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)

This report describes the simultaneous manifestation of ischemic heart disease and nephrotic syndrome in a 37-year-old woman presenting with acute anterior myocardial infarction. Symptoms of nephrotic syndrome, such as facial and peripheral edema accompanied by proteinuria and hyperlipidemia, and onset of severe retrosternal pain developed within 24 h. Coronary angiography revealed a complete thrombotic occlusion of the proximal portion of the left anterior descending artery with no evidence of arteriosclerotic lesions. Histologic examination of renal biopsy, including electron microscopy, revealed evidence of minimal change glomerulonephritis. Ultrastructural studies demonstrated widespread effacement of epithelial foot processes. Elevated levels of circulating fibrinogen appeared to be an important factor for the hypercoagulable state in this patient, suggesting a causative relationship between coronary thrombosis and nephrotic syndrome.
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PMID:Simultaneous manifestation of acute myocardial infarction and nephrotic syndrome. 966 62

Glycoprotein IIIa/IIb is a membrane receptor for fibrinogen and von Willebrand factor that plays an important role in platelet aggregation. The beta integrin chain of this receptor, GPIIIa, is polymorphic, and the allele known as PlA2 has been associated with coronary thrombosis. The GPIIIa genotype of a cohort of 119 consecutive renal allograft recipients (46.3 +/- 13 yr; 85 M/34 F; 24.4% diabetic patients) was determined by PCR-restriction fragment length polymorphism, and those patients were followed for at least 12 mo. From 119 patients with at least 1 yr of follow-up, those who suffered an acute rejection (n = 52) showed a lower proportion of HLA-DR beta1 identity with the donor (7.7% versus 23.9%; P = 0.03), a higher proportion of cytomegalovirus-positive (CMV+) donors/CMV- recipients (21% versus 7.5%; P = 0.05), and the PlA2 allele was more frequent (48.1% versus 26.9%; P = 0.02) compared with patients free of acute rejection (n = 67). No other variable was associated with acute rejection in the univariate analysis. The impact of the three above-mentioned significant variables on acute rejection was analyzed by stepwise logistic regression. The presence of the PlA2 allele yielded an odds ratio of 2.75 (95% confidence interval, 1.01 to 7.93) and an HLA-DR beta1 identity of 0.2 (95% confidence interval, 0.06 to 0.99) for suffering an acute rejection episode. In addition, the serum creatinine at discharge was higher in PlA2-positive versus PlA2-negative patients (2.2 +/- 1.6 versus 1.5 +/- 0.6 mg/dl, respectively; P = 0.01), and the prevalence of proteinuria >1.5 g/d 1 yr after transplantation was significantly higher among patients showing the PlA2 allele (16% versus 3%; P = 0.02). Finally, in the entire cohort of patients, the 2-yr graft survival was significantly lower in PlA2-positive (n = 43) compared with PlA2-negative (n = 76) patients (85.7% versus 97.2%; P = 0.015). No differences were found in patient survival (95.2% versus 98.7%, respectively). Proportional hazards regression analysis (Cox regression model) confirmed that serum creatinine level at discharge is the best predictor of allograft survival, followed by CMV status, delayed graft function, and the glycoprotein IIIa/IIb genotype. The PlA2 polymorphism is an independent risk factor for acute renal graft rejection, affecting short-term graft survival. Future studies aimed at preventing the hemostatic imbalance favoring platelet aggregation associated with this polymorphism may be important in preventing acute rejection and its impact on chronic rejection.
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PMID:The PlA2 polymorphism of the platelet glycoprotein IIIA gene as a risk factor for acute renal allograft rejection. 1058

A 41-year-old woman presented with acute angina in the emergency unit. Additionally, she reported pain in both legs and a weight loss of 5 kilograms within the last 10 days. ECG revealed an acute anterior myocardial infarction. However, immediate coronary angiography showed open arteries with minimal arteriosclerosis. A characteristic rise of cardiac enzymes together with an akinesis of the anterior wall and an adjacent mural thrombus was highly suggestive of a transient coronary thrombosis. Further investigations showed occlusion of multiple arteries in both legs and a splenic infarct. Although there was a typical risk profile including smoking, hyperlipidemia and regular estrogen medication, a further work-up was started. Urin analysis was decisive for the presence of proteinuria and a severe nephrotic syndrome. The definite diagnosis was made by direct biopsy of the kidney that revealed the characteristic findings of a minimal change glomerulopathy. Rapid remission could be induced by high-dose oral steroids. During routine work-up of coronary syndromes, especially in those with normal coronaries, rare but treatable causes of myocardial infarction and coagulopathy have to be thought of and should carefully be excluded.
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PMID:[41-year-old female patient with ST-elevation myocardial infarction and multiple arterial emboli]. 2043 64