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)

A patient with dermatitis herpetiformis, proteinuria and reduced renal function is described. A renal biopsy studied by light and immunofluorescence microscopy revealed a glomerulonephritis with deposits of predominantly IgA and complement C3. Deposits of IgA and C3 were also demonstrated in a biopsy from normal skin, and a common pathway for the skin and renal lesions is suggested.
 ...
PMID:Glomerulonephritis in dermatitis herpetiformis. A case study. 35 98

Eleven cases of mesangial proliferative glomerulonephritis whose kidney biopsies were studied with light, immunofluorescent, and electron microscopy are described. Nine patients presented with nephrotic syndrome, one with proteinuria and hematuria, and one with proteinuria alone. Morphologically mesangial proliferative glomerulonephritis was characterized by diffuse mesangial cell proliferation and some increase in mesangial matrix. On immunofluorescence, mesangial IgM deposition was observed in all cases and was considered a distinct feature of mesangial proliferative glomerulonephritis. Electron microscopy showed electron-dense granular deposits within the mesangial matrix in four cases. The clinical course was variable. Of the eight cases with nephrotic syndrome, four treated with steroids alone and four treated with steroids and cytotoxic drugs, one in each group achieved remission while the remaining patients continued to have steroid dependency or resistance. Two of these latter patients manifested steroid responsiveness, steroid resistance, and spontaneous remission at different times in their courses. Renal function remained normal in all. These cases demonstrate that mesangial proliferative glomerulonephritis is an entity characterized by increased mesangial cellularity, deposition of IgM in a mesangial distribution, a relatively benign course, and variable response to treatment.
 ...
PMID:Mesangial proliferative glomerulonephritis. 35 24

Proliferative glomerulonephritis with proteinuria was induced in Wistar rats by bovine serum albumin (BSA). Rats were first immunized with 1 mg or 2.5 mg of BSA and complete Freund's adjuvant (CFA) and eight weeks later 1 mg of BSA were given intravenously six times a week for four weeks. Immunofluorescence revealed granular deposits of IgG, C3, and BSA in the mesangial area with or without deposition of the same components along the capillary wall. Evaluation of the circulating antibody disclosed an apparent correlation between the level of antibody and histological findings. Rats with an intermediate amount of antibody production developed mesangial widening with mesangial immune deposits and no proteinuria. Rats with a low response developed proliferative glomerulonephritis with immune deposits along the capillary wall as well as in the mesangial area and proteinuria.
 ...
PMID:Bovine serum albumin (BSA) nephritis in rats. I. Experimental model. 36 54

The present study describes 3 patients with the simultaneous occurrence of diabetic nephropathy and immune-complex mediated glomerulonephritis. Renal manifestation included proteinuria and hematuria which were preceded by or co-existent with an infectious process. Renal manifestation included proteinuria and hematuria which were preceded by or co-existent with an infectious process. Renal histology showed the characteristic change of diabetic nephropathy along with those of immune complex glomerulonephritis. Immunofluorescence studies showed a linear pattern with a superimposed granular pattern of IgG and C3 deposits. Renal function and urinary findings improved in the 2 patients who were followed up.
 ...
PMID:Diabetes mellitus with immune complex glomerulonephritis. 37 11

We studied the interaction of two different forms of immune glomerular damage occurring simultaneously: anti-glomerular basement membrane (GBM) antibody fixation and immune elimination of bovine serum albumin (BSA). 125I-radiolabelled BSA anti-BSA immune complexes, formed in response to a single small intravenous dose (150 mg/kg) of 125I BSA, did not cause proteinuria in control animals within 15 days, despite evidence of immune elimination of the antigen. Similarly, a small dose of nephrotoxic globulin (NTG)(3.0 mg/kg) did not cause immediate proteinuria in controls. Test animals received the BSA injection followed by the NTG injection 5, 7 or 9 days later. In this way, antibody fixed to glomerular basement membrane antigens at various times after BSA anti-BSA complexes first appeared in the circulation. Animals were killed on day 15. Fifteen of the eighteen test animals developed moderate to severe clinical nephritis. The onset of the nephritis coincided with BSA elimination irrespective of when the NTG was given. Greatly increased amounts of nonlinear immunofluorescent deposits were demonstrated in the glomeruli of test animals. We concluded that there was a marked synergistic effect between two forms of immune glomerular damage (i.e. that mediated by anti-GBM antibody and immune complexes), which appeared to be due to the increased deposition of complex material in the presence of active fixation of anti-GBM antibody. The relevance of this finding to human glomerulonephritis is discussed.
 ...
PMID:The interaction of anti-glomerular basement membrane antibody deposition with immune elimination of bovine serum albumin in the rabbit. 37 80

A brief review of the classical and the alternative pathways of complement activation is presented. Clinically, according to the complement system, we can divide the children with glomerulonephritis into two groups, normocomplementemic and hypocomplementemic. In addition, inherited complement deficiencies can be identified associated with renal diseases. We discuss the three possible sources of complement in urine, although more control studies are necessary in patients with different causes of proteinuria in order to define the clinical significance of complementuria. The immunohistological results of glomerular nephritic biopsy material by the fluorescence antibody technique is analyzed with respect to clinical diagnosis and evaluation of the treatment. The nature of C3NeF as an antibody to factor B-C3 complex is demonstrated by different groups and in different diseases. Finally, the presence of a receptor for complement in the glomerulus, is explained in human disease by the deposition of immune complexes into the renal glomeruli.
 ...
PMID:The complement system in pediatric renal disease. 39 7

Five of six lactating rats did not develop proteinuria after an injection of nephrotoxic serum, whereas four out of five non-lactating, non-pregnant rats showed the usual proteinuric response (P = 0.06). The amount of heterologous IgG deposits was similar in both groups, but the lactating rats had significantly less autologous IgG (P = 0.004) in the glomerular basal membrane. It is suggested that hormonal factors influence the development of experimental glomerulonephritis in lactating rats.
 ...
PMID:Suppressed development of experimental glomerulonephritis in lactating rats. 39 36

A patient with disseminated malignant melanoma developed mild renal failure with proteinuria four months following the diagnosis of his neoplasm. Renal biopsy showed a membranoproliferative glomerulonephritis. Electron microscopy revealed intramembranous dense deposits in the glomeruli as well as in tubular basement membranes and Bowman's capsule. Immunofluorescence microscopy demonstrated granular staining for C3 in these same locations and granular deposits of immunoglobulins in the glomerular capillary loops. Light and electron microscopy of the autopsy kidney obtained 5 months later revealed progression of the number, size and density of the deposits. Eluates from both autopsy and biopsy kidney contained melanoma antigen and anti-melanoma antibodies. This case illustrates the association between the dense deposits and neoplasia with the dense deposits representing immune complexes with the tumor as antigen.
 ...
PMID:Malignant melanoma with renal dense deposits containing tumor antigens. 39 45

In a comprehensive survey the diagnostic and therapeutic problems of pyelonephritis and glomerulonephritis are discussed. The importance of thorough nephrological diagnostics is pointed out. The first section of the paper describes the diagnostic procedures such as x-ray and laboratory work (tubular proteinuria, antibody-coated bacteria) and the chemotherapy in pyelonephritis. The second part deals with glomerulonephritis, the aspects of histological classification, etiology, pathogenesis, diagnostic principles, prognosis, and results of therapy with penicillin G (acute form), corticosteroids, azathioprine, indomethacin, and cyclophosphamide.
 ...
PMID:[Diagnosis and therapy of pyelonephritis and glomerulonephritis]. 41 72

Rats given N,N'-diacetyl benzidine (N,N'-DAB) by intraperitoneal injections were studied to further characterize the ensuing renal disease. Significant proteinuria and albuminuria occurred at 10 weeks and thereafter and was enhanced by prior unilateral nephrectomy. Glomerular epithelial cell vacuolization and cyst formation were marked in proteinuric rats. Focal glomerular sclerosis and synechia were present, but proliferative crescent formation was not. Glomerular fibrinogen was noted, but no immunoglobulins or C3 was detected by immunofluorescence microscopy. Glomerular epithelial cell cysts and disruption were noted ultrastructurally, but no electron-dense deposits were seen. Tubular basement membrane thickening and wrinkling were noted in N,N'-DAB rats, and maximum urine osmolarlity was decreased. None of the animals developed renal insufficiency. Parenteral N,N'-DAB-induced renal disease is different from crescentic glomerulonephritis noted in rats fed N,N'-DAB and has similarities to an experimental model of aminonucleoside induced focal sclerosis, supporting the theory of primary glomerular epithelial cell injury mediating proteinuria and focal sclerosis.
 ...
PMID:Characterization of chronic N,N'-diacetylbenzidine-induced nephropathy. 42 29


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>