Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Glomerulomegaly is a histologic finding present in idiopathic pulmonary hypertension, congenital cyanotic heart disease, morbid obesity associated with sleep apnea syndrome, sickle cell disease, and polycythemic states. This study examines the case of a 34-yr-old woman with idiopathic pulmonary artery hypertension who presented with nephrotic-range proteinuria. Kidney biopsy revealed enlarged glomeruli with mesangial-proliferative glomerulonephritis. A review of the pertinent literature and a discussion of the proposed pathophysiologic mechanisms leading to glomerulomegaly are presented.
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PMID:Glomerulomegaly and proteinuria in a patient with idiopathic pulmonary hypertension. 940 1

We report an unusual case in which infectious endocarditis presented systemic vasculitis and glomerulonephritis as the initial manifestation of the disease. The patient was a 16-year-old girl with congenital cyanotic heart disease who presented with skin purpura, proteinuria, and hematuria. She had hypergammaglobulinemia, cryoglobulinemia, and positive circulating immune complexes. Renal biopsy revealed crescentic glomerulonephritis. Her serum C3 level, which was initially normal, became decreased, and prednisolone and azathioprine were administered with a tentative diagnosis of systemic lupus erythematosus (SLE). Soon after, she developed fever and renal failure. Blood culture grew Streptococcus pyogenes, and the diagnosis of infectious endocarditis was made. Eight cases of systemic vasculitis and glomerulonephritis associated with infectious endocarditis have been described in the literature. Infectious endocarditis should be included in the differential diagnosis of systemic vasculitis and glomerulonephritis.
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PMID:Vasculitis associated with septicemia: case report and review of the literature. 1179 7

Pulmonary thromboembolism (PTE) is rarely diagnosed in cats, and the clinical features of the disease are not well known. PTE was diagnosed at postmortem examination in 17 cats, a prevalence of 0.06% over a 24-year period. The age of affected cats ranged from 10 months to 18 years, although young (<4 years) and old (>10 years) cats were more commonly affected than were middle-aged cats. Males and females were equally affected. The majority of cats with PTE (n = 16) had concurrent disease, which was often severe. The most common diseases identified in association with PTE were neoplasia, anemia of unidentified cause, and pancreatitis. Cats with glomerulonephritis, encephalitis, pneumonia, heart disease, and hepatic lipidosis were also represented in this study. Most cats with PTE demonstrated dyspnea and respiratory distress before death or euthanasia, but PTE was not recognized ante mortem in any cat studied. In conclusion, PTE can affect cats of any age and is associated with a variety of systemic and inflammatory disorders. It is recommended that the same clinical criteria used to increase the suspicion of PTE in dogs should also be applied to cats.
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PMID:Pulmonary thromboembolism in cats. 1532 May 93

End-stage renal disease (ESRD), due to its high morbidity and mortality as well as social and financial implications, is a major public health problem. Outcome depends not only on different modalities of treatment like hemodialysis and peritoneal dialysis, but also on existing co-morbidities, age, duration on dialysis, supportive therapies and infection control strategies. Thus, a detailed study becomes necessary to improve health care delivery, provide medical care and to establish a geographical reference. The present study was undertaken to characterize the ESRD patients by their demographic and co-morbid conditions and relate this to the morbidity and mortality trends. The medical records of 110 ESRD patients seen over a five-year period (June 1995 to December 1999) in two tertiary-care hospitals in Riyadh, Saudi Arabia were studied retrospectively. There were 79 (64.5%) males and 31 (35.5%) females; their age ranged from 17 to 92 years (mean age 53.8 +/- 17.8 years). Diabetes was the commonest cause of ESRD seen in 26 (26.6%) followed by nephrosclerosis, unknown etiology, lupus nephritis, pyelonephritis and primary glomerulonephritis. Diabetes mellitus was the most prevalent co-morbidity seen during the study period and occurred in 65 patients (59%) followed by heart disease in 36 (32.7%), liver disease in 30 (27.3%), cerebrovascular accidents in 13 (11.8%) and neoplasm in 11 (10%). Seven (6.3%) patients only were smokers. Hemodialysis was the most frequent treatment choice as renal replacement therapy. Among the causes of hospitalization, cardiovascular conditions were the leading single cause (19.1%), followed by access related reasons and infections (11.5% each). The overall hospitalization rate was 11.2 days/year. The overall mortality rate was 8.07 deaths/year. The leading cause of death was cardiovascular in 15 (51.7%) followed by unknown/sudden death in eight (27.5%). Other causes of death included fluid overload, gastrointestinal hemorrhage, septicemia, liver disease and pulmonary embolism. Diabetes was the commonest co-morbid cause among the deceased. Old age, diabetes mellitus, prolonged duration on dialysis and cardiac diseases were the common causes of mortality. Our findings are consistent with worldwide reports. The study provides a reference data and will hopefully be helpful in improving the medical care.
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PMID:Morbidity and mortality in ESRD patients on dialysis. 1766 Jun 70

The term 'cardiorenal syndrome' (CRS) has increasingly been used in recent years without a constant meaning and a well-accepted definition. To include the vast array of interrelated derangements, and to stress the bidirectional nature of the heart-kidney interactions, the classification of the CRS today includes 5 subtypes whose etymology reflects the primary and secondary pathology, the time frame and simultaneous cardiac and renal codysfunction secondary to systemic disease. The CRS can generally be defined as a pathophysiological disorder of the heart and kidneys whereby acute or chronic dysfunction in one organ may induce acute or chronic dysfunction in the other organ. Type I CRS reflects an abrupt worsening of cardiac function (e.g. acute cardiogenic shock or decompensated congestive heart failure) leading to acute kidney injury. Type II CRS describes chronic abnormalities in cardiac function (e.g. chronic congestive heart failure) causing progressive and permanent chronic kidney disease. Type III CRS consists in an abrupt worsening of renal function (e.g. acute kidney ischemia or glomerulonephritis) causing acute cardiac disorder (e.g. heart failure, arrhythmia, ischemia). Type IV CRS describes a state of chronic kidney disease (e.g. chronic glomerular disease) contributing to decreased cardiac function, cardiac hypertrophy and/or increased risk of adverse cardiovascular events. Type V CRS reflects a systemic condition (e.g. diabetes mellitus, sepsis) causing both cardiac and renal dysfunction. Biomarkers can help to characterize the subtypes of the CRS and to indicate treatment initiation and effectiveness. The identification of patients and the pathophysiological mechanisms underlying each syndrome subtype will help to understand clinical derangements, to make the rationale for management strategies and to design future clinical trials with accurate selection and stratification of the studied population.
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PMID:The cardiorenal syndrome. 1916 27

The term cardiorenal syndrome (CRS) has increasingly been used in recent years without a constant meaning and a well accepted definition. To include the vast array of interrelated derangements, and to stress the bi-directional nature of the heart-kidney interactions, the classification of the cardiorenal syndrome includes today five sub-types whose etymology reflects the primary and secondary pathology, the time-frame and simultaneous cardiac and renal co-dysfunction secondary to systemic disease. The cardiorenal syndrome can be generally defined as a pathophysiologic disorder of the heart and kidneys whereby acute or chronic dysfunction in one organ may induce acute or chronic dysfunction in the other organ. Type I CRS reflects an abrupt worsening of cardiac function (e.g. acute cardiogenic shock or decompensated congestive heart failure) leading to acute kidney injury. Type II CRS describes chronic abnormalities in cardiac function (e.g. chronic congestive heart failure) causing progressive and permanent chronic kidney disease. Type III CRS consists in an abrupt worsening of renal function (e.g. acute kidney ischaemia or glomerulonephritis) causing acute cardiac disorder (e.g. heart failure, arrhythmia, ischemia). Type IV CRS describes a state of chronic kidney disease (e.g. chronic glomerular disease) contributing to decreased cardiac function, cardiac hypertrophy and/or increased risk of adverse cardiovascular events. Type V CRS reflects a systemic condition (e.g. diabetes mellitus, sepsis) causing both cardiac and renal dysfunction. Biomarkers can help to characterize the subtypes of the CRS and to indicate treatment initiation and effectiveness.
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PMID:[Cardiorenal syndrome, current understanding]. 1955 20

The complement system is an important part of innate immunity; however, as with other parts of the immune system, the complement system can become pathologically activated and create or worsen disease. Anticomplement reagents have been studied for several years, but only recently have they emerged as a viable therapeutic tool. Here, we describe the role of the complement system in a wide array of diseases, as well as the use of anticomplement therapy as treatment for these diseases in animal models and in human clinical trials. Specifically, we will discuss the role of anticomplement therapy in paroxysmal nocturnal hemoglobinuria, glomerulonephritis, and heart disease, including coronary artery disease, myocardial infarction, and coronary revascularization procedures such as percutaneous coronary angioplasty and coronary artery bypass graft surgery.
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PMID:Anticomplement therapy. 1970 48

To include the vast array of interrelated derangements, and to stress the bidirectional nature of the heart-kidney interactions, the classification of the cardiorenal syndrome (CRS) includes today five subtypes whose etymology reflects the primary and secondary pathology, the time-frame and simultaneous cardiac and renal codysfunction secondary to systemic disease. The CRS can be generally defined as a pathophysiologic disorder of the heart and kidneys, whereby acute or chronic dysfunction in one organ may induce acute or chronic dysfunction in the other organ. Type 1 CRS reflects an abrupt worsening of cardiac function (e.g. acute cardiogenic shock or decompensated congestive heart failure) leading to acute kidney injury. Type 2 CRS describes chronic abnormalities in cardiac function (e.g. chronic congestive heart failure) causing progressive and permanent chronic kidney disease. Type 3 CRS consists in an abrupt worsening of renal function (e.g. acute kidney ischemia or glomerulonephritis) causing acute cardiac disorder (e.g. heart failure, arrhythmia, ischemia). Type 4 CRS describes a state of chronic kidney disease (e.g. chronic glomerular disease) contributing to decreased cardiac function, cardiac hypertrophy and/ or increased risk of adverse cardiovascular events. Type 5 CRS reflects a systemic condition (e.g. diabetes mellitus, sepsis) causing both cardiac and renal dysfunction. The identification of patients and the pathophysiological mechanisms underlying each syndrome subtype will help to understand clinical disorders and to design future clinical trials.
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PMID:Cardiorenal syndromes: definition and classification. 2042 91

Kidney disease is a rare complication in patients with the Down's syndrome. However, with increased survival, it appears that a growing number of these patients present with glomerulonephritis. Most cases have been reported as case reports and include lesions such as mesangiocapillary glomerulonephritis with hypo-complementemia, crescentic glomerulonephritis with anti-neutrophil cytoplasmic antibodies (ANCA), amyloidosis and immunotactoid glomerulopathy. We report the observation of a 38-year-old man with the Down's syndrome who presented with severe renal failure, proteinuria and microscopic hematuria evolving over two months. There was no history of congenital heart disease or urinary symptoms. Percutaneous renal biopsy revealed fibrous crescents, rupture of Bowman's capsule and peri-glomerular granuloma; there were no deposits on immunofluorescence study. Thoracic computerized tomography scan showed alveolar congestion. The patient tested negative for ANCA. At the time of reporting, the patient is on regular chronic hemodialysis. Our case illustrates a distinct entity that further expands the spectrum of renal disease known to occur in the Down's syndrome. Early detection of the renal disorders may prevent or slow down the progression.
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PMID:Pauci-immune crescentic glomerulonephritis in the Down's syndrome. 2423 90

We report a case of a 21-year-old young man with underlying congenital heart disease who developed Bartonella henselae endocarditis of the right ventricular outflow tract (RVOT) conduit of his Melody transcatheter (percutaneous) pulmonary valve (TPV), with an initial presentation of glomerulonephritis with a dominant C3 pattern, with renal failure and circulating cryoglobulins. There are few reports of a glomerulonephritis with a dominant C3 pattern presenting as a manifestation of B. henselae endocarditis. While most cases of B. henselae endocarditis affect the aortic valve, in this case the valve damage was to the RVOT of the Melody TPV, a percutaneous transcatheter valve delivery system that had previously replaced his pulmonary homograft, which had become dysfunctional as a result of prior Streptococcus viridans endocarditis. The pulmonary homograft had been in place since childhood as a result of a Ross procedure to repair his congenital aortic stenosis. The patient's renal failure significantly improved after surgical resection of the infected RVOT and institution of appropriate antibiotic therapy.
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PMID:Bartonella henselae endocarditis and glomerulonephritis with dominant C3 deposition in a 21-year-old male with a Melody transcatheter pulmonary valve: case report and review of the literature. 2489 98


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