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)

Serum C4 and C3 concentration and binding of double-stranded-DNA (ds-DNA) were measured in sera from ninety-nine patients with systemic lupus erythematosus and clinical evidence of nephritis. C3 and C4 concentrations correlated poorly with ds-DNA binding. In sera from fifty-three patients, precipitating antibody was sought using the counterimmunoelectrophoretic technique. Precipitating antibody was detected on at least one occasion in 44% of the patients, and these sera with precipitating antibody showed higher binding of ds-DNA and lower C4 concentrations than those without precipitating antibody. In thirty-two patients, serial assessments of the activity of the renal disease were made using decline or improvement in glomerular filtration rate, degree of proteinuria, oedema and hypertension as indices of "activity". All patients were receiving immunosuppressive drugs. Active nephritis was rarely found in patients showing, at that time, a normal serum C4 or normal ds-DNA binding; but a raised ds-DNA binding or lowered serum C4 were found in both active and inactive nephritis. There was no correlation of activity with serum concentrations of C3, or the presence or absence of precipitating antibody. We conclude that measurements of serum-complement concentrations and binding of ds-DNA are of most use in the diagnosis of systemic lupus erythematosus, and that in patients with nephritis and taking immunosuppressive drugs, these tests are of limited use in guiding treatment.
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PMID:Disease activity in the nephritis of systemic lupus erythematosus in relation to serum complement concentrations. DNA-binding capacity and precipitating anti-DNA antibody. 108 78

Humoral immune processes mediate alterations in glomerular basement membrane (GBM) permeability by two mechanisms. One requires complement and polymorphonuclear leukocytes and the second is complement- and polymorphonuclear leukocyte-independent. The structural basis for enhanced GBM permeability induced by anti-GBM antibody is not clear. Experimental anti-GBM glomerulopathy was induced in guinea pigs by immunization with human GBM in complete Freund's adjuvant. Control animals received injections of complete Freund's adjuvant alone. Light, immunofluorescent, and electron microscopic studies were done on eight heavily proteinuric animals, four immunized nonproteinuric animals, three controls, and two normal animals. All animals that received injections of GBM had intense linear deposits of gamma2 anti-GBM antibody. Complement deposition was not demonstrable in vivo, and anti-GBM antibody deposits did not fix complement in vitro. Histologic abnormalities in proteinuric animals were confined to the GBM, which was of variable density and had a characteristic beaded thickening, with numerous areas of electron lucency most prominent in the outer aspect of GBM in peripheral portions of capillary loops. The inner margin and endothelium were normal. Ultrastructural tracer studies with ferritin demonstrated increased permeability confined to portions of GBM demonstrating ultrastructural lesions. The urine protein excreted by animals with ultrastructural GBM lesions was largely albumin. The absence of complement deposition accompanying anti-GBM antibody deposits in vivo and the unique GBM lesion in this model differ from the findings in nephritis induced by most heterologous nephrotoxic antibodies and suggest that GBM injury in this model is mediated by autologous antibody through complement-independent mechanisms. The selective proteinuria and ultrastructural lesions suggest a derangement in glomerular permeability functionally localized to the epithelial side of the GBM and could reflect an antibody-mediated abnormality in GBM biosynthesis.
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PMID:Experimental glomerulonephritis in the guinea pig. II. Ultrastructural lesions of the basement membrane associated with proteinuria. 108 38

Significant changes in glomeruli on light microscopy has been observed in 27 of 109 cadaveric renal allografts which functioned beyond 6 months. Tissue was available for study from all but two allografts. The histologic lesions were classified as follows: recurrent glomeruloneophritis, 9 cases (3 focal scierosis, 2 mesangial immunoglobulin A[IgA] disease, 2 mesangiocapillary glomerulonephritis, 1 dense deposit disease, 1 familial nephritis); de novo glomerulonephritis, 1 case (diffuse proliferative glomerulonephritis with crescents); and glomerular change of uncertain etiology, 17 cases (10 mesangiocapillary, 5 focal scierosis, 1 focal proliferative and 1 mesangial proliferative). These lesions were not distinguishable on light, fluorescent and electron microscopy from those in patients with spontaneous renal disease. All patients with glomerular lesions had proteinuria, and all but 3 had microscopic hematuria. Glomerular lesions were not significantly associated with early clinical rejection episodes or HLA compatibility. Presensitization of HLA antigens was significantly related to the occurence of a nonrecurrent glomerular lesion. Vescoureteral reflux was significantly more frequent in those with glomerular change (14 of 24) than in those without (13 of 48). Glomerular lesions were associated with a higher rate of graft loss due to renal transplant failure; renal function in survivors was significantly worse than in those without glomerular lesions.
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PMID:Glomerular lesions after renal transplantation. 109 56

Serial serum samples from a large number of patients with immunologic renal disease, normal healthy controls, acute infections as well as non-immunological renal disease were studied for the presence, nature and properties of cryoproteins, and these correlated with serial renal functional, morphologic, immunohistologic and clinical fingings as well as serologic observations. A high incidence of cryoproteins were found in renal disease thought to be mediated by immune complexes. Cryoprecipitates were not detected in the other patients. The presence of fibrinogen in a serum cryoprecipitate was always associated with rapidly progressive disease and poor prognosis. An association between the detection of cryoproteins and the clinical and morphological activity of disease was observed. Persistence of cryoproteinemia was associated with progression and apparent disappearance with resolution or progression to end stage renal disease. In patients with hematuria or proteinuria of questionable significance cryoprotein detection was always associated with immune complex nephritis. Renal transplantation in the presence of cryoproteinemia was associated with recurrent nephritis in the graft. Cryoproteins were found to have biologic properties attributable to antigen-antibody complexes, to contain immune complexes of antigen and antibody and to have serologic factors concentrated. The detection of serum cryoglobulins was found to be a better index of clinical and morphologic activity of immune complex renal disease than was serum complement. As in our previous studies, these proteins appear to be of diagnostic and prognostic value in renal disease and provide a method of antigen identification in these disorders.
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PMID:Cryoglobulins. III. Further studies on the nature, incidence, clinical, diagnostic, prognostic, and immunopathologic significance of cryoproteins in renal disease. 110 Dec 84

We describe three patients with arrested hydrocephalus in whom glomerulonephritis developed secondary to Staphylococcus epidermidis bacteremia from an infected ventriculoatrial shunt. Investigation of the immune-mediated renal disease associated with this chronic infection showed that (1) complement depletion during the acute phase of bacteremia and nephritis was predominantly via the classic pathway; (2) rheumatoid factor was associated with bacteremia, fever, proteinuria and low complement levels; (3) early complement components (C1q, C4, C3), immunoglobulin (predominantly immunoglobulin M [IgM], Staph. epidermidis antigen(s) and electron denxe subendothelial deposits were localized within the renal glomerulus; (4) C1q, and IgM derived from patient serums, were the most prominent in vitro immunoreactants to Staph. epidermidis cell walls; and (5) the causative organisms, Staph. epidermidis, shared common antigens with Staph. aureus, and antibody from patient serums cross reacted with extracts from both of these organisms.
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PMID:The role of complement, immunoglobulin and bacterial antigen in coagulase-negative staphylococcal shunt nephritis. 110 92

In guinea-pig nephrotoxic nephritis induced by a sheep antibody there was minimal glomerular capillary deposition of C3 and accumulation of polymorphonuclear leucocytes (PMN) in the heterologous phase. The C4-deficient strain developed the same injury as normal Duncan-Hartley animals. Complement depletion with cobra venom factor, polymorph depletion with nitrogen mustard or anti-PMN serum and treatment with antihistamines provided no protection. The relationship between the dose of nephrotoxic antibody and the proteinuria was similar for gamma1 and gamma2 subclasses and the F(ab')2 fragment of gamma1 antibody. However, the F(ab') and F(ab) antibody fragments, though fixing on the glomerular basement membrane, did not cause proteinuria. It is concluded that the development of proteinuria in this system: is largely independent of the complement-polymorph system; is due to the fixation of the F(ab')2 fragment of the antibody molecule; and does not depend on an intact Fc piece.
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PMID:Guinea-pig nephrotoxic nephritis. I. The role of complement and polymorphonuclear leucocytes and the effect of antibody subclass and fragments in the heterologous phase. 110 14

Pressures and flows were measured in surface glomerular capillaries, efferent arterioles, and proximal tubules of 22 Wistar rats in the early autologous phase of nephrotoxic serum nephritis (NSN). Linear deposits of rabbit and rat IgG and C3 component of complement were demonstrated in glomerular capillary walls by immunofluorescence microscopy. Light microscopy revealed diffuse proliferative glomerulonephritis, and proteinuria was present. Although whole kidney and single nephron glomerular filtration rate (GFR) in NSN (0.8 plus or minus 0.04 SE2 ml/min and 2 plus or minus 2 nl/min, respectively) remained unchanged from values in 16 weight-matched NORMAL HYDROPENIC control rats (0.8 plus or minus 0.08 and 28 plus or minus 2), important alterations in glomerular dynamics were noted. Mean transcapillary hydraulic pressure difference (deltaP) averaged 41 plus or minus 1 mm Hg in NSN versus 32 plus or minus 1 in controls (P LESS THAN 0.005). Oncotic pressures at the afferent (piA) end of the glomerular capillary were similar in both groups ( 16 mm /g) but increased much less by the efferent end (piE) in NSN (to 29 plus or minus 1 mm Hg) than in controls (33 plus or minus 1, P less than 0.025). Hence, equality between deltaP and piE, denoting filtration pressure equilibrium, obtained in control but not in NSN rats. While glomerular plasma flow rate was slightly higher in NSN (88 plus or minus 8 nl/min) than in controls (76 plus or minus 6, P greater than 0.2), the failure to achieve filtration equilibrium in NSN rats was primarily the consequence of a marked fall in the glomerular capillary ultrafiltration coefficient, Kf, to a mean value of 0.03 nl/(s times mm Hg), considerably lower than that found recently for the normal rat, 0.08 nl/(s times mm Hg). Thus, despite extensive glomerular injury, evidenced morphologically and by the low Kf, GFR remained normal. This maintenance of GFR resulted primarily from increases in deltaP, which tended to increase the net driving force for filtration, and thereby compensate for the reduction in Kf.
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PMID:Determinants of glomerular filtration in experimental glomerulonephritis in the rat. 112 1

The levels of serum orosomucoid, haptoglobin, and seromucoid were evaluated as possible quantitative criteria for the estimation of drug efficiency in adjuvant arthritis and nephrotoxic serum nephritis. In adjuvant arthritis, haptoglobin, seromucoid, and chiefly orosomucoid serum levels were generally very sensitive to anti-inflammatory agents such as phenylbutazone and pyridinol carbamate, and to immunosuppressive agents such as L-asparaginase. There was a significant correlation between the serum levels of these glycoproteins and the arthritis scores. In nephrotoxic serum nephritis, seromucoid levels were correlated with the proteinuria of the autologous phase and were found to be a good complementary criterion for the analysis of the efficiency of pyridinol carbamate, colchicine, iysine acetylsalicylate, and L-asparaginase.
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PMID:Biochemical criteria for the evaluation of drug efficiency on adjuvant arthritis and nephrotoxic serum nephritis in the rat: studies with phenylbutazone, L-Asparaginase, colchicine, lysine acetylsalicylate, and pyridinol carbamate. 114 23

A patient with hydrocephalus and a ventriculojugular shunt presented with acute nephritis, nephrotic syndrome (proteinuria 10 g/24 hours), decreased complement levels, circulating immune complexes and diminished creatinine clearance (41 ml/min). Seven blood cultures grew Corynebacterium bovis. A renal biopsy specimen revealed mesangiocapillary glomerulonephritis by light microscopy, and thickened glomerular basement membranes with areas of increased granular density by electron microscopy. Immunofluorescent examination of the biopsy specimen demonstrated 2+ granular glomerular basement membrane deposits of immunoglobulin M (IgM), with trace third component of complement (C-3), fourth component of complement (C-4) and immunoglobulin G (IgG). Rabbits immunized with C. bovis produced a line of partial identity in agar with patient serum against a sonicate of C. bovis. Indirect fluorescein staining of the biopsy specimen with the rabbit antiserum demonstrated 1+ granular glomerular basement membrane deposits. Potassium thiocyanate microelution of sections prior to examination markedly diminished staining with antihuman antiserum, but did not affect staining with rabbit antiserum. Following initial therapy with intravenous penicillin for six weeks the bacteremia cleared, serum complement levels returned to normal, proteinuria decreased and creatinine clearance increased. A relapse occured four weeks later with decreased complement levels, increased proteinuria and decreased creatinine clearance. Blood cultures were again positive for C. bovis. Following therapy with erythromycin and rifampin, the bacteremia cleared and there was a sustained improvement of all parameters. To our knowledge, this is the first time an association has been noted between C. bovis ventriculojugular shunt infection and glomerulonephritis. These findings support the potential role of C. bovis as an etiologic agent in human renal disease and further define the immune complex nature of shunt nephritis.
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PMID:Ventriculojugular shunt nephritis with Corynebacterium bovis. Successful therapy with antibiotics. 116 49

Mesangial deposits of IgA, occurring in the absence of systemic disease known to be associated with nephritis, were detected by immunofluorescence microscopy in renal biopsy specimens from 25 patients (4% of 630 specimens studied). Associated deposits of C3 were always present, usually with IgG, but IgM deposits were less common and C1q was never seen. On light microscopy most of the biopsy specimens showed mesangial of focal nuclear proliferation though some were normal. Fifteen of the 25 patients presented with macroscopic haematuria, which was usually recurrent and preceded by a sore throat, whereas the remaining, and usually older, patients presented with persistent proteinuria and were more likely to have impaired renal function. This incidence of "mesangial IgA disease" is less than that reported by French workers. There was a significantly high incidence of familial renal disease among these patients. No abnormalities of serum complement or IgA concentration were found.
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PMID:Isolated glomerulonephritis with mesangial IgA deposits. 116 37


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