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 distribution of heparan sulfate proteoglycan (HS-PG) was examined electron microscopically by the high iron diamine (HID) method in puromycin aminonucleoside (PAN) nephrosis, accelerated Masugi nephritis (NTN), and serum sickness nephritis induced by bovine serum albumin (BSA nephritis) in the rat. In PAN nephrosis rats, no change was observed in the distribution of HS-PG in the lamina rara externa (LRE) of the glomerular basement membrane (GBM) throughout the experiment. In NTN rats, however, the loss of HS-PG was observed, and it was associated with subepithelial electron dense deposits formed possibly by serum sickness mechanism, but not with inflammatory cell infiltration. In BAS nephritis, immune deposits were seen in mesangial, subendothelial, intramembranous and subepithelial areas. The deposits in the former three areas seemed to have little reciprocity with the loss of HS-PG and proteinuria. Urinary protein increased in accordance with the development of subepithelial deposits and the loss of HS-PG in the area of the deposits in the LRE. These results indicate that HS-PG could be preserved even in marked proteinuric states in morphologically intact basement membrane, but altered and lost distribution of HS-PG associated with subepithelial immune deposits could in turn result in the development of proteinuria.
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PMID:Altered glomerular localization of heparan sulfate proteoglycan in experimental nephritides. 294 56

To evaluate the role of macrophages in glomerulonephritis, the relationship between the existence of macrophages and proteinuria in the long course of glomerulonephritis was studied in accelerated Masugi nephritis in the rat. Non-specific esterase staining was used as a marker of macrophages and the kinetics of glomerular macrophages was analysed by an image processor. Macrophages became detectable 48 hours after nephrotoxic serum injection and their accumulation reached a maximum level at 5 days. At 1 month, they had clearly decreased. At 3 months, however, many macrophages were found within the capsular drop-like lesions and crescents. Urinary protein excretion took roughly the same time course as the number of macrophages for 2 weeks. However, at 1 month, whereas macrophages had decreased, the proteinuria kept a persistently high level. At 3 months it showed a tendency to decrease. The correlation between the rate of appearance of macrophages and the urinary protein excretion assessed in 20 cases exhibited no significance. In addition, discrepancy in their time course was evident at 1 month. Although macrophages may happen to contribute to the tissue injury resulting in proteinuria in the early phase of nephrotoxic serum nephritis, factors other than macrophages should be considered in the subsequent duration of proteinuria in this model.
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PMID:Macrophages in glomerular injury. I. The kinetics of macrophages in accelerated Masugi nephritis in the rat. 315 78

Experiments were undertaken to clarify whether a large dose of methylprednisolone (MPSL) could have any suppressive effect on progressive Masugi nephritis in the rabbit. Progressive crescentic Masugi nephritis could be induced with high reproducibility by preimmunization with a small amount of nephrotoxic duck gamma-globulin incorporated with complete Freund's adjuvant, followed by an intravenous injection 4 days later. Two groups of rabbits treated with 80 mg/kg of MPSL either before or after the development of proteinuria, showed a significant decrease in both antibody titers and serum creatinine levels during treatment. Histologically, the prominent diffuse intracapillary proliferation and crescent formation observed in controls, were markedly diminished. Accumulations of monocytes in the intra- and extracapillary space were also decreased. These results suggest that suppression of antibody production by a large dose of MPSL is one of its most fundamental actions, and can prevent the processes leading to crescentic glomerular lesions.
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PMID:Effect of methylprednisolone on progressive Masugi nephritis in the rabbit. I. Suppression of antibody production and crescent formation. 611 Nov 56

Experiments were undertaken to ascertain whether progression of crescentic Masugi nephritis in rabbits could be prevented by the administration of Bredinin (BR). Crescentic glomerulonephritis can be induced with high reproducibility by intramuscular preimmunization on day 1, followed by intravenous injections on days 3 and 5 of nephrotoxic duck gamma-globulin (NTD gamma-gl). 30 rabbits were divided into 3 groups including controls (group 1). Two groups of 10 nephritic rabbits were each treated with 10 mg/kg of BR either after or before the development of proteinuria (groups 2 and 3). In group 3, the onset of proteinuria showed a significant delay and duration of survival was significantly prolonged, compared with controls. Serum antibody titers after day 8 and creatinine levels after day 10, as well as the initial amounts of proteinuria, were also significantly lower during treatment in group 3 than in controls. Histologically, the prominent diffuse intra- and extra-capillary proliferation with monocyte accumulations observed in the control group were markedly diminished in group 3. These results suggest that early treatment in crescentic glomerulonephritis with BR will suppress the production of humoral antibody and prevent progression of the glomerular lesions.
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PMID:Modification of crescentic Masugi nephritis in the rabbit by Bredinin, a new immunosuppressant. 613 99

Nephrotoxic activity of rabbit antisera to glomerular basement membrane (GBM) from three different donors (rat, gerbil, and man) was examined in mice of various strains. Animals receiving a small dose (0.1 ml) of anti-rat GBM or a large dose (0.3 ml X 2) of anti-gerbil GBM developed massive proteinuria and irreversible glomerular lesions which were identical to those seen in rats receiving anti-rat GBM, i.e. rat Masugi nephritis. Linear deposition of rabbit IgG, host's immunoglobulins and C3 was characteristically seen. Necrotizing changes and crescent formation accompanied by plasmic exudation, cellular proliferation and/or infiltration of PMNs and monocytes occurred after the injection. In animals receiving anti-human GBM, linear deposition of rabbit IgG and less marked glomerular changes were seen. The finding of no specificity in species between GBM antigens of rat and mouse indicates the usefulness of rat GBM for mouse Masugi nephritis or anti-GBM disease.
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PMID:Masugi nephritis produced by the antiserum to heterologous glomerular basement membrane. I. Results in mice. 701 88

Anti-rat glomerular basement membrane (GBM) rabbit serum was produced by immunizing rabbits with the supernatant substance of trypsin-digested rat GBM. Nephritis was induced in rats by a single intravenous administration of 0.25 ml of anti-serum and changes in pathohistological and biochemical parameters during the process of the disease were investigated in comparison with those of Masugi nephritis and the modified type of Masugi nephritis previously reported. In light microscopic studies, histological changes seen in the kidneys closely resembled those of typical human glomerulonephritis. Changes such as hypercellularity, adhesion between capillary wall and Bowman's capsule, crescent formation and hyalinization in glomeruli and interstitial infiltration were the most pronounced on the 30th day after the anti-serum injection. In immunofluorescent studies, a linear fixation of rabbit IgG was observed along the GBM from the 1st day and the staining of a certain intensity was preserved throughout the experimental periods. A linear staining with anti-rat IgG serum was recognized from the 10th day. The fixation of fibrinogen was also seen in not only the glomerular capillary walls, but also in Bowman's space after the 10th day. Proteinuria significantly increased from the 1st day, reached a peak of 12 times the control level, and thereafter gradually decreased. The patterns of progress of urinary alkaline phosphatase and N-acetyl-beta-glucosaminidase activities were much the same as those seen in cases of proteinuria and the levels at their peak times were about 10 and 3 times control levels, respectively. Plasma urea nitrogen level transiently increased on the 5th day and then reverted to the control level by the 30th day. Plasma cholesterol levels were significantly high from the 5th to the 20th days. It is concluded that glomerular damages in this model are more severe, so-called, "nephritic type" and continue for longer periods than in cases of Masugi nephritis, however, do not differ in degree and duration from findings in the modified type of Masugi nephritis.
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PMID:[Pharmacological studies on experimental nephritic rats (11). Changes in pathohistological and biochemical parameters in anti-rat GBM rabbit serum-induced nephritis (author's transl)]. 728 45

The role of cell-mediated immunity in glomerular injury has been extensively studied, but the precise mechanism remains obscure. This study was undertaken to determine whether the homologous glomerular basement membrane (GBM) combined heterogeneous anti-GBM antibody would induce cell-mediated immunity. Wistar-Kyoto rats were divided into three groups; group I rats were immunized with homologous GBM antigen that was derived from Masugi nephritis and emulsified in complete Freund's adjuvant (CFA); group II rats were immunized with homologous GBM antigen that was derived from normal rats and emulsified in CFA; group III rats were immunized with CFA only. Group I rats demonstrated proteinuria on days 7 and 10 after immunization. Histologically, mesangial cell proliferation and cell infiltration were observed in the glomeruli. No changes in tubulointerstitial tissue. CD4-positive cells, CD8-positive cells and macrophages were found in the glomeruli, and mononuclear cells were found in the glomerular capillary lumen. Group II and Group III rats demonstrated no proteinuria and no histological changes. These findings indicated that the altered GBM obtained antigenicity and induced cell-mediated immunity in the glomeruli.
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PMID:[Studies on cell-mediated immunity (CMI) in the glomeruli: immunization with GBM antigen from Masugi nephritis in Wistar-Kyoto rats]. 813 54

The effects of Dilazep on immunologically induced glomerular injuries were examined. Accelerated Masugi nephritis in rats produced glomerulosclerosis with proteinuria following administration of a single dose of nephrotoxic serum (NTS). When 5 mg/kg/day of Dilazep had been administered prior to the NTS injection, the proteinuria was resolved rapidly after reaching a maximum level. The glomeruli 3 months later showed significant suppression of glomerulosclerosis and lesser adhesive lesions as compared to those in control rats with Masugi nephritis. On the other hand, when Dilazep was administered from 2 weeks after the injection of NTS, the rats displayed persistent proteinuria and glomerulosclerosis at similar levels to those in the Masugi group. Dilazep appears to exert some protective effects in the early stages of glomerular injuries induced by immunological mechanisms.
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PMID:Dilazep prevents glomerulosclerosis in accelerated Masugi nephritis in the rat. 834 Oct 8

Intercellular adhesion molecule-1 (ICAM-1, CD54), an adhesion molecule of the immunoglobulin superfamily, is an endothelial cell surface ligand for such leukocyte integrins as lymphocyte-function-associated molecule 1 (LFA-1, CD11a/CD18), Mac-1 (CD11b/CD18) and CD43. These molecules mediate adhesive interactions between leukocytes and endothelial cells and are critically involved in infiltration of leukocytes into inflammatory lesions. We examined the expression of ICAM-1 in renal tissues of Masugi nephritis rats and directly examined the role of ICAM-1 by administration of neutralizing monoclonal antibodies (MAbs) to rat ICAM-1, LFA-1 alpha-subunit (LFA-1 alpha), beta-subunit (LFA-1 beta) and Mac-1 alpha-subunit (Mac-1 alpha). Within 3 h after injection of nephrotoxic serum, increased expression of ICAM-1 was detected in the glomeruli by in situ hybridization and an immunofluorescence study. Proteinuria was significantly suppressed by the MAbs against ICAM-1, Mac-1 alpha and LFA-1 beta. Neutrophil infiltration into the glomeruli was significantly prevented by injection of the MAbs against ICAM-1, LFA-1 alpha and LFA-1 beta. These results indicate that both ICAM-1/LFA-1 and ICAM-1/Mac-1 pathways are involved in neutrophil infiltration into the glomeruli. On the other hand, monocytic infiltration was prevented by the MAbs against ICAM-1, LFA-1 alpha and LFA-1 beta but not by anti-Mac-1 alpha MAb. Due to these results, ICAM-1 is considered to be a critical molecule involved in the pathogenesis of the leukocyte infiltration into the glomeruli in the heterologous phase of Masugi nephritis. Anti-ICAM-1 antibody may be beneficial in the treatment of leukocyte-mediated glomerular diseases.
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PMID:The critical role of intercellular adhesion molecule-1 in Masugi nephritis in rats. 877 54

The ability of macrophages to cause acute inflammatory glomerular injury is well-established; however, the role of macrophages in the fibrotic phase of chronic kidney disease remains poorly understood. This study examined the role of macrophages in the fibrotic phase (days 14 to 35) of established crescentic glomerulonephritis. Nephrotoxic serum nephritis (NTN) was induced in groups of eight Wistar-Kyoto rats that were given a selective c-fms kinase inhibitor, fms-I, or vehicle alone from day 14 until being killed on day 35. Rats killed on day 14 NTN had pronounced macrophage infiltration with glomerular damage, fibrocellular crescents in 50% of glomeruli, tubulointerstitial damage, heavy proteinuria, and renal dysfunction. Glomerulosclerosis was more severe by day 35 in vehicle-treated rats, as was periglomerular and interstitial fibrosis, while proteinuria and renal dysfunction continued unabated and some parameters of tubular damage worsened. During the day 14-to-35 period, glomerular and interstitial macrophage infiltration decreased with an apparent change from a proinflammatory M1 phenotype to an alternatively activated M2 phenotype. Treatment with fms-I over days 14 to 35 selectively reduced blood monocyte numbers and abrogated glomerular and interstitial macrophage infiltration. This resulted in improved renal function, significantly reduced glomerular and interstitial fibrosis, and protection against further peritubular capillary loss. However, sustained proteinuria, tubular damage, and interstitial T cell infiltration and activation were unaffected. In conclusion, this study demonstrates that macrophages contribute to renal dysfunction and tissue damage in established crescentic glomerulonephritis as it progresses from the acute inflammatory to a chronic fibrotic phase.
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PMID:Role of macrophages in the fibrotic phase of rat crescentic glomerulonephritis. 2340 65


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