Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020639 (hypoproteinemia)
 1,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 26-year old woman, who was diagnosed as having systemic lupus erythematosus at the age of 23 year old, presented diarrhea and headache. She showed severe hypoproteinemia (serum total protein 3.7 g/dl, serum albumin 1.4 g/dl) and hyperlipidemia. She revealed to have protein-losing enteropathy with the result of alpha-1-antitrypsin clearance test using stool. Increase of prednisolone improved the loss of albumin into the bowel and abnormal laboratory findings. She also showed watershed infarction in the area of middle cerebral artery and posterior cerebral artery. Protein-losing enteropathy is a rare complication of SLE, only 18 cases are available on literature. No case is found to have cerebral infarction in patients with protein-losing enteropathy associated with SLE. It is known that blood levels of anticoagulation factors decrease in protein-losing enteropathy due to the leakage of plasma protein into intestinal lumen. Serum antithrombin III was decreased in this case. Hyperlipidemia found in this case seems to be caused by same mechanism in nephrotic syndrome. Lupus anticoagulant was also positive in this patient. These factors seems to be related to the occurrence of cerebral infarction. This case suggests the possibility of cerebral infarction in patients with protein-losing enteropathy in SLE.
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PMID:[Protein-losing enteropathy and cerebral infarction associated with systemic lupus erythematosus]. 814 30

A 21-year-old man was admitted to our hospital because of leg edema. Because laboratory findings revealed massive proteinuria and hypoproteinemia, he was diagnosed as having nephritic syndrome caused by minimal change disease. He was given a continuous heparin infusion and intravenous steroid therapy, at a prednisolone dose of 1 mg/kg per day, and his condition gradually improved. Five months after discharge, the patient's proteinuria relapsed. He was readmitted to our hospital and we restarted anticoagulant treatment with intravenous heparin and 60 mg prednisolone. On the third hospital day, he complained of chest pain with sudden onset and dyspnea. He quickly developed shock and died. The findings of an autopsy confirmed the presence of diffuse fibrin thrombi in bilateral pulmonary arteries, and we diagnosed the cause of death as diffuse pulmonary artery thrombosis. A coagulation test for activated partial thromboplastin time (aPTT) had already shown that aPTT was prolonged before the initiation of treatment. There may have been a deficit of antithrombin III (ATIII) - a cofactor of heparin - because of the proteinuria; thus, the continuous heparin treatment might not have been effective for the prevention of thrombosis. Alternatives to heparin treatment that do not suppress AT III, such as nafamostat mesilate or argatroban, which do not require the presence of AT III for their anticoagulant action, should be considered in cases similar to the that in the patient reported here. In patients with nephrotic syndrome who exhibit altered coagulation test results, the choice of anticoagulation therapy for treatment of the hypercoagulabilty status associated with nephrotic syndrome should be carefully considered.
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PMID:Fatal diffuse pulmonary arterial thrombosis as a complication of nephrotic syndrome. 1808 94

Nephrotic syndrom is an association of proteinuria>3g/d or 50mg/kg/d, an hypoalbuminemia<30g/L and a hypoproteinemia<60g/L. Primary etiologies are minimal glomerular injury, focal segmental glomerulosclerosis and non membranous glomerulonephritis. Secondary etiologies are diabetes, high blood pressure and amyloidosis. We present four cases about nephrotic syndrome after thromboembolic disease. In every case, patients show a pulmonary embolism symptomatic of a nephrotic syndrom, whose diagnostic could be delayed up to six months after first pulmonary symptoms. This raised the problem of renal biopsy in these patients who need anticoagulation. In minimal change nephrosis, without hematuria, high blood pressure or renal dysfonction, a corticosteroid therapy test could be done assuming that is corticosensitive minimal glomerular injury. In every case, anticoagulation course must be completed and maintained in case of patent nephrotic syndrom with an albuminemia under 20g/L. In case of pulmonary embolism or deep vein thrombosis, idiopathic-looking, a nephrotic syndrome must be sought-after. The two diagnosis ways are the proteinuria on the urine dipstick and the hypoproteinemia on usual biology. The main mechanism is the coagulation factor leak, side effect of the nephrotic syndrom, notably because of the antithrombin III.
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PMID:[Nephrotic syndrome revealed by pulmonary embolism: about four cases]. 2528 96

The aims of this study were to evaluate the characteristics of hypercoagulable states in patients with membranous nephropathy (MN) via thromboelastography (TEG) and to identify risk factors. 235 MN patients who had undergone TEG examinations from 2011 to 2014 were included. An abnormality in at least two TEG parameters is considered a hypercoagulable state. Patient data was compared between the hypercoagulable and non-hypercoagulable groups. Potential risk factors for hypercoagulability were analyzed by logistic regression models. Subgroup analysis was performed in hypercoagulable patients. Compared to the non-hypercoagulable MN patients, the hypercoagulable patients showed a significantly higher proportion of female patients, urinary protein, platelet count, triglyceride and fibrinogen level, along with more severe hypoproteinemia and a reduction of serum antithrombin III. Correlation analysis showed that hypoproteinemia was the primary risk factor for hypercoagulability in MN patients. Among the hypercoagulable MN patients, a subgroup TEG parameter analysis showed that glucocorticoids-used subgroup and smoker subgroup had shortened time to initial fibrin formation (R value) and increased coagulation index respectively (P < 0.05), indicating a more serious hypercoagulable state. Meanwhile, the time to initial fibrin formation (R value) and time to clot formation (K value) of the statin-used patients were remarkably higher than those of the non-statin patients. TEG examinations facilitated the detection of hypercoagulable states in MN patients, and hypoproteinemia was the most important risk factor for hypercoagulability in these patients. The use of glucocorticoids and smoking may help to aggravate hypercoagulable states, while statin drugs may alleviate hypercoagulability.
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PMID:Hypercoagulable state evaluated by thromboelastography in patients with idiopathic membranous nephropathy. 2615 97