration, age, and diagnosis of diabetes each remained statistically significant. Together, factors included in the model accounted for 41% of the variability in peak VO2 (P = 0.0001). Among factors not correlating significantly with peak VO2 were resting blood pressure, serum carnitine level, and urea clearance assessed by Kt/V. Findings show the range of exercise impairment among clinically stable ambulatory hemodialysis patients, which may be sufficient to interfere with normal daily activities for many of these patients. Although this impairment may be broadly attributable to physiological consequences of uremia, the degree of impairment for individual patients is predicted by demographic factors, coexistent disease, and factors potentially modified by medical therapeutics.
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PMID:Clinical and demographic predictors of exercise capacity in end-stage renal disease. 1177 5

There are almost one hundred inborn errors of metabolism which can start in the neonatal period, but less than 20 are amenable to treatment. In general, an extremely evocative clinical setting is the course of a full-term baby born after normal pregnancy and delivery who, after an initial symptom-free period deteriorates relentlessly for no apparent reason and does not respond to symptomatic therapy. Investigations routinely performed in all sick neonates yield normal results. Emergency treatment must be undertaken in parallel with investigations. Five main presentations can be observed: a neurologic deterioration 'intoxication' type mostly suggests maple syrup urine disease, methylmalonic, propionic, isovaleric acidaemias and urea cycle disorders. Isolated seizures is the revealing symptom of pyridoxine-responsive and folinic acid responsive seizures. A jaundice or a liver failure suggest galactosaemia, fructosaemia, tyrosinaemia type I (after 3 weeks), phosphomannoisomerase deficiency or bile acid synthesis defects. Cardiac failure and heartbeat disorders should first suggest mitochondrial fatty acid oxidation (FAO) disorders. Persistent hypoglycaemia is the presenting sign of glyco/gluconeogeneis defects, hyperinsulinism and FAO disorders. The first line investigation relies upon the collection at the same time of a few samples including blood gases electrolytes, prothrombin time, transaminases, ammonia and lactic acid, and the search for ketonuria. The storage of plasma, urine and blood (on filter paper) is an important element in the diagnosis. The utilization of these samples should be carefully planned after taking advice from specialists in inborn errors.
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PMID:Clinical approach to inherited metabolic disorders in neonates: an overview. 1206 34

During the neonatal period, inborn errors of metabolism mostly present with an overwhelming illness that requires prompt diagnosis and both supportive and specific treatments. The most frequent situations are due to branched-chain organic acidurias that present with ketoacidosis and urea cycle defects that are characterized by hyperammonaemia. During both situations, toxin removal procedures and nutritional support with a free-protein and high-energy diet are pivotal treatments. In patients presenting with hypoglycaemia blood glucose levels must be corrected. Progress following glucose provision is useful in recognizing the disorders that are mainly implicated. Hyperinsulinism requires high-glucose infusion. Glycogen storage diseases and gluconeogenesis defects are easily treated with a permanent glucose provision while hypoglycaemias quickly recur. In patients with galactosaemia, hereditary fructose intolerance or tyrosinaemia type I, the presentation is dominated by a liver failure requiring galactose and fructose exclusion associated with a low-protein diet. Many patients with beta-oxidation defects may present with hypoglycaemia that is usually easily corrected. The precise diagnosis can be easily missed in those patients that do well in the following weeks but may develop cardiac failure, arrhythmia and/or liver failure. Patients presenting with intractable convulsions, vitamin responsiveness to biotin, pyridoxine and folate must be considered.
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PMID:Management and emergency treatments of neonates with a suspicion of inborn errors of metabolism. 1206 35

BACKGROUND: Two separate cohorts of consecutive patients admitted to hospital with a primary diagnosis of heart failure were studied, the first in 1986 in Rochdale, and the second in 1995 in Brighton. METHODS: We observed the clinical profile, treatment and mortality during hospital admission and reviewed their status at 6 months. There were 132 patients in the Rochdale cohort and 223 in the Brighton cohort. RESULTS: The Rochdale cohort was characterised by a lower mean age and longer hospital stay. Significant differences were also observed in co-morbidity and the use of ACE inhibitors, but hospital mortality was almost identical (25% in Rochdale and 24% in Brighton). A low systolic blood pressure, hyponatraemia, hyperkalaemia and a raised blood urea at presentation were independent adverse prognostic factors. In contrast, prior treatment with ACE inhibitors in patients with congestive cardiac failure led to a more favourable hospital outcome. Age, gender and co-morbidity did not affect mortality apart from patients with acute myocardial infarction. Follow-up of these cohorts showed that mortality of the two groups remained high at 180 days after admission (40% in Rochdale and 39% in Brighton). There were marked differences in the use of ACE inhibitors in survivors, but target doses of ACE inhibitors (enalapril 20 mg/day or equivalent) were only achieved in 31%, despite direct communication between the hospital and primary care physicians. CONCLUSIONS: Although clinical and treatment profiles differed between the two periods studied, the hospital and 6-month mortality of patients with heart failure remained high. More emphasis needs to be given to optimising ACE inhibitor use in primary care.
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PMID:Heart failure in patients admitted to hospital: mortality is still high. 1214 9

This study was undertaken to: (i) determine the prevalence, pattern and outcome of systemic complications of acute glomerulonephritis (AGN), and (ii) evaluate some clinicolaboratory features of the disease in Nigerian children. Clinical and laboratory records of consecutive cases of AGN seen over a period of 3 years in our unit, were prospectively entered into nephrology record forms and later analysed. Some of the analysed data included age, sex, blood pressure, types of systemic complication, haematocrit, plasma electrolytes, urea, creatinine, protein and albumin. Fractional excretion of filtered sodium (FeNa, %) and 24-hours urinary protein concentration data were also analysed. Majority of the patients (18/29) were under 6 years of age, with peak age incidence of 3 years. The hospital incidence of AGN and prevalence of systemic complications were 10 new cases per year and 41.38%, respectively. Heart failure (HF) and acute renal failure (ARF) were sole systemic complications in 7 and 2 AGN patients, respectively. Three patients had double systemic complications: one each of hypertensive encephalopathy (HTE)+HF, HTE+ARF and ARF+HF. Ten of 29 patients (34.48%) had nephrotic range proteinuria. None of the AGN patients except those with ARF had FeNa >1%, plasma bicarbonate <15 mmol/l, urea 225 mmol/l and creatinine 2400 mmol/l. Two of the patients died: one each of ARF and ARF+HF, giving a case fatality and mortality rate of 6.90% and 0.08%, respectively. ARF is clearly the principal risk factor for mortality in our AGN patients. Its early detection and aggressive but purposive management which must include dialysis, will certainly improve outcome in AGN cases complicated by ARF.
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PMID:Systemic complications of acute glomerulonephritis in Nigerian children. 1216 79

In renal failure, blood urea nitrogen and serum creatinine usually rise in tandem; the normal BUN: Cr ratio is 10-15: 1. Disproportionate rises in BUN: Cr (> 20: 1) often imply pre-renal azotemia but may be caused by increased protein catabolism or an excessive protein load. In this study we looked at intensive care patients who acutely developed markedly increased BUN (> or = 100 mg/dL) with only modest elevation of Cr (< or = 5 mg/dL) for possible causes of the disproportionate azotemia. There were 19 such cases collected over 6 months, nine women and ten men, with mean age 69.2 +/- 4.4 years (13/19 > 75 years). Peak BUN was 156 +/- 11 mg/dL; peak Cr 4.3 +/- 0.5 mg/dL. Eleven patients expired. Mean serum albumin at the time of consultation was 2.7 +/- 0.2 g/dL; mean total lymphocyte count 1.0 +/- 0.1/mm3. Of possible factors causing the azotemia, nine patients had documented hypovolemia; eight had congestive heart failure; six were in septic or hypovolemic shock, and two received high-dose steroids. As contributing factors, eight patients had Salb < 2.5 g/dL; eight were given a high protein intake > 100 g/d; two had HIV, and two others had gastrointestinal bleeding. Infection was present in 14 patients; seven had sepsis (bacteremia with hypotension). All patients had at least one of these factors present and 16/19 had two or more. Fractional Na excretion was < 1% (consistent with pre-renal azotemia) in only four of the 11 patients in whom it was measured. We conclude that severely disproportionate BUN : Cr is frequently multifactorial and is most common in the elderly, perhaps due to their lower muscle mass, and in ICU patients given a high protein intake. It is often not indicative of uncomplicated renal hypoperfusion, although low renal perfusion (hypovolemia, shock, or heart failure) is common. Mortality is high due to the severe illnesses, especially infection, worsened by decreased renal function and hypercatabolic state.
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PMID:Massive and disproportionate elevation of blood urea nitrogen in acute azotemia. 1254 57

We conducted a study of the influence of the vasoactive peptides atrial natriuretic peptide (ANP) and neuropeptide Y (NPY) on survival of patients on hemodialysis and their association and relative importance with cardiac and clinical variables. Thirty-three hemodialysis patients were characterized by age, sex, diagnosis, blood pressure, serum (S)-albumin, serum (S)-urea, hemoglobin, dialysis dose, weight gain, duration of dialysis, cardiac hypertrophy, volume, failure, and ischemia and plasma levels of ANP and NPY. The outcomes were analyzed for early deaths (< 1 year) and for all deaths. The association of the variables to early deaths and all deaths, respectively, was studied in Cox proportional hazard analyses. The variables were also studied in three hierarchical steps: clinical variables only, clinical and cardiac variables, and all variables. For all deaths, the independent variables were plasma NPY (pmol/L) (hazard ratio [HR] = 1.035, p = 0.004), heart volume (ml/m2) (HR = 1.009, p = 0.001), and S-albumin (g/L) (HR = 0.750, p = 0.034). For early deaths, the independent variables were predialysis ANP (pmol/L) (HR = 1.008, p = 0.034) and NPY (pmol/L) (HR = 1.031, p = 0.026). In the hierarchical study, excluding the vasoactive peptides, heart volume, heart failure and S-albumin were independently associated with all deaths, and mean arterial blood pressure was associated with early death. When also excluding the cardiac parameters, S-albumin was associated with all deaths and mean arterial blood pressure with early death. In conclusion, plasma levels of the vasoactive peptides ANP and NPY are the most important group in a hierarchy of variables that predict imminent death in hemodialysis patients, and NPY is associated with late death. ANP and NPY apparently sum up the detrimental influence of many factors in hemodialysis patients.
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PMID:Neuropeptide-Y and atrial natriuretic peptide as prognostic markers in patients on hemodialysis. 1255 11

Atrial natriuretic peptide (ANP), a small peptide consisting of 28 amino acids, has been applied in clinical treatment for heart failure, but it can encounter proteolytic degradation during its expression in host cells. Therefore, it is usually reported that ANP was expressed as a part of fusion protein. The aim of our study was to use an overexpression system to express the fusion protein REF-ANP and to optimize a purification method. First, Escherichia coli DH5alpha was transformed with constructed expression vector containing two tandem copies of ref-anp gene and the fusion protein REF-ANP was overexpressed in shaking flask culture. Subsequently, the inclusion bodies were purified with reverse phase chromatography and pooled fractions were lyophilized. After this step, REF-ANP can be solubilized under native conditions without urea. After cleavage reaction, the sample was subjected to size exclusion chromatography and then rANP was polished with reverse phase chromatography. The final purity of rANP was more than 98% and the recovery of rANP per liter of shaking flask culture was more than 3mg. Such methods as mass spectrometry, capillary isoelectrofocusing analysis, and N-terminal amino acid sequence were used to identify rANP. The capillary isoelectrofocusing analysis showed that the pI of ANP was about pH 9.7. In this study, an efficient refolding and purification process should make scaling-up procedures easier and more successful than earlier reports. Moreover, it is possible that the refolding and purification method along with the overexpression system described in this article may offer new ideas on optimizing expression and purification of other kinds of short peptides.
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PMID:Overexpression and purification of recombinant atrial natriuretic peptide using hybrid fusion protein REF-ANP in Escherichia coli. 1265 Nov 6


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