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)

The sudden onset of pulmonary edema in patients with renal artery stenosis is an increasingly recognized entity. Some data also support an association between renal artery stenosis and chronic cardiac failure. We report a 60-year-old man with chronic renal failure who had most normal arterial blood pressure despite highly severe chronic congestive heart failure. Renovascular disease was suspected and an arteriography revealed very tight bilateral artery stenosis. Removal of stenosis led to both renal and cardiac functions improvement.
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PMID:Chronic congestive heart failure associated with bilateral renal artery stenosis. 924 81

Clinical presentation, laboratory findings, renal biopsy findings and subsequent clinical course were studied retrospectively in 90 children with acute renal failure to intrinsic renal damage. The mean age at presentation was 8.1 years. Diagnosis and number of patients were as follows: Hemolytic uremic syndrome (HUS) in 32 patients, tubulo-interstitial nephritis in 19, idiopathic nephrotic syndrome in 10, IgA nephropathy on 9, membranoproliferative glomerulonephritis in 8, lupus in 5, poststreptococcal glomerulonephritis in 4, cortical necrosis in 1, Henoch Schoenlein purpura nephritis in 1 and anti-neutrophil cytoplasmic antibody associated glomerulonephritis in 1. Thirty-nine patients needed dialysis, but 36 of these were able to stop dialysis, 3 patients with HUS without gastrointestinal symptoms needed chronic dialysis. The mean follow-up period was 7.3 years from onset, and the the latest follow-up 82 patients had normal renal function, 3 showed chronic renal failure, 2 had regular dialysis, 2 had successful renal transplantation, an 1 had died due to heart failure. A poor outcome was associated with diffuse crescents and the presence of severe vascular changes. The early biopsy findings were very useful for the management of children with acute renal failure.
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PMID:[A clinicopathological study of 90 children with acute renal failure]. 928 14

A 36-year-old man known as chronic alcohol abuser presently suffered from arthralgia and showed bilateral petriefied kidneys by sonography and computed tomography. Because of an unclear renal failure a kidney biopsy was performed and presented typical chronic renal oxalosis with massive oxalate crystal deposits, tubular atrophy and interstitital fibrosis. Since the man had never shown signs of hyperoxaluria in his life before, a secondary oxalosis was supposed. The subsequently prompted exploration established a three to four times abuse of rocket fuel with cola lemonade 12 years before during the patient's army time as a marine soldier. Such fuels contain ethylene glycol (glysantin) as antifreeze commonly known to cause in toxic doses acute renal tubular necrosis with hyperoxaluria. The presented case, however, suggests a rare sublethal ethylene glycol poisoning with initial renal tubular damage, oxalate crystal deposition and subsequent chronic interstitial oxalate nephritis with tubular atrophy, interstitial fibrosis and chronic renal failure. Undergoing chronic hemodialysis, the patient died 5 months after the kidney biopsy diagnosis by acute heart failure. At autopsy, progressed chronic renal oxalosis could be confirmed. Decompensated oxalate cardiomyopathy with disseminated myocardial oxalate crystal deposits caused acute heart failure promoted by myocardial hypertrophy in renal hypertension.
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PMID:[Fatal chronic oxalosis after sublethal ethylene glycol poisoning]. 938 Jun 7

End-stage renal disease (ESRD) patients, whether they are treated with hemodialysis or continuous ambulatory peritoneal dialysis, frequently suffer from protein-energy malnutrition, which is associated with increased morbidity and mortality. The protein requirements in dialysis patients are increased compared to those of healthy individuals and nondialyzed patients with chronic renal failure. The intake of protein and energy is frequently reduced because of the underlying disease, comorbidity, psychosocial factors, and uremic anorexia (underdialysis). There are several factors in ESRD patients that may enhance protein catabolism and increase protein requirements, such as low energy intake, amino acid abnormalities, metabolic acidosis, endocrine abnormalities (insulin resistance, hyperglucagonemia, hyperparathyroidism, insensitivity to growth hormone and insulin-like growth factor-1, cardiac failure, infection and inflammation, anemia, and physical inactivity. The dialytic procedures per se may enhance protein catabolism due to dialytic losses of protein and amino acids and, in hemodialysis, an inflammatory response to blood-dialyzer interaction. The relative importance of the various factors which cause anorexia and stimulate protein catabolism is still not well understood.
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PMID:Factors contributing to catabolism in end-stage renal disease patients. 939 22

A 77-year-old woman with severe valvular heart disease and chronic renal failure was admitted to hospital for control of her heart condition and to improve her ability to perform activities of daily living. In the past 2 years, she had been admitted to hospital four times due to severe congestive heart failure, and she was bedridden because of muscle weakness. A multidisciplinary approach was taken. A cardiologist reassessed her medications and determined an exercise level in co-operation with a physical therapist. After 40 days of rehabilitation, the patient was able to walk 200 m without the help of a cane. With an increase in the exercise level, her cardiothoracic ratio increased from 68 to 74%. The furosemid was then increased from 40 to 60 mg per day and 20 mg of denopamine was added, which resulted in a decrease of the cardiothoracic ratio to 66%. Dietary assessment revealed her usual salt intake was more than 10 g per day, and the dietitian advised the patient that her daily salt intake should be lower than 7 g and water intake less than 800 ml per day. Consultations with social-service personnel made revealed problems in her family and living environment, and she was advised of available social services. For good compliance, the patient had her medication explained by a pharmacist. Assessment of activities of her daily living and intensive education about congestive heart failure were performed by the nurse in charge. After discharge, a nurse team visited her home every two weeks and watched for signs of heart failure. This comprehensive intervention prevented an exacerbation of heart failure and readmission for nine months.
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PMID:[Multidisciplinary approach to an elderly patient with severe congestive heart failure]. 949 70

1. Transport of L-arginine was investigated under zero-trans conditions in human erythrocytes from healthy donors and patients with heart failure. 2. Saturable influx of L-arginine was mediated by the classical cationic amino acid transport systems y+ and y+L. 3. The Vmax for L-arginine transport via system y+ increased from 292 to 490 mumol h-1 l-1 of cells in heart failure. 4. With system y+ inhibited by N-ethylmaleimide (0.2 mmol/l), the Vmax for the transport of L-arginine via system y+L was unaffected in erythrocytes from patients with heart failure. 5. The inhibition of L-arginine and L-leucine influx by NG-monomethyl-L-arginine was similar in erythrocytes from control and heart failure patients. 6. Plasma L-arginine levels were reduced in patients with heart failure (59 mumol/l) compared with controls (125 mumol/l). Plasma from patients with heart failure also contained the endogenous L-arginine analogue NG-monomethyl-L-arginine, which was undetectable in plasma from controls. 7. Intracellular concentrations of L-arginine and NG-monomethyl-L-arginine were significantly elevated in erythrocytes from patients with heart failure compared with controls, consistent with an increased transport capacity for L-arginine and NG-monomethyl-L-arginine. 8. The present study provides the first evidence that system y+ mediates the increased transport of L-arginine in human erythrocytes from patients with chronic heart failure. These findings are similar to our previous results obtained in patients with chronic renal failure. Since both pathologies seem to present with an increased synthesis of nitric oxide, studies of L-arginine transport in erythrocytes may provide a valuable paradigm to study abnormalities of the L-arginine-nitric oxide signalling pathway.
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PMID:Increased L-arginine transport in human erythrocytes in chronic heart failure. 950 65

Only 10 years ago, the vasoconstricting peptide endothelin was discovered; it is produced by endothelial cells. Different isoforms and receptors of endothelin have been identified. The effects of endothelin-I, the most important isoform, are mainly vasoconstriction and proliferation of cells. In the last few years endothelin receptor antagonists have become available, which can delineate the clinical importance of the endothelin system. Possible indications for endothelin receptor blockers are renal disease (acute and chronic renal failure) and cardiovascular disease (heart failure; restenosis after percutaneous transluminal coronary angioplasty (PTCA); pulmonary hypertension; systemic hypertension). There is also a possible role for endothelin receptor blockers in oncology (prostatic carcinoma). Currently clinical trials are being carried out to determine the efficacy of these compounds for the above-mentioned indications.
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PMID:[Endothelins: possibly a new pharmacological approach in cardiovascular diseases, kidney diseases and oncological disorders]. 954 34

We present the case of a 39-year-old woman with aortic regurgitation that may have been induced by primary antiphospholipid syndrome. The patient had suffered recurrent miscarriages, thrombocytopenia, and deep-vein thrombosis for the previous 16 years, and had been diagnosed as having primary antiphospholipid syndrome 9 years previously because of a high titer of anticardiolipin antibody. She had been receiving medication for moderate hypertension for 7 years. The patient was admitted to Tenri Hospital because of heart failure, which was thought to be caused by moderate aortic regurgitation, moderate hypertension, and mild chronic renal failure. Echocardiography revealed thickened aortic and mitral valves. Primary antiphospholipid syndrome might have induced valve regurgitation as a result of valvular thickening.
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PMID:Aortic regurgitation in a patient with primary antiphospholipid syndrome--a case report. 958 54

Ischemic hepatitis, a relatively infrequent disorder occurring in 0.16% to 0.50% of patients admitted to medical intensive care units, often follows episodes of hypotension or acute heart failure. Investigating the clinical characteristics of patients with ischemic hepatitis may add to our understanding of the pathogenesis and significance of this syndrome. We therefore conducted a retrospective analysis of 34 patients to examine the possible contribution of the various baseline characteristics to the severity of the hepatic damage. In all patients liver disease was unexpected and in some, liver dysfunction dominated the clinical picture. All patients had high serum glutamic pyruvic transaminase (SGPT) and lactic dehydrogenase (LDH) levels (mean +/- SE, 2073 +/- 255 international units and 6085 +/- 748 international units, respectively). The mean SGPT/LDH ratio was 0.34. Most patients had coagulopathy with a prolonged prothrombin time (mean +/- SE, 5.86 +/- 1.37 international normalized ratio [INR]). The most common diagnosis on admission was respiratory distress secondary to various causes. Before the development of the hepatic dysfunction, respiratory failure and hypoxemia were observed in 68% of the patients, whereas hypotension was observed in only 38%. More than 90% of the patients had three or more associated comorbid conditions. The most frequent of these were left heart failure (88.2%), right heart failure (67.6%), chronic obstructive lung disease (58.8%), and chronic renal failure (55.9%). During the acute episode, more than 90% of the patients had transient deterioration of their renal functions. Hypoglycemia was noted in 11 patients (32.4%), and the glucose level was inversely correlated with the SGPT level (r = -0.43, p = 0.01). Stepwise multiple regression analysis showed that left heart failure, systolic blood pressure lower than 90 mm Hg, and female gender, together, accounted for 34% of the variance of the peak SGPT levels (p = 0.002). Fourteen (41.2%) patients died during the 3-month follow-up period, but none from the hepatic injury. None of the clinical or laboratory parameters measured predicted mortality. Clearly, ischemic hepatitis is associated with a high risk of death. The characteristic patients are those with multiple underlying systemic diseases and conditions, especially those with left heart failure. Liver function test results and levels of liver enzymes should be monitored in these patients, particularly when they are admitted for respiratory deterioration and episodes of hypotension.
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PMID:Ischemic hepatitis: clinical and laboratory observations of 34 patients. 960 Mar 66

All consecutive cases of chronic renal failure (CRF) seen over a twelve-month period (January-December 1992) were evaluated. Those that fulfilled strict diagnostic criteria for hypertension induced CRF (HICRF) were further studied to determine peculiarities of its clinico-pathological features that may render this possibly preventable condition readily identifiable. Twenty one (23.1%) of the 91 cases of CRF satisfied these criteria. There was a male preponderance (M.F.4.3:1). Nocturia was a prominent symptom predating other symptoms of CRF in all. Throbbing frontal headache necessitating significant consumption of analgesic was found in 13(61.9%). Hypertension had been diagnosed in the patients for periods ranging from 2-15 years and compliance to therapy was adjudged poor. Ten smoked cigarette in significant quantities. Hypertension occurred in 8 of the families of the patients. Hypertension was severe in all, with evidence of accelerated phase in 19(90.5%). A majority (71.4%) presented with severe uraemia (serum creatinine > or = 100 umol/l). Target organ damage, evident in cardiomegaly with heart failure occurred in 15, while ultrasonographic features of bilateral shrunken kidneys was seen in all. Blood pressure control was largely inadequate with a combination of 3 drugs. Mortality rate was 51% in the first year. Renal histopathological findings of glomerular sclerosis, malignant arteriolar changes with absence of glomerular cellular proliferation were observed in renal biopsies and 6 autopsy tissues. It is concluded that HICRF is a major cause of mortality; renal failure is often advanced at presentation, and blood pressure is usually in the accelerated phase. Significant cigarette smoking, severe headache necessitating consumption of significant quantity of analgesics, and a family history of hypertension are striking features.
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PMID:Hypertension induced chronic renal failure: clinical features, management and prognosis. 971 16


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