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

In a retrospective study the outcome of 40 pregnancies in 20 women with a high titer of anti-RNP antibodies was evaluated. In the 18 pregnancies that occurred after disease onset, transient proteinuria was noted in 3 and transient thrombocytopenia in 2. Deep venous thrombosis was observed in one patient. Preeclampsia in another woman necessitated cesarean sections in 2 pregnancies with successful outcome. The observed complications may all be seen in normal pregnancies. There was no evidence of exacerbation of maternal disease during pregnancy or in the postpartum period. Our study indicates that in women with high anti-RNP titer the risk of fetal loss or maternal worsening of disease seems slight.
 ...
PMID:Pregnancy outcome in patients with high titer anti-RNP antibodies. A retrospective study of 40 pregnancies. 171 70

A 13-year-old boy was admitted to this hospital for evaluation of pitting edema of both legs. Three years ago, he had been diagnosed to have nephrotic syndrome. Two and half years ago, because of persistent heavy proteinuria, poor response to steroids and frequent relapse of disease, a renal biopsy was done; characteristics of IgM nephropathy was shown. About a year previously, the patient felt dizziness and weakness of the left side of his body upon awakening one morning. Neurologic examination showed loss of muscle tone, muscle power and deep tendon reflexes. Sensory and cranial nerve function were intact. Blood pressure was normal. The CT scan of brain showed a patch of low attenuation area in the right temporal region, obliteration of the right cortical sulci and mild compression of right lateral ventricle. A diagnosis of nephrotic syndrome with right cerebral infarction was made. The patient's condition became stable two days later after mannitol infusion, correction of electrolytes, and supportive therapy. According to literature, most cases of nephrotic syndrome complicate with renal thrombosis, pulmonary emboli, and deep vein thrombosis. Few cases complicate with cerebral thrombosis and infarction. If patient have low plasma albumin and anti-thrombin III level, hyperfunction of platelet aggregability and use long-term diuretic therapy, they may be at higher risk of thromboembolic complications. If thromboembolic complications exist, anticoagulation treatment should be instituted. Prophylactic therapy with aspirin or dicumarol is not currently recommended.
 ...
PMID:[Nephrotic syndrome complicated with cerebral infarction: report of one case]. 182 17

We describe two children with an otherwise unexplained deep vein thrombosis associated with high titer anticardiolipin antibodies (ACA) of the IgG class and circulating lupus anticoagulant (LAC). One of these patients had persistent proteinuria but neither had systemic lupus erythematosus. Our observation suggests that ACA and LAC assays should be performed in children with thromboembolic disease even when no underlying autoimmune disease can be found.
 ...
PMID:Anticardiolipin syndrome in childhood: a report of two cases. 211 74

Twenty cases of primary nephrotic syndrome were treated with urokinase at a dosage of 60,000 units per day for two successive weeks. The results showed that after treatment the concentrations of fibrinogen, urine FDP, alpha 2-plasma inhibitor and plasminogen were significantly decreased (P value less than 0.01, less than 0.01, less than 0.001, less than 0.005 respectively). The concentration of antithrombin III was significantly increased (P less than 0.05). It is suggested that the treatment obviously increased the fibrinolytic activity and improved the hypercoagulated state. The clinical data showed that in addition to decrease of proteinuria and obvious increase of urine volume, the clinical manifestations and laboratory parameters showed no significant difference. Further study on the dosage and indications of urokinase is needed and the activity of coagulation and fibrinolysis in patients with deep vein thrombosis of lower extremities was also discussed.
 ...
PMID:[Primary nephrotic syndrome treated with urokinase--a report of 20 cases]. 258 15

125I-Antithrombin III metabolism studies were performed in 2 patients with ischemic and ulcerative colitis, respectively. Both patients had acquired antithrombin III deficiency and objectively diagnosed deep venous thrombosis. A decreased 125I-antithrombin III plasma disappearance halflife and an increased fractional catabolic rate was found in both patients. The transcapillary flux ratio was elevated in the patient with ischemic colitis. A follow-up study of the first patient during a period when no signs of an ischemic colitis were present and no medication was taken showed completely normal tracer data. The data are consistent with both gastrointestinal loss and intravascular consumption of antithrombin III. The antithrombin III deficiency could not be explained by other causes such as proteinuria, liver dysfunction, or obvious disseminated intravascular coagulation. Reduced antithrombin III plasma levels were considered to have contributed to the development of deep venous thrombosis in both patients.
 ...
PMID:Antithrombin III metabolism in two colitis patients with acquired antithrombin III deficiency. 400 29

In three different disease entities associated with acquired antithrombin III (AT III) deficiency some of the pathogenetic mechanisms were studied. In liver cirrhosis (23 patients) the AT III level was closely correlated to the activity of hepatocellular synthesized clotting factors, indicating decreased AT III synthesis. In glomerular proteinuria (20 patients not on steroid therapy) the plasma level of AT III correlated inversely to the renal AT III clearance. In contrast to liver cirrhosis and proteinuria, in septicaemia (33 patients) the ratio between AT III antigen (radial immunodiffusion) and functional AT III (heparin cofactor assay using a chromogenic substrate) demonstrated an excess of AT III antigen probably due to inactive AT III-enzyme complexes. Therefore consumption of AT III appears to be an important cause of AT III deficiency in septicaemia. There was an inverse correlation between this ratio and the plasma AT III activity. It is well documented that congenital AT III deficiency predisposes to deep venous thrombosis (DVT) and sometimes to disseminated intravascular coagulation. A similar clinical relevance may be assumed for an acquired AT III deficiency, though so far a relationship between AT III deficiency and DVT has been only established in the nephrotic syndrome.
 ...
PMID:[Pathogenetic mechanism and clinical relevance of acquired anti-thrombin III deficiency in internal medicine (author's transl)]. 702 26

Intravenous immune globulin (IVIg) is advocated as a safe treatment for immune-mediated neurologic disease. We reviewed the medical records of 88 patients who were given IVIg for a neurologic illness. Major complications in four patients (4.5%) included congestive heart failure in a patient with polymyositis, hypotension after a recent myocardial infarction, deep venous thrombosis in a bed-bound patient, and acute renal failure with diabetic nephropathy. Other adverse effects included vasomotor symptoms 26, headache 23, rash 5, leukopenia 4, fever 3, neutropenia 1, proteinuria (1.9 g/day) 1, viral syndrome 1, dyspnea 1, and pruritus 1. Fifty-two patients (59%) had some adverse effect of IVIg infusion, most commonly vasomotor symptoms, headaches, fever, or shortness of breath in 40 (45%), which improved with reduced infusion rate or symptomatic medications. Five (6%) had asymptomatic laboratory abnormalities and seven (8%) had other minor adverse effects. Adverse effects led to discontinuation of therapy in 16% and permanent termination of therapy in 10% of patients. There was no mortality or long-term morbidity. Although adverse effects were frequent, serious complications were rare except in patients with heart disease, renal insufficiency, and bed-bound state.
 ...
PMID:Complications of intravenous immune globulin treatment in neurologic disease. 930 72

A young male patient with a recent history of meningococcemia was referred to our hospital in his recovery period. He had signs suggesting deep venous thrombosis in the legs but no other abnormalities on physical examination at admission. Laboratory results showed proteinuria (3.1 g/day), prolonged activated partial thromboplastin time (56.3 s), low level of C3c (0.19 g/l), high titers of both IgM (27.04 MPLU/ml) and IgG (74.88 GPLU/ml) anticardiolipin antibodies and recanalized thrombotic changes in the deep veins of the lower extremities on venography. Histopathological diagnosis of the kidney disease was membranous glomerulonephritis. He was started on an angiotensin-converting enzyme inhibitor to reduce proteinuria and an oral anticoagulant to prevent thromboembolic events. Since no reduction in proteinuria was observed at the 10th month of therapy, the angiotensin-converting enzyme inhibitor was discontinued. On his last follow-up, approximately 1.5 years after meningococcemia, he had no complaints and no abnormal findings on physical examination. While both IgM and IgG anticardiolipin antibody titers returned to the normal range, he still had persistent proteinuria and hypocomplementemia.
 ...
PMID:Membranous glomerulonephritis, antiphospholipid syndrome, and persistent low C3 levels associated with meningococcal disease. 1205 76

Venous thrombophilia is the result of clotting changes namely of a hypercoagulable state together with blood flow and vessel wall changes. There is no need for all these components to be present in order for thrombosis to occur. As the matter of fact, thrombosis may occur even if only one of these conditions is present. In clinical practice a combination of factors is usualy seen. In comparison with arterial thrombophilia, clotting changes and blood flow seen to play a major role in venous thrombosis. Venous thrombophilia may remain asynptomatic or may result in a series of clinical syndromes. The commonest of these are: 1. Superficial vein thrombosis, 2. Deep vein thrombosis of legs, 3. Deep vein thrombosis of arms, 4. Caval veins thrombosis, 5. Portal vein thrombosis, 6. Hepatic veins thrombosis, 7. Renal vein thrombosis, 8. Cerebral sinuses thrombosis, 9. Right heart thrombosis, 10. Miscellaneous (ovarian, adrenal veins thrombosis, etc.). Since the first two are widely and easily recognized, these is no need for an extensive discussion. Deep vein thromboses of upper limbs are not as frequent as those of lower limbs or of superficial phlebitis but they can still be recognized on clinical grounds and non invasive techniques. The remaining 7 syndromes are less common and therefore less frequently suspected and recognized. Of particular interest, among these less common manifestations of venous thrombophilia are hepatic vein and renal vein thrombosis. Hepatic veins thrombosis, sometimes part of inferior vena cava thrombosis is most frequently due to an isolated occlusion of hepatic veins thereby causing a form of venocclusive disease. Occasionally diagnosis may be difficult because of slow onset of symptoms (hepatomegaly, right flank pain, fever, ascites etc.). The same is true for renal vein thrombosis which may also be of difficult diagnosis since it causes proteinuria and flank pain. The proteinuria is often interpreted as due to a nephrotic syndrome which, incidentally, may cause by its turn renal vein thrombosis. Portal vein thrombosis and cerebral sinuses thrombosis on the contrary are more easily suspected because of ascites, adominal pain, jaundice or headache, eye proptosis, vomiting. Right heart thrombosis should be suspected in cases of recurrent pulmonary embolization. Ovarian or adrenal veins thrombosis are rare. The competent physician should always consider, given certain congenital or acquired conditions, the possibility to be facing a special form of venous thrombosis or a venous thrombosis in unusual sites. An early diagnosis, as often in medicine, is of paramount importance for a prompt treatment and a satisfactory outcome.
 ...
PMID:Clinical aspects of venous thrombophilia. 1367 53

A 28-year-old man presented with mental retardation, peculiar facial features, radioulnar synostosis, hypogonadism, aplasia of the right kidney, a moderate degree of proteinuria, and peripheral cyanosis. The activated partial thromboplastin time was shortened, and the level of plasma factor VIII was high. A chromosomal analysis revealed a 49, XXXXY karyotype. From the 10th hospital day, he suffered from sudden dyspnea following swelling of the left leg. He was diagnosed as having deep vein thrombosis and pulmonary embolism, and was successfully treated with anticoagulant therapy. This is the first case of the 49, XXXXY syndrome complicated with unilateral renal aplasia, proteinuria, and venous thromboembolism.
 ...
PMID:49, XXXXY syndrome with unilateral renal aplasia, proteinuria, and venous thromboembolism. 1564 56


1 2 3 4 Next >>