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)

Antibodies directed against tubular brush border antigens (RTE) are used to induce heterologous immune-complex nephritis. Among these antigens a glycoprotein with a molecular weight of 330 kilodaltons (gp330) has been shown to be of pathogenetic significance. We investigated whether antibodies other than those directed against gp330 are present in anti-RTE and whether they play a pathogenetic role. By using enzyme-linked immunosorbent assay techniques and Western blotting, we investigated polyclonal antibodies directed not only against crude RTE but also against RTEgp, a purified glycoprotein fraction of RTE, with respect to activity against glomerular basement membrane (GBM) components laminin, fibronectin, and type IV collagen. Both antibody preparations showed reactivity predominantly to the 220 kilodaltons subunit of laminin. Lower but nevertheless distinct reactivity to fibronectin and type IV collagen was also found. The antibody fraction directed against components of the GBM, which was isolated from anti-RTE IgG by affinity chromatography, showed linear binding to the GBM in indirect immunofluorescence studies. Injection of these antibodies into the renal artery also led to linear binding to the GBM with linear deposition of complement factors 3 and 9 and induced a weak and transient proteinuria. Immunoelectron microscopy revealed binding of the antibodies to glomerular epithelial and endothelial cell surfaces adjacent to the GBM. Injection of anti-RTE antibody absorbed to GBM components resulted in binding of antibodies and complement factors 3 and 9 in a fine granular pattern along the GBM, whereas injection of unabsorbed anti-RTE led to a course granular pattern. We conclude that the presence of antibodies (cross-)reacting with laminin, fibronectin, and type IV collagen in anti-RTE antibody has pathogenetic effects and could explain differences in pathogenicity between monospecific anti-gp330 antibody and polyclonal anti-RTE antibody.
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PMID:Antibodies to purified renal tubular epithelial antigens contain activity against laminin, fibronectin, and type IV collagen. 327 61

The effect of lysozyme on intraglomerular immune complex deposition was examined in NZB/W F1 mice undergoing unilateral nephrectomy. Unilateral nephrectomy enhanced the glomerular immune complex deposition and glomerular lesions, which were suppressed by repeated intraperitoneal injections of lysozyme, in spite of unaltered serum anti-DNA antibody titers. DNA binding to the glomerular basement membrane (GBM) examined in vitro and that to glomeruli examined in vitro were also suppressed by lysozyme. An increased survival rate and decreased proteinuria were also induced by this basic protein. The mechanisms of the ameliorative effect were studied in vitro. DNA was bound to the GBM only in the presence of serum, plasma, or fibronectin. A similar inhibitory effect on DNA binding was also obtained by another polycation, hexadimethrine, in place of lysozyme. The in vitro findings suggest that DNA binding to the GBM is mediated by fibronectin, and that lysozyme electrostatically inhibits this binding, thereby possibly reducing the in situ DNA-anti-DNA complex formation in the GBM.
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PMID:Inhibitory effect of lysozyme on the intraglomerular immune complex formation in lupus mice. 334 56

The determinants of plasma colloid osmotic pressure were studied in 32 patients with preeclampsia and their matched control subjects. Although plasma colloid osmotic pressure was significantly related to preeclampsia, its severity, and proteinuria, it was most highly correlated with an elevated fibronectin level, suggesting that endothelial injury, rather than proteinuria, is the major mechanism of reduced colloid osmotic pressure in preeclampsia.
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PMID:Mechanisms for reduced colloid osmotic pressure in preeclampsia. 360 41

The teratogenic effects of the dioxin 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) have previously been studied in several species, and hydronephrosis has been reported to be a frequent abnormality in near-term fetuses. C57BL/6N female mice, given 12 micrograms/kg TCDD, P.O., on day 10 of gestation were killed on days 14, 15, and 16; fetal kidneys were collected and prepared for either immunofluorescent localization of several extracellular matrix components (ECM) or transmission electron microscopy (TEM). The TCDD-treated and control kidneys showed the same pattern of staining for fibronectin, but TCDD-treated kidneys displayed a diminished overall intensity. The intensity of laminin and type IV collagen immunofluorescence also appeared to be decreased, and deviations in the pattern of antibody binding were detected for differentiating TCDD-treated nephrons. Binding of the laminin antibody to the basal lamina was decreased in the parietal layer of Bowman's capsules in more advanced stages of differentiation. TEM analysis focused on the basal lamina of the tubules and Bowman's capsule. In TCDD-exposed kidneys, ECM components adjacent to differentiating nephrons were less abundant, and the basal lamina of the developing Bowman's capsules had a diminished lamina densa. The earliest nephrons to develop display these defects and comprise the first functional filtration units of the metanephric kidney. These ultrastructural changes noted in TCDD-exposed nephrons may promote proteinuria, a condition normally observed in the developing kidney when the filtration barrier is immature.
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PMID:TCDD alters the extracellular matrix and basal lamina of the fetal mouse kidney. 362 14

The possible relationship among blood rheology pattern, renal hemodynamics and proteinuria was investigated in 22 long-term insulin-dependent diabetic patients with overt nephropathy. Higher blood, plasma and serum viscosity and lower erythrocyte filtrability were found in our patients with overt nephropathy, than in patients without renal microvascular complications. Several negative correlations between blood viscosity and renal hemodynamic parameters (i.e., glomerular filtration rate and renal plasma flow) were demonstrated in the diabetics with overt nephropathy. Furthermore increased plasma fibrinogen, fibronectin and acute-phase protein levels were found in diabetics with overt nephropathy, compared to diabetics without renal changes. The data may suggest a pathogenetic role for blood rheology changes in the progression of diabetic glomerular complications.
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PMID:Hemodynamic alterations in long-term insulin-dependent diabetic patients with overt nephropathy: role of blood hyperviscosity and plasma protein changes. 366 7

Plasma fibronectin might play a role in the pathogenesis and progression of diabetic microvascular disease. To test this hypothesis we measured plasma fibronectin, von Willebrand factor antigen, fibrinogen, erythrocyte filtrability, whole-blood viscosity, proteinuria and albuminuria in 25 control subjects and 29 diabetic patients with and without microvascular complications. Plasma fibronectin was significantly higher in the diabetic patients, especially in those with retinopathy and nephropathy. A significant correlation between fibronectin and von Willebrand factor antigen was found in both patients with and without microangiopathy (p less than 0.001). In diabetic patients with and without microvascular complications, several significant correlations were found between increased fibronectin levels and reduced erythrocyte filtrability (p less than 0.001) and between the increase of fibronectin and whole-blood viscosity (p less than 0.001). Furthermore, a significant correlation was found between plasma fibronectin levels, proteinuria (p less than 0.001) and albuminuria (p less than 0.001). The relationship between plasma fibronectin and changes of blood rheology may be important for the occurrence and progression of diabetic microangiopathy.
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PMID:Plasma fibronectin, von Willebrand factor antigen, and blood rheology. Association with diabetic microvascular disease. 387 55

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

Plasma fibronectin levels increased significantly over time in MRL/l mice with progressive autoimmune disease. At 100 and 120 days of age both male and female MRL/l mice exhibited significantly higher fibronectin (Fn) levels than the more resistant MRL/l controls. Male mice at early time points had Fn levels no greater than controls due perhaps to the later onset of disease in MRL/l males. In contrast, female MRL/l mice, when compared with MRL/n controls, had higher Fn levels from 40 days of age. The proteinuria in these animals was also above MRL/n controls from the first time point taken (Day 40). In a temporal study with female MRL/l mice, Fn levels peaked at age 120 days and reflected the pattern of the survival curve, indicating that plasma Fn levels have an association with disease activity.
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PMID:The relationship between plasma fibronectin levels and autoimmune disease activity in MRL/l mice. 403 27

The distribution of fibronectin (FN) and the depositions of fibrinolytic components in human renal glomeruli with a variety of pathologic disorders were examined on biopsy specimens by immunofluorescence and immunoenzymatic methods. In a majority of the cases with thickening of capillary walls and/or with fibrin deposits in the capillary walls, staining for FN along the walls of the capillary loops (capillary pattern) was noted in addition to the staining in the mesangial area. In the capillary pattern with fibrin deposition, deposits of alpha 2-plasmin inhibitor and plasminogen, which are major components of the fibrinolytic system, were also seen along the capillary walls with a high frequency of occurrence. Plasminogen deposits, however, were found only in the glomeruli with deposits of alpha 2-plasmin inhibitor. There was no direct relationship between the degree of proteinuria and the appearance of the capillary pattern of FN or the deposition of the fibrinolytic components. These findings suggest that the appearance of FN in the walls of the capillary loops has some causal relationship with the local activation of blood coagulation factors which is frequently followed by activation of the fibrinolytic enzyme system.
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PMID:Fibronectin and deposits of fibrinolytic components in glomerular capillary walls. 405 Aug 85

We have measured plasma von Willebrand factor (VWF) as the factor VIII-related antigen, plasma fibronectin, and two of the serum somatomedins, insulin-like growth factor I (IGF I) and IGF II, in 51 diabetic patients and 25 nondiabetic control subjects. VWF was significantly higher in the diabetic group than in the controls (173 +/- 9% SEM versus 101 +/- 9%, P less than 0.001), as has been reported by others. However, within the diabetic group there was no significant difference in VWF between those patients without retinopathy, those with background or proliferative retinopathy, or those with macular edema. There was also no difference in VWF between the diabetic subjects with and those without proteinuria. These results rule against a previously advanced hypothesis that the increase in VWF in patients with diabetes is secondary to microangiopathy. No significant difference was observed in fibronectin, IGF I, or IGF II between the diabetic and control groups, between the diabetic group without retinopathy and the retinopathic subgroups, and between the diabetic subjects with and without proteinuria. In the diabetic patients, there was no correlation between diabetic control as assessed by glycosylated hemoglobin and glycosylated serum protein, and the plasma levels of VWF, fibronectin, IGF I, or IGF II. The results of this study strongly suggest that neither plasma VWF, fibronectin, IGF I, nor IGF II plays an important primary role in the pathogenesis of diabetic microvascular disease, although one or more of these factors might play a permissive role.
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PMID:Von Willebrand factor (VIII R:Ag), fibronectin, and insulin-like growth factors I and II in diabetic retinopathy and nephropathy. 636 66


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