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)

Thromboses and disorders of hemostasis in nephrotic syndrome. Thromboembolic complications are common in nephrotic syndrome (NS). This article reviews the factors of thrombogenesis in NS, including: 1) a hypercoagulable state with platelet hyperaggregability, hyperfibrinogenemia and elevated factor VIII, decrease in plasma levels of coagulation inhibitors antithrombin III and free protein S, reduced fibrinolytic activity; 2) excessive intravascular thrombin formation marked by increased plasma levels of fibrinopeptide A. The intensity of hemostasis disorders coincides with that of NS. Most disorders are related to hypoalbuminemia and proteinuria. In agreement with experimental data, the role of intraglomerular activation of coagulation during active phases of glomerulopathies has to be considered. This could explain the predominance of renal vein thrombosis in several glomerulopathies with NS. Several coagulation disorders in SN have implications for therapy.
 ...
PMID:[Thrombosis and disorders of hemostasis in nephrotic syndrome]. 140 55

Nephrotic syndrome (NS) is associated with several disorders of hemostasis: thrombocytosis and platelet hyperaggregability; increased plasma levels of factors V and VIII, and of fibrinogen with blood hyperviscosity; decreased plasma levels of natural anticoagulants: free protein S, and antithrombin III compensated by increased levels of alpha 2-macroglobulin; lowered fibrinolytic activity. Intensity of hypercoagulability is related to the degree of hypoalbuminemia; however, the role of hypercoagulability in the increased incidence of thromboembolic events, including renal vein thrombosis, is not proved. Clotting disorders are due to urinary losses of anticoagulants or to increased liver synthesis of procoagulants stimulated by hypoalbuminemia. Moreover, changes in clotting factors levels may be due to intravascular thrombin formation (marked by increased plasma levels of fibrinopeptide A). During active phases of glomerulonephritides (GN) with NS, thrombin formation might in fact arise in glomeruli, following activation of the glomerular hemostasis system. Isolated glomeruli from human crescentic GN, rabbit nephrotoxic GN and rat HgCl2 autoimmune GN produce excessive amounts of procoagulant (tissue factor) activity (PCA). Sequential studies of the self-limited HgCl2 GN showed that glomerular PCA, proteinuria and glomerular fibrin deposits peaked concomitantly at the acme of the disease, suggesting that immunologically mediated glomerular damage had triggered the extrinsic coagulation pathway.
 ...
PMID:Coagulation factors in nephrotic syndrome. 225 77

The cause of the thrombotic tendency in nephrotic patients is unknown. Recent reports of thrombotic complications in patients with deficiencies of protein C or protein S (natural inhibitors of coagulation) have raised the possibility that decreased levels of these proteins may play a role in the hypercoagulable state of nephrotic patients. We measured the levels of protein C, total protein S, and free protein S antigens in 42 patients (21 nephrotic and 21 non-nephrotic) with one of four types of glomerular pathology: diabetic nephropathy (DM), focal glomerular sclerosis (FGS), membranous glomerulonephritis (MGN), and chronic renal failure due to hypertension (CRF). Protein C and total protein S antigen levels were significantly higher in FGS and MGN than they were in DM or CRF. Free protein S levels were lower in DM than they were in MGN. Protein C, total protein S, and free protein S levels did not significantly correlate with either serum albumin or degree of proteinuria. The mean levels of the three proteins did not differ between nephrotic and non-nephrotic patients. Free protein S and protein C were, however, significantly correlated (P less than .005 and P less than .002, respectively) with the type of glomerular pathology, independent of differences in age, sex, serum albumin, or degree of proteinuria. These data suggest that abnormalities of free protein S and protein C are related to the nature of the underlying renal disease, rather than to the degree of proteinuria.
 ...
PMID:Protein S and C antigen levels in proteinuric patients: dependence on type of glomerular pathology. 252 34

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)
 ...
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.
 ...
PMID:Plasma concentrations of the natural anticoagulants protein C and protein S in patients with proteinuria. 316 Aug

Thromboembolic events remain one of the most serious complications in patients with nephrotic syndrome (NS). The natural anticoagulant system protein C-protein S was evaluated in patients with proteinuria and NS. Protein C levels were found to be normal or increased in NS. Protein C levels correlated positively with proteinuria, cholesterol and triglycerides and negatively with serum albumin. All of the 17 patients with NS exhibited urinary loss of protein C. Total protein S and C4BP were increased in mild and moderate forms of NS. Free protein S was identical in controls and NS patients. Nine of ten patients had urinary loss of protein S. No correlation was found between protein S and the various usual biologic parameters of NS. However, two patients with NS and thrombosis of the renal veins had an acquired deficit in either free protein S or protein C. Thus, in some patients, an acquired deficit in free protein S and/or protein C may contribute to the development of thrombotic complications in NS.
 ...
PMID:[Proteins C and S of coagulation: new markers of thrombotic risk in nephrotic syndromes?]. 328 98

A 42-yr-old woman with hypertension and renal involvement due to systemic lupus erythematosus (SLE) developed unilateral headache followed by the sudden onset of confusion and a grand mal convulsion. Cerebral computed tomography was normal. A magnetic resonance imaging angiogram revealed cerebral venous thrombosis and a venous infarct. Nephrotic syndrome had resulted in an acquired protein S deficiency. A review of previous cases suggests that either renal disease with proteinuria or features of the antiphospholipid syndrome are prerequisites for the development of cerebral venous thrombosis in SLE. Low free-protein S levels may be an additional risk factor. Furthermore it is likely that this condition is underdiagnosed.
 ...
PMID:Cerebral venous thrombosis and acquired protein S deficiency: an uncommon cause of headache in systemic lupus erythematosus. 763 1

Nephrotic syndrome (NS) is associated with an increased incidence of various thromboembolic complications in adult patients. It was found to be due to elevated factor IX (FIX) F.VII, F.VIII, F.V, fibrinogen, thrombocytosis and increased platelet reactivity. Acquired AT-III deficiency, reduced functional levels of protein S and reduced activity of protein C were also reported. We evaluated 15 children aged 1 to 13 years. Thirteen of these children suffered from nephrotic syndrome and two others had non-nephrotic proteinuria. All patients but one were normotensive. Two patients were not steroid responsive. Serum creatinine was normal for age in 14 patients. Kidney biopsy was carried out only in three children. Haemostatic parameters included protein C and S antigenicity in plasma and urine. Plasma levels of protein C and protein S were within the normal range. Protein C antigenicity in urine was increased in five children out of 14 examined. Protein S in urine was increased in seven out of 12 children examined. No thromboembolic phenomena were documented even though protein C and protein S antigenicity were identified in the urine.
 ...
PMID:Protein C and protein S in pediatric nephrotic patients. 904 58

A case of significant proteinuria occurred as a result of bilateral renal vein thrombosis secondary to dehydration, which resolved after treatment with urokinase. The patient developed nausea and vomiting from viral gastroenteritis with subsequent volume contraction. He later noted the onset of aching lower abdominal and flank pain. On admission, he was noted to have a serum creatinine of 1.7 mg/dL, and 4+ proteinuria on urinalysis. A 24-hour urine collection showed 2.34 g protein. A renal venogram showed bilateral renal vein thrombosis (RVT) without involvement of the inferior vena cava. Therapy was initiated with heparin at 1,000 U/hr, followed by intravenous (IV) urokinase, 4,400 U/kg bolus, followed by 4,400 U/kg/hr with continuous infusion for 12 hours. A repeat renal venogram done at this time showed partial resolution of thrombosis bilaterally. A second 12-hour infusion of urokinase at 5,000 U/kg/hr was performed; at this time, the patient reported resolution of his flank and abdominal pain. A repeat 24-hour urine collection showed 60 mg protein with a normal creatinine clearance. Levels of antithrombin III, protein C, and protein S were all normal. A renal biopsy was performed and showed normal histology on light, immunofluorescent, and electron microscopic evaluation. The patient has done well on no therapy and has had no recurrence of thrombosis or proteinuria after 2.5 years. This is a US government work. There are no restrictions on its use.
 ...
PMID:Resolution of proteinuria secondary to bilateral renal vein thrombosis after treatment with systemic thrombolytic therapy. 910 53

To elucidate the relationship between glomerular deposition of protein S (PS) and renal lesions or dysfunction, 30 patients with various glomerulopathies were examined. Glomerular PS deposition was found in 20 patients (group A), and other 10 patients showed no deposition (group B). PS was found mainly along the capillary loops and segmentally in the mesangium. Group A showed significantly more severe proteinuria than group B (p < 0.05). Group A patients showed significant decreases in glomerular filtration rate (p < 0.01). Patients in group A had significantly lower plasma levels of plasmin-alpha2-plasmin inhibitor complexes (p < 0.05) and thrombin-antithrombin III complexes (p < 0.01) than those in group B. Group A showed significant decreases in the mean values of plasma total PS (p < 0.01) and protein C (PC) antigens (p < 0.01) and C4b-binding protein (C4bp; p < 0.05) as compared with group B patients. There was a positive correlation between plasma PS and C4bp (p < 0.02). Histologically, group A showed a significantly higher incidence of glomerular deposition of factor XIII (subunit a), alpha2-plasmin inhibitor, PC (p < 0.05), and C4bp (p < 0.01). The present study demonstrates that glomerular PS deposition indicates the existence of PC and C4bp in the glomeruli and suggests that the glomerular PS deposition may modify the activation of fibrinolytic and coagulation systems within the glomeruli in various glomerulopathies.
 ...
PMID:Significance of glomerular deposition of protein S in various glomerulopathies. 945 2


1 2 Next >>