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)

To study the possible role of an "increased thrombotic tendency" in the vascular complications of diabetes several tests of haemostatic function were carried out on 91 men and 63 women with diabetes aged 35-54 years and the results compared with findings in 686 men and 393 women of the same age in the Northwick Park Heart Study. Mean values for factors VII and X, fibrinogen, and platelet adhesiveness were higher in the diabetics, but mean fibrinolytic activity and whole blood platelet counts were lower. Antithrombin III values were also higher in the diabetics, which may have constituted a protective response to other changes favouring the onset of vascular disease. Diabetics with retinopathy had higher factor VII and antithrombin III values, and those with proteinuria had higher values for factor VII, fibrinogen, and platelet adhesiveness than those without these complications. These findings suggest a potentially important association between a thrombogenic tendency and vascular disease in diabetes. Nevertheless, prospective data are needed to clarify whether the haemostatic abnormalities precede the onset of clinically manifest vascular complications or are a consequence of them.
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PMID:Haemostatic variables associated with diabetes and its complications. 50 77

Antithrombin III (AT II/III) was determined immunologically and by means of a heparin cofactor assay in plasma samples and 24-hour urine of 15 patients with various degrees of proteinuria, being predominantly of glomerular origin. In urine the AT II/III concentrations were significantly correlated to the concentrations of albumin, plasminogen and IgG. One third of the patients had AT II/III plasma levels below the normal range. The plasma levels showed a significant inverse correlation to the AT II/III and albumin clearance rates. Similarily, the plasminogen concentrations in plasma were decreased in two thirds of the patients, being inversely correlated to the renal plasminogen clearance values. It is proposed that AT II/III deficiency in the nephrotic syndrome is an important pathogenetic factor in venous thrombosis.
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PMID:Acquired antithrombin III deficiency in patients with glomerular proteinuria. 68 89

Antithrombin III levels were studied in relation to the occurrence of thromboembolism in 48 patients with various degrees of proteinuria. Nine of these patients had clinical signs of thrombosis, including four with renal vein thrombosis. In eight of these nine patients, antithrombin III concentrations were below 70 per cent. There was a significant negative correlation between the antithrombin III concentration and the urinary protein excreation (P less than 0.001). Antithrombin III was found in the urine of 32 of 42 patients. There was a significant correlation between the renal clearance and the degree of antithrombin III serum deficiency (P less that 0.001). The clearance and serum level of albumin closely paralleled these changes. We conclude that thrombosis in patients with severe proteinuria is associated with a deficiency of antithrombin III due to urinary excretion of this protein.
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PMID:Acquired antithrombin III deficiency and thrombosis in the nephrotic syndrome. 70 21

Antithrombin III (AT-III) activity was measured and compared in 29 patients with preeclampsia and 31 women with normal pregnancies. AT-III levels were 83 +/- 25% in preeclamptic patients with greater than 5 g/l proteinuria compared with 102 +/- 11% in the controls. Less severe proteinuria was not associated with decreased AT-III levels. Multivariate analysis revealed that the duration of pregnancy and the degree of proteinuria had an independent negative effect on AT-III levels. AT-III activity correlated poorly with platelet counts and blood pressure measurements. We conclude that urinary loss appears to be the major mechanisms of lower AT-III levels observed in our patients with preeclampsia.
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PMID:Antithrombin III levels in preeclampsia. 232 33

The protein C-protein S natural anticoagulant system was evaluated in 32 patients with proteinuria, 11 without nephrotic syndrome (NS) and 21 with NS of different grade. Antithrombin III (AT III), factors II, VII, X were also measured in the same groups of patients. In addition to plasma levels of these proteins, urinary loss of protein C was evaluated in concentrated urine specimens from 17 of the 21 patients with NS. The protein C antigen level was found to be normal or high in NS, but the difference between the control group and nephrotic patients was statistically significant only in severe NS. For all proteinuric patients, the plasma concentration of protein C correlated positively with the degree of proteinuria, cholesterol level, triglyceride level, and correlated inversely with serum albumin concentration; 17/17 patients with NS exhibited urinary loss of protein C and the degree of protein C excretion correlated positively with the degree of proteinuria. Plasma protein S antigen was measured in only 11 patients with NS and was found to be significatively increased, with a negative correlation with serum albumin concentration. AT III did not differ between the control group and the proteinuric patients with or without NS. Factors II and X were in the normal range for all patients. Factor VII was increased even in mild NS. Thus, the plasma levels of protein C and protein S antigens were normal or increased in patients with NS and this is probably related to an increased liver synthesis rate of these proteins, which is secondary to proteinuria.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Study of the protein C-protein S system in glomerulopathies and nephrotic syndrome]. 295 50

We measured the plasma concentrations of the natural anticoagulant protein C and its cofactor protein S in 17 patients with severe proteinuria. In addition, prothrombin and antithrombin III levels were measured in the same group of patients. These results were compared with results obtained in 26 healthy controls and a group of 14 patients with chronic renal insufficiency (CRI) but minimal proteinuria. Protein C, protein S, and prothrombin levels were not significantly different between healthy controls and patients with CRI. However, protein C, protein S, and prothrombin levels were significantly elevated in 71%, 82%, and 76%, respectively, of patients with proteinuria. Antithrombin III levels were decreased in three of these 17 patients with proteinuria. Plasma concentrations of protein C, protein S, and prothrombin correlated significantly with each other and were inversely correlated with serum albumin concentrations. In three patients, high protein C, protein S, and prothrombin levels returned to normal during remission of the proteinuric state. Proteins C and S were not detectable in the urine of two patients with high-grade proteinuria. Thus, the plasma levels of the vitamin K-dependent, natural anticoagulant protein C and its cofactor protein S are increased in patients with proteinuria. The elevated plasma levels of other vitamin K-dependent proteins, such as prothrombin, suggest a generalized elevation in vitamin K-dependent protein synthesis in patients with proteinuria.
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PMID:Plasma concentrations of the natural anticoagulants protein C and protein S in patients with proteinuria. 316 Aug

Plasma Antithrombin III (AT III) has been shown to be elevated in certain conditions like diabetes mellitus and coronary artery disease as well as in situations where there is increased platelet turnover. This study attempts to define the role of platelet injury in Clinical Nephrology and assesses the clinical value of ATT III. In IgA Nephritis, plasma AT III levels (105 +/- 10%) in 97 patients were higher than those of normal controls (96 +/- 5%) (p less than 0.0005). AT III levels were significantly correlated with proteinuria (p less than 0.0001), segmental sclerosis (p less than 0.01), crescents (p less than 0.01), medial hypertrophy (p less than 0.001) and intensity of IgA staining on IMF (p less than 0.02). Patients with IgA nephritis with raised AT III had more proteinuria (p less than 0.003), more segmental sclerosis (p less than 0.007) as well as a greater intensity of IgA on IMG (p less than 0.02) when compared to patients with normal AT III levels. The data suggest that plasma AT III may serve as a marker of disease activity in IgA nephritis. Plasma AT III levels in hemodialysis patients, low prior to dialysis, improved after dialysis (p less than 0.01). Pre and post hemodialysis platelet counts however did not change significantly. In peritoneal dialysis patients, AT III levels which were normal before dialysis, increased significantly after peritoneal dialysis (p less than 0.01). The platelet counts before and after peritoneal dialysis also improved (p less than 0.005). No correlation was found between AT III levels and platelet counts. Although platelet damage has a contributory role in increasing AT III levels during hemodialysis, the data on peritoneal dialysis suggest that there may be other factors affecting platelets and AT III during dialysis.
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PMID:Galloway memorial lecture. Platelet injury and antithrombin III in clinical nephrology. 389 86

Antithrombin III activity and plasma fibronectin levels were determined in patients with preeclampsia. In several cases low antithrombin III and high plasma fibronectin concentrations could be related to proteinuria. Altered plasma fibronectin and antithrombin III concentrations might contribute to a hypercoaguable state in patients with preeclampsia.
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PMID:Low antithrombin III and high plasma fibronectin in pre-eclampsia. 400 30

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.
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PMID:Antithrombin III metabolism in two colitis patients with acquired antithrombin III deficiency. 400 29

Plasma Antithrombin III (A T III) was measured in 97 patients with IgA nephritis, 30 patients with non IgA idiopathic mesangial proliferative glomerulonephritis and 40 healthy subjects. The mean plasma A T III levels in the patients with IgA nephritis (105 +/- 10%) was significantly higher than those of normal controls (96 +/- 5%) (p less than 0.0005). The mean plasma A T III levels in the patients with non IgA nephritis (101 +/- 10%) was not different from those of the normal controls or the patients with IgA nephritis. A T III levels were significantly correlated with proteinuria (p less than 0.0001), segmental sclerosis (p less than 0.001), crescents (p less than 0.01), medial hypertrophy (p less than 0.001) and intensity of IgA staining on IMF (p less than 0.02). Patients with IgA nephritis with raised A T III levels had significantly more proteinuria (p less than 0.003), more segmental sclerosis (p less than 0.007) as well as a greater intensity of IgA staining on IMF (p less than 0.02) when compared to patients with normal A T III levels. The data suggest that raised plasma A T III levels may serve as a prognostic marker in IgA nephritis.
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PMID:Antithrombin III in mesangial IgA nephritis. 408 21


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