Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 40-year-old woman was admitted because of increasing exertional dyspnea. Right heart failure was suggested by the presence of hepatomegaly, pretibial edema and also echocardiographic findings. Physical examination and echocardiography showed no evidence of valvular disease or congenital heart disease except for right ventricular dilatation and tricuspid regurgitation. The ventricular septum deviated toward the left ventricle throughout the cardiac cycle, but left ventricular function was preserved. Severe pulmonary hypertension averaging 44 mmHg was revealed by cardiac catheterization. Digital subtraction angiography and pulmonary blood flow scintigraphy showed no evidence of pulmonary artery embolism, and no interstitial pulmonary lesions that might have caused pulmonary hypertension were recognized. Hypergammaglobulinemia suggested an autoimmune disorder, and signs of systemic lupus erythematosus (SLE), such as pleural effusion, proteinuria, lymphocytopenia, LE cell phenomenon and antinuclear antibodies were present. Several autoimmune diseases are known to be causative factors of pulmonary hypertension. However, only ten cases of SLE complicated by pulmonary hypertension have been reported the present one. These cases were characterized by a high incidence of Raynaud's phenomenon and positivity for anti-RNP antibody. In our present case, SLE activity was suppressed using prednisolone, but pulmonary hypertension persisted and the patient eventually died due to right cardiac failure. Judging from the clinical course of the ten reported cases of SLE-pulmonary hypertension, there seems to be no hope of improving the pulmonary hypertension once it has become established. Therefore it is important to detect and cure pulmonary hypertension as early as possible.
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PMID:[A case of lupus erythematosus preceded by right heart failure due to pulmonary hypertension]. 174 69

A 43 year old woman was admitted to our hospital in April 1987 due to shortness of breath and pedal edema. She had a history of sepsis associated with the crisis of hyperthyroidism 15 years prior to the admission. Physical examination revealed a badly nourished with ascites: weight was 56 kg and height 156 cm. The heart sounds were distant with mild holosystoric murmur (grade I/VI) at xiphoisternum. The chest X-ray showed cardiomegaly (CTR: 72.3%) with pleural effusion. The electrocardiogram showed atrial fibrillation, low voltage and right ventriculer hypertrophy. The echocardiogram showed marked dilatation of right atrium and ventricle with very short septal leaflet of tricuspid valve. The anterior and posterior leaflets were undetected. The tricuspid regurgitant doppler signal was recorded up to hepatic vein. No other abnormalities were noted in other valves. The white cell count was 4900 with lymphocytopenia (26%; T-cell 82%, B-cell 13%). Serum total protein was reduced to 3.4 g/dl with albumin 1.64 g/dl. Immunoelectrophoresis showed normal IgG, IgA and IgM. Proteinuria was not recognized. Fecal excretion of polyvinylpyrrolidone-131I (PVP) was elevated to 2.8%, The systolic pressure in pulmonary artery, right ventricle, right atrium, superior and inferior vena cave were almost equal as 26 mmHg. The pulmonary arterial scintigraphy disclosed multiple peripheral defects in both lungs. Two weeks after the operation of tricuspid valve replacement based on the diagnosis of protein-losing enteropathy due to isolated tricuspid regurgitation, serum total protein and albumin were normalized to 6.8 g/dl and 3.6 g/dl respectively, but the lymphocytopenia was persistent. She become very well, with free of ascites and edema.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of isolated tricuspid regurgitation associated with protein-losing gastroenteropathy]. 273 14

Renal responses to atrial natriuretic peptide were examined in conscious dogs with congestive heart failure (tricuspid insufficiency) and in conscious rats with nephrotic syndrome (adriamycin). Heart-failure dogs displayed elevated atrial pressure and heart weights, blunted natriuresis to a saline load, and ascites. Nephrotic rats displayed proteinuria, hypoproteinemia, sodium retention, and ascites. In control animals, atrial natriuretic peptide increased absolute and fractional urine flow rate and urinary sodium excretion. Although atrial natriuretic peptide increased absolute and fractional urine flow rate and urinary sodium excretion in conscious heart-failure dogs and nephrotic rats, the responses were markedly blunted. In heart-failure dogs, infusion of atrial natriuretic peptide increased plasma concentrations of norepinephrine and epinephrine. In nephrotic rats, renal denervation reversed the blunted diuretic and natriuretic responses to atrial natriuretic peptide. Mean arterial pressure, glomerular filtration rate, and p-aminohippurate clearance were affected similarly by atrial natriuretic peptide in heart-failure dogs or nephrotic rats vs. control animals. Conscious congestive heart-failure dogs and conscious nephrotic rats have blunted diuretic and natriuretic responses to atrial natriuretic peptide.
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PMID:Blunted natriuresis to atrial natriuretic peptide in chronic sodium-retaining disorders. 295 52

We report a case of IgA-dominant postinfectious glomerulonephritis in a 49-year-old man presenting with acute kidney injury, nephrotic range proteinuria and hematuria. He suffered from ischemic heart disease, cardiac insufficiency, mitral regurgitation, tricuspid insufficiency, septal aneurysm and hypertension. Renal biopsy revealed segmental and focal endocapillary and mesangial hypercellularity, and thickening of the glomerular capillary wall. Immunofluorescence showed co-dominant strong coarse granular immunostaining of IgA, IgG and C3 mainly along the glomerular capillary wall. On electron microscopy some large subepithelial hump-shaped deposits were present. In summary, this case demonstrates the presence of a broad spectrum of glomerular histological findings in postinfectious glomerulonephritis.
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PMID:An unusual case of IgA-dominant postinfectious glomerulonephritis: a case report and review of the literature. 2754 74

We herein report two cases of proteinase 3-anti-neutrophil cytoplasmic antibody (PR3-ANCA)-related nephritis in infectious endocarditis. In both cases, the patients were middle-aged men with proteinuria and hematuria, hypoalbuminemia, decreased kidney function, anemia, elevated C-reactive protein (CRP) levels, and PR3-ANCA positivity. Each had bacteremia, due to Enterococcus faecium in one and Streptococcus bovis in the other. One patient received aortic valve replacement therapy for aortic regurgitation with vegetation, and the other underwent tricuspid valve replacement therapy and closure of a ventricular septic defect to treat tricuspid regurgitation with vegetation. These patients' urinary abnormalities and PR3-ANCA titers improved at 6 months after surgery following antibiotic treatment without steroid therapy.
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PMID:Two Cases of Proteinase 3-Anti-Neutrophil Cytoplasmic Antibody (PR3-ANCA)-related Nephritis in Infectious Endocarditis. 2790 14