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)

The plasma levels of factor VIII related antigen (FVIIIRA), factor VIII coagulant activity (FVIIIC) and the ratio between them were evaluated in 57 patients with kidney disease of diverse etiology, and with either normal (49) or impaired (8) renal function. Renal biopsy specimens were obtained from 47 patients with normal renal function. No correlation was observed between the increased plasma values of FVIIIRA and FVIIIC and renal function, histologic findings, and the pattern of deposition of immunoglobulin and complement. In contrast, plasma levels of both components of factor VIII were positively correlated with the magnitude of proteinuria. In the authors' opinion, the determination of factor VIII components is of no value in establishing the diagnosis and prognosis of patients with kidney disease. The finding on immunofluorescence of simultaneous deposition of factor VIII and C3 in the arteriolar walls might suggest incipient atherosclerotic damage. The FVIIIRA/FVIIIC ratio was increased in 87% of the patients and particularly in those with membrano-proliferative glomerulonephritis and chronic renal failure; however, the clinical relevance of this finding remains to be elucidated. The significant correlation between the two components suggests that in renal disease a simultaneous aggregation of the two proteins in factor VIII takes place.
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PMID:Clinical significance of plasma factor VIII levels in renal disease. 679 66

Levels of factor VIII/von Willebrand factor were measured in 105 patients affected by glomerulonephritis either of primary origin or associated with systemic diseases. The median plasma concentration of factor VIII-related antigen was significantly higher in the patients than in healthy controls. Amongst patients with primary glomerulonephritis, higher levels were observed in minimal change nephropathy than in other types. In patients with secondary glomerulonephritis, plasma factor VIII-related antigen was particularly elevated in lupus nephritis and in renal amyloidosis. Altogether, patients with the nephrotic syndrome showed higher levels than patients with lesser degrees of proteinuria. A negative correlation was found between the plasma concentration of factor VIII-related antigen and that of serum albumin but no correlation was observed with the extent of proteinuria. In 48 patients, plasma factor-VIII procoagulant activity was also measured and found to be elevated to the same extent as factor VIII-related antigen in the majority of cases. The urinary excretion of factor VIII-related antigen, evaluated in 72 patients, was found in variable amounts in 31 cases without any correlation with proteinuria. Glomerular deposits of factor VIII-related antigen were an uncommon finding. After 24 months, there was no clear evidence of an unfavourable association between increased plasma levels of factor VIII-related antigen and the course of the disease. Our findings suggest that the measurement of levels of factor VIII/von Willebrand factor in plasma or urine must be interpreted with caution in predicting the clinical course of patients affected by glomerular disease.
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PMID:Factor VIII/von Willebrand factor in glomerular nephropathies. 679 18

Factor XII clotting activities and antigen levels were assayed in 14 plasma samples from 10 patients with nephrotic syndrome; the group was heterogeneous clinically and histologically. Factor XII was low at initial sampling in 7 of the 10 patients; in 7 of the 14 samples, factor XII antigen was in excess over clotting activity. Inhibition of factor XII could not be demonstrated; excess plasma antigen and urinary antigen (when present) had normal patterns on crossed-immunoelectrophoresis, indicating no major changes in charge or size. In 3 patients tested more than once, plasma levels of factor XII were increased up to 6fold in steroid-induced remission. Of other hemostatic factors assessed for comparison, factor VIII was elevated in 11 of the 14 samples; eight of these had elevated factor VII levels as well. Eight samples from six patients showed low antithrombin III levels; one of these patients had recurrent thromboses. Antithrombin III levels correlated with the serum albumin concentration. Only two of the eight urines tested had detectable factor XII antigen; a third had factor IX and prothrombin and no factor XII. Plasminogen and antithrombin III were readily demonstrated in all urine samples with higher concentrations in those patients with less selective proteinuria. Urinary and plasma levels were not correlated, suggesting that increased consumption or turnover was not simply related to increased filtration.
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PMID:Factor XII and other hemostatic protein abnormalities in nephrotic syndrome patients. 681 92

Factor VIII coagulant activity (VIII C) and factor VIII-related antigen (VIII R:Ag) were studied in 86 insulin-dependent diabetic children. All children were without signs of vascular disease based on a negative funduscopy, negative fluorescein angiography, normal serum creatinine levels, and absence of proteinuria. Age ranged from 4 to 17 yr; duration of clinical diabetes ranged from 1 to 12 yr. The children were grouped according to their urinary sugar excretion, the HbA1 levels, and the duration of clinical diabetes. The group with high urinary sugar excretion and the group with high HbA1 levels had a significantly higher VIII C than the group with low urinary sugar excretion and the group with low HbA1 levels. VIII C levels did not differ significantly in the groups with a different duration of clinical diabetes, but VIII R:Ag was significantly higher in the group with the longest duration of diabetes as compared with the group with the shortest duration. VIII R:Ag levels did not differ significantly in the groups with different degrees of urinary sugar excretion or different HbA1 levels. The results show that in children without vascular disease, and even in children with a short duration of diabetes, alterations of the factor VIII complex can be demonstrated.
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PMID:Elevated factor VIII activity and factor VIII-related antigen in diabetic children without vascular disease. 681 42

The interaction of the endogenous vasoconstrictors endothelin (ET), angiotensin II (Ang II) and catecholamines with the kallikrein-kinin-, prostaglandin and renin-aldosterone systems in the pathogenesis of acute renal failure (ARF) is still to be defined. In 18 anesthesized pigs the influence of i.v. bolus applications of ET (2 micrograms/kg), Ang II (10 micrograms/kg) and norepinephrine (NE; 20 micrograms/kg) on hemodynamics, plasmatic coagulation and fibrinolysis system, prostaglandins and renal function was studied. ET induced a biphasic change in blood pressure, starting with an initial short-lasting reduction followed by a long-lasting elevation of systolic and diastolic blood pressure. Endothelin bolus resulted in a significant increase of 6-keto-PGF1 alpha, PGE2 and TXB2 plasma levels (P < 0.05 against preinjection values), whereas prostaglandins remained unchanged in the Ang II and NE groups. There was a distinct correlation between the plasma ET and 6-keto-PGF1 alpha levels (r = 0.82). In contrast to Ang II or NE, ET induced a shortening of the activated partial thromboplastin time (aPTT) and increase of antithrombin III levels (ATIII), fibrin monomers (FM), prekallikrein (PKK) and factor VIII activity at the beginning. Finally a pronounced decrease of ATIII, FM and PKK occurred, indicating a consumptive coagulopathy. At the end of the experiment, elevated plasma renin activity and pCO2, significantly decreased creatinine clearance, blood pH, pO2, base excess, HCO3-, oxygen saturation (P < 0.01), a distinct glomerular proteinuria, and a final anuria were observated. These results reveal that ET activates the plasmatic coagulation system and induces an ARF accompanied by impairment of pulmonary function.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of endothelin on hemodynamics, prostaglandins, blood coagulation and renal function. 775 79

Morphological examination of renal biopsies from 90 women with preeclampsia (PE), assessment of the clinical data and clinicomorphological correlations produced the following results: 1. By light-microscopy the renal lesions in PE imitate a picture of glomerulonephritis of mesangial type with different degrees of severity. 2. Morphometric investigations confirmed the impression gained by light-microscopy of swelling of endothelial cells and podocytes as well as endocapillary cell proliferation and enlargement of the glomeruli. 3. The immunohistological findings are non-specific and argue against immune complex deposition, but are suggestive of insudative processes. In addition immunohistological investigations of fibronectin and factor VIII-associated antigen reveal a pathogenetic relevant alteration of endothelial cell. 4. Electronmicroscopy is the most valid diagnostic method allowing subdivision of the quantitative different lesions in various degrees of severity. Furthermore the use of this method allows elucidation of the dynamics of the underlying disease process, which progresses through successive stages i.e. early, fully developed and late stage, supporting the reversibility of these glomerular lesions. 5. Close correlations are found between the clinical parameters and morphological findings in nephropathy in pregnancy-induced hypertension. The hypertension, proteinuria and nephrotic syndrome, which characterize the clinical picture, correlate with the severity of the glomerular lesions and the further course of the disease. Moreover, hypertension also correlates with mesangial and subendothelial deposits and with focal segmental hyalinosis and sclerosis, occurring in some cases. The focal segmental hyalinosis and sclerosis should be regarded as hyperperfusion-lesions indicating benign nephrosclerosis and developing only facultatively in PE. 6. The first morphological substrate of nephropathy in pregnancy-induced hypertension with the key to pathogenesis present itself as endothelial lesion, possibly caused by oxygen free radicals, lipid-peroxides or hyperfusion. In result of the endothelial lesion an imbalance of the different mediator systems i.e. thromboxane-prostacyclin, endothelin-EDRF with dominance of vasoconstrictive reactions would be effective. Thus the following induction of coagulative, vasoconstrictive and proliferative processes results in the characteristic glomerular lesions in PE.
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PMID:[Nephropathy in pregnancy--an endothelial lesion?]. 817 90

In search of the basic defect and cell type responsible for the massive treatment-resistant proteinuria of congenital nephrotic syndrome of the Finnish type (CNF), we examined tissue samples of CNF kidneys using established antibody and lectin markers of various glomerular cell types. Markers of vascular endothelium (antibodies to factor VIII and a human homologue of podocalyxin (anti-PHM5) and UEA I lectin) showed no qualitative changes in the endothelial cells of glomeruli or peritubular areas in CNF as compared with controls. Markers of glomerular mesangial cells (antibodies to desmin, smooth muscle actin, RCA I lectin) revealed a secondary increase in mesangial reactivity reflecting the sclerosis and expansion of the mesangial areas in CNF. Markers of visceral epithelial cells (antibodies to a human homologue of podocalyxin, C3b receptor, vimentin, common lymphocytic leukemia antigen, gp44, and the WGA, LFA and, after neuraminidase treatment, PNA lectin) failed to show appreciable qualitative changes in CNF kidney samples. Interestingly, the alpha 2 beta 1 integrins appeared greatly reduced in all CNF samples studied, possibly explaining the mechanisms of CNF-associated proteinuria.
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PMID:Glomerular antigens in severe hereditary nephrosis. 854 48

A 1-year-old boy with hemophagocytic lymphohistiocytosis exhibited proteinuria 1 month after unrelated cord blood cell transplantation, which persisted without hematuria. Laboratory study showed an increase of factor VIII-related antigen and total plasminogen activator inhibitor, suggesting endothelial injury. Histological examination of autopsy materials showed increased mesangial matrices and double-contoured basement membranes, and ultrastructurally, swelling of the endothelial cells and widening of the subendothelial space with mesangial interposition. Thrombosis was not observed at any of the sites. This case may be vasculopathy distinct from thrombotic microangiopathy (TMA) or a variant form of TMA following blood stem cell transplantation (BSCT). This vasculopathy should be considered in the differential diagnosis of proteinuria in the early stages after BSCT.
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PMID:Glomerular vasculopathy after unrelated cord blood transplantation. 1270 Sep 71

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.
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PMID:49, XXXXY syndrome with unilateral renal aplasia, proteinuria, and venous thromboembolism. 1564 56

We encountered a 2-year-old boy with acquired haemophilia, which rarely occurs in children, who was complicated with nephrotic syndrome. In mid-August 2001, he was diagnosed to have nephrotic syndrome based on the presence of massive proteinuria and hypoalbuminaemia. Activated partial thromboplastin time (APTT) was normal at 42.4 s at that time. After starting prednisone administration of 2 mg kg(-1) day(-1), the proteinuria disappeared immediately. However, in early October the same year, subcutaneous ecchymosis and intramuscular bleeding occurred for no apparent reason, and from the examination results his APTT was 106.4 s, factor VIII (FVIII) activity was <1%, and the anti-FVIII inhibitor titre was 6.9 BU ml(-1). As a result, he was diagnosed to have acquired haemophilia. The anti-nuclear antibody and anti-phospholipid antibody were negative. With recombinant activated FVII, haemostasis was obtained, and after administering three courses of steroid pulse therapy (methyl prednisolone: 20 mg kg(-1) day(-1) x 3 days), the anti-FVIII inhibitory activity disappeared. An analysis of the immunological and coagulation properties of his FVIII autoantibodies showed the anti-FVIII inhibitory activity to be mediated by IgG(1) antibody. In other words, his FVIII inhibitor was a Th1 dominant and it provided a good response to treatment. These findings correlate with those of previous reports. The patient thereafter frequently demonstrated a recurrence of nephrotic syndrome. As a result, he is presently being managed with cyclosporine. However, no recurrence of the anti-FVIII titre has been observed.
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PMID:Successful steroid pulse treatment in childhood acquired haemophilia with nephrotic syndrome. 1587 76


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