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)

We describe a case of a three year old unvaccinated child who developed a fulminant diphtheric myocarditis and nephritis four days after the onset of a tonsillar diphtheria. Despite of the administration of antitoxin on day three and four the child died within 48 hours from the beginning of rhythm disturbances. The cardiac involvement rapidly progressed from bradyarrhythmias with the necessity of a temporary pacemaker to ventricular rhythm disturbances with cardiac failure and final ventricular fibrillation.
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PMID:[Fulminant diphtheria myocarditis in an unvaccinated preschool child]. 1059 28

Three children with renal hypertension are described. Two had histories of neuroblastoma treated by surgical resection and chemotherapy. They both presented later with unilateral atrophic kidney and marked hypertension. Only the child with severe cardiac failure demonstrated high plasma brain natriuretic peptide (BNP) concentrations. The remaining patient had a history of chronic nephritis treated with continuous ambulatory peritoneal dialysis. She also had chronic hypertension and severe cardiac failure. This child demonstrated high plasma BNP levels. The endogenous secretion of BNP is not triggered by hypertension alone, even though exogenous BNP has the pharmacological effect of reducing renin activity.
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PMID:Plasma brain natriuretic peptides and renal hypertension. 1095 34

Clinical course of infectious endocarditis (IE) was analysed for 43 intravenous drug abusers. 42 of them had primary IE, one patient--secondary. Acute course and high activity of the disease were registered in 86% of the patients. IE was provoked by Staphylococcus aureus (50%), Staphylococcus epidermidis 920%), Staphylococcus haemolyticus (11%), E. coli (8%), Pseudomonas aeruginosa (2%), Candida albicans (2%), mixed microflora (7%). Vegetations were detected on the tricuspid, mitral and aortic valves (52, 23 and 19%, respectively), on more than one valve (6%). Pneumonia, pleuricy, hydrothorax, enlargement of the liver, spleen, nephritis and anemia were found in 76, 44, 9, 100, 75, 70 and 88% of the patients, respectively. Cardiac failure aggravated the disease in half of the patients, lethality was 18%. Thus, IE in intravenous drug abusers is characterized by a primary form, acute active course, prevalent damage to the tricuspid valve, polyorganic involvement, high lethality. IE cure in such patients is feasible only in adequate antibacterial therapy, timely surgical correction and giving up drug abuse.
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PMID:[Infectious endocarditis in intravenous drug abusers]. 1101 26

Eculizumab (5G1.1), a humanized monoclonal antibody that prevents the cleavage of human complement component C5 into its pro-inflammatory components, is under development by Alexion as a potential treatment for several chronic inflammatory diseases, including rheumatoid arthritis (RA) and nephritis [190673], [292328]. In January 2002, a phase IIb trial was initiated for RA [437814]. This trial was ongoing in April 2002, at which time, eculizumab was also in phase II trials for the treatment of membranous nephritis and lupus nephritis, and in earlier stage clinical trials for dermatomyositis and pemphigoid [446377]. The company is also developing a single-chain version of this antibody, pexelizumab, for use in acute cardiovascular indications [188760]. In October 2000, eculizumab was granted Orphan Drug status by the FDA for the treatment of dermatomyositis [385057]. In February 2002, the product received Orphan Drug designation for its use in patients with membranous nephritis [440583]. In September 2001, analysts at US Bancorp Piper Jaffray predicted eculizumab's launch for dermatomyositis and pemphigus in 2003, RA and nephritis in 2004, and chronic heart failure (CHF) after 2006 [426537]. In March 2002, analysts at US Bancorp Piper Jaffray predicted that the product would have peak worldwide sales in RA of US $175 million and US $400 million for nephritis. Sales for the RA indication are predicted to reach US $35 million in 2006, rising to US $110 million in 2008, and US $10 million in 2006, rising to US $50 million in 2008, in the US and the rest of the world, respectively. For the nephritis/other indication(s), sales are pegged at US $50 million in 2006, rising to US $200 million in 2008, and US $15 million in 2006, rising to US $100 million in 2008, again in the US and the rest of the world, respectively [446992].
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PMID:Eculizumab (Alexion). 1218 61

The majority of patients seen at the renal clinic of the University Hospital of the West Indies (UHWI) are of African descent. The case notes of patients with systemic lupus erythematosus (SLE) with class 4 nephritis and who were given standard pulse intravenous cyclophosphamide therapy during the period 1990-2000 were retrospectively reviewed. Primary outcomes were doubling of serum creatinine and development of end stage renal disease (ESRD). Secondary outcomes were return of proteinuria to normal and renal remission. A total of 117 patients had a renal biopsy for SLE nephritis at the UHWI between 1990 and 2000. Of the patients, 34 (29%) had diffuse proliferative glomerulonephritis (WHO class 4), of which 29 were reviewed. Twenty-two patients of 24 in whom it was measured (92%) had significant proteinuria at presentation. The 24-hour proteinuria was measured at final review in 16 patients and in 10 patients it went into complete remission. At the beginning of therapy, 24 patients (83%) had renal impairment. Of the 18 who had final creatinine values, the renal function returned to normal in eight patients (44%) and an additional six patients showed a significant improvement in renal function at final review. Six patients developed end stage renal disease (ESRD). The risk (95% confidence interval) of developing ESRD at one year was 16.2% (CI, 6.4-37.6) and at two years was 23.2% (CI, 10.0-48.5). There were three deaths, two from sepsis and one from heart failure. The one-year mortality (95% CI) was 8% (CI, 2.0-28.5), the two-year mortality was 15.6% (CI, 4.9-43.5) and the five-year mortality was also 15.6% (CI, 4.9-43.5). Intravenous pulse cyclophosphamide for Jamaican patients with SLE and diffuse proliferative glomerulonephritis is an ineffective form of treatment.
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PMID:Severity of systemic lupus erythematosus with diffuse proliferative glomerulonephritis and the ineffectiveness of standard pulse intravenous cyclophosphamide therapy in Jamaican patients. 1294 26

Alkavervir (Veriloid(R)), a new derivative of veratrum viride was used in the treatment of hypertension in ten children with acute nephritis. The patients had a variety of complications associated with hypertension-heart failure, convulsions, vomiting and headache. In all of them the blood pressure decreased soon after the drug was given.
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PMID:Hypertension in childhood; treatment of acute nephritis with a derivative of veratrum viride. 1331 38

Blockade of the renin-angiotensin system has been established as a treatment for heart failure with hypertension and left ventricular hypertrophy, and for progressive kidney diseases. The present study was conducted to examine whether spironolactone, a mineralocorticoid receptor antagonist, alone or in combination with cilazapril, an angiotensin converting enzyme (ACE) inhibitor, ameliorates proteinuria and renal lesions in an immune-initiated progressive nephritis model. Wistar rats were uninephrectomized 7 days before injection of anti-Thy-1 monoclonal antibody 1-22-3 to induce progressive glomerulonephritis. The nephritic rats were untreated or treated with spironolactone (400 mg/kg body weight/day), cilazapril (1 mg/kg body weight/day), or both for 10 weeks. Proteinuria was increased in the untreated rats 1 week after nephritis induction and was maintained throughout the experiment. Compared with the untreated animals (212.9+/-49.2 mg/day), proteinuria was significantly reduced in the spironolactone-treated group (62.0+/-4.0 mg/day, p=0.0046) and the cilazapril-treated group (71.8+/-26.0 mg/day, p=0.0048) on day 70 after antibody injection. Further reduction of proteinuria (42.4+/-4.5 mg/day, p=0.0019 vs. the untreated group) and less renal cortex interstitial fibrotic change (fibrosis score: 142.0+/-18.4 vs. 80.3+/-18.5 in the untreated group, p=0.0123) were detected in the spironolactone plus cilazapril-treated group. Blood pressure did not differ among the three treatment groups. In conclusion, spironolactone ameliorates proteinuria to the same degree as cilazapril, and concomitant use of spironolactone and an ACE inhibitor further suppresses renal disease progression. These data suggest that concomitant treatment with spironolactone and an ACE inhibitor has beneficial effects on immune-initiated progressive kidney disease.
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PMID:Spironolactone in combination with cilazapril ameliorates proteinuria and renal interstitial fibrosis in rats with anti-Thy-1 irreversible nephritis. 1589 38

Although still incompletely understood, the etiology of systemic lupus erythematosus (SLE) is considered to involve both genetic and environmental factors. We encountered two boys with severe SLE from unrelated families and analyzed the gene that encodes cytotoxic T-lymphocyte-associated (CTLA)-4, a protein important in T-cell activation and immune tolerance. Abnormal function of the gene may participate in causation of autoimmune disease, including SLE. In family 1, a boy showed serious cardiovascular complications associated with heart failure, and his mother also had clinically active SLE, including nephritis. A boy in family 2 developed severe renal complications and peripheral vasculitis accompanied by disseminated petechiae in the lower extremities. His paternal grandfather had died from fibrinous pneumonia caused by SLE. They showed high SLE Disease Activity Index (SLEDAI) score. Analysis of the CTLA-4 gene indicated that the boy in family 1 and his mother and the boy in family 2 possess a GG genotype in CTLA-4 exon 1 at +49 together with a 106-bp fragment length of the 3' untranslated region (UTR) in exon 4. No association with disease activity was found for polymorphism of the promoter region in exon 1 at -318 in either family. Disorders of the CTLA-4 gene, especially a GG genotype in exon 1 at +49 and/or 106-bp fragment length of the 3'UTR in exon 4, may be involved in early development of SLE in Japanese children, such as the boys described here.
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PMID:Clinical manifestations and analyses of the cytotoxic T-lymphocyte associated-4 gene in two Japanese families with systemic lupus erythematosus. 1818 8

Recent clinical studies on chronic kidney disease (CKD) reported that renal dysfunction was a critical risk factor for cardiovascular events (CVE), which lead us to reconsider the effect of cardioprotective agents on the kidney. Glomerulonephritis, which is the major cause of CKD, is characterized by mesangial cell proliferation and extracellular matrix deposition. Nicorandil, a therapeutic drug for angina and acute heart failure, have been reported to show antiproliferative activity in mesangial cells. In this study, we first investigated the in vivo effects of nicorandil in anti-Thy1 nephritis rats. In male F344 rats, anti-Thy1 nephritis was induced by the injection of an anti-Thy1 antibody. From three days before induction, nicorandil (10, 30 mg/kg per day) was administered in the drinking water for 12 consecutive days. Anti-Thy1 nephritis resulted in a significant increase in proteinuria and glomerular mesangial cell proliferation. In nephritis rats, nicorandil (30 mg/kg per day) significantly suppressed increase in proteinuria, mesangial cell proliferation (the number of glomerular cell and glomerular area), and renal hypertrophy without affecting blood pressure. Nicorandil significantly prevented the overexpression of type I collagen, fibronectin, transforming growth factor (TGF)-beta, and platelet-derived growth factor (PDGF) mRNA. These results suggest that nicorandil may have renoprotective effects in mesangioproliferative glomerulonephritis.
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PMID:Nicorandil improves glomerular injury in rats with mesangioproliferative glomerulonephritis via inhibition of proproliferative and profibrotic growth factors. 1972 33

In nephrosclerosis (Volhard and Fahr classification of nephritis) there was no decrease in the plasma proteins. With heart failure the ratio of albumin to globulin fell from the normal 1.7 +/- 0.3 to about 1. There is a sharp difference between the two types of glomerulonephritis in the effect on plasma proteins. In the vascular-interstitial type the effect was the same as in nephrosclerosis. There was no decrease in the plasma proteins until shortly before death. In the glomerulotubular or nephrotic type, active or recently active, the total plasma proteins were less than 5 gm. per 100 cc. This decrease from the normal 5.5 to 7.5 occurred whether edema was present or absent. The decrease affected chiefly the albumin, the globulin being usually diminished but little, and sometimes slightly increased. Consequently the ratio of albumin to globulin was reduced to less than 1, and occasionally to 0.6. In nephrosis similar changes were found in the total protein concentration but in severe cases the decrease in albumin was greater than in nephrotic glomerulonephritis while the globulin was either very slightly reduced or was increased. The albumin : globulin ratio was therefore lower than in nephrotic glomerulonephritis, ranging down to 0.26. With the disappearance of edema there was usually an increase in the plasma protein concentration, but this was not invariable, and concentrations of 4.5 per cent or less were compatible with the persistent absence of edema. The ratio of albumin to globulin showed an irregular tendency to rise. Whenever the total concentration was less than 4 per cent there was some edema present, but it was sometimes slight in amount. With recovery in acute cases, and remission with decrease of proteinuria in chronic cases, normal concentrations were regained. The albumin : globulin ratio remained low in some instances for a longer period on account of an absolute increase in globulin concentration. In "functional proteinuria" no change in plasma proteins was found. Low plasma protein concentrations were always associated with considerable losses of protein in the urine, but these losses did not provide an explanation for all our observations. A disturbance in the production of the plasma proteins appears probable.
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PMID:THE CONCENTRATION OF THE PLASMA PROTEINS IN NEPHRITIS. 1986 91


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