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)

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

Renal failure secondary to crescentic glomerulonephritis developed in a patient who had typical serologic features of drug-induced systemic lupus erythematosus after two years of therapy with procainamide. Renal function and proteinuria improved after the drug was discontinued and steroid therapy begun. A review of previously reported cases of glomerulonephritis in association with drug-induced systemic lupus erythematosus revealed a high incidence of renal failure. Crescentic glomerulonephritis has not to our knowledge been previously documented in drug-induced systemic lupus erythematosus.
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PMID:Renal manifestations of drug-induced systemic lupus erythematosus. 701 25

We reviewed the clinical and renal biopsy information of 115 patients who presented with renal disease after the age of sixty years. The major clinical presentations were renal insufficiency in 57 patients, nephrotic syndrome in 35 patients, and hematuria with variable amounts of proteinuria in 23 patients. Crescentic glomerulonephritis, diagnosed in 19 patients, was the most common cause of renal insufficiency. Membranous glomerulonephritis and minimal change nephrotic syndrome were noted in 15 and 9 patients, respectively. While patients with crescentic glomerulonephritis had an unfavorable outcome, patients with minimal change nephrotic syndrome and diffuse proliferative glomerulonephritis had a benign course. We conclude that even in the elderly, the natural history of renal disease is similar to that of younger patients, and the clinical course appears to depend on the nature of the underlying renal disease.
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PMID:Renal disease in the elderly: clinicopathologic analysis of renal disease in 115 elderly patients. 722 80

Crescentic glomerulonephritis (GN) demonstrates immunopathological features of a T helper (Th)1-directed delayed-type hypersensitivity (DTH) response. The capacity of Th2 cytokines to attenuate crescentic glomerular injury in this disease was examined by administering interleukin (IL)-4 and IL-10, singly and in combination. GN was induced by i.v. administration of sheep anti-mouse glomerular basement membrane (GBM) globulin to mice sensitized to sheep globulin 10 days earlier. Treatment (2.5 microg, i.p.) with IL-4, IL-10, or both IL-4 and IL-10 (IL-4 + 10), was started 1 h before sensitization and continued daily until the end of the study (10 days after administration of anti-GBM globulin). Control mice treated with PBS developed GN with glomerular accumulation of T cells and macrophages, crescents in 42.5 +/- 4.5 % of glomeruli (normal 0 %), proteinuria (8.3 +/- 0.9 mg/24 h, normal 0.74 +/- 0.08 mg/24 h, p <0.001) and renal impairment (creatinine clearance [cr/cl]: 93 +/- 12 microl/min, normal 193 +/- 10 microl/min, p < 0.001). Treatment with either IL-4, IL-10, or IL-4 + 10 prevented crescent formation (crescentic glomeruli: 0.8 +/- 0.5, 1.2 +/- 0.9, and 1.4 +/- 1.0 %, respectively, all p < 0.01 compared to control) and attenuated proteinuria (3.6 +/- 1.0, 2.2 +/- 0.5, and 2.9 +/- 0.5 mg/24 h, respectively, all p < 0.01 compared to control). IL-4 + 10 prevented development of renal impairment (cr/cl: 183 +/- 22 microl/min); IL-10 given alone limited the decline in renal function (cr/cl: 150 +/- 20 microl/min), but IL-4 alone did not provide any significant protection (cr/cl: 121 +/- 17 microl/min). All treatments markedly diminished glomerular T cell and macrophage accumulation, reduced interferon-gamma production by splenic T cells, prevented cutaneous DTH to the disease-initiating antigen and reduced antigen-specific immunoglobulin of the IgG2a and IgG3 isotypes. These data demonstrate that crescentic GN and renal impairment can be prevented by administration of Th2 cytokines and that this effect is associated with attenuation of the Th1 response to the disease-initiating antigen.
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PMID:Immune modulation with interleukin-4 and interleukin-10 prevents crescent formation and glomerular injury in experimental glomerulonephritis. 904 27

Idiopathic crescentic glomerulonephritis (GN) often presents with a rapid loss of renal function and pathology showing extensive crescent formation. The disease is caused by different immunopathogenetic mechanisms, pauci-immune, often antineutrophil cytoplasmic antibody (ANCA)-positive microvasculitis, antiglomerular basement membrane (GBM) antibody disease, and immune complex formation. Historical reviews reveal poor renal prognosis, even after treatment with oral steroids and cytotoxic drugs. Prognosis has improved in the last decade. In this article, evidence-based recommendations for management are presented. Because of the high risk of end-stage renal disease (ESRD), early aggressive therapy is recommended, despite weak supporting evidence. Treatment for anti-GBM antibody-induced crescentic GN should be initiated early and should include pulse methylprednisolone, a two-week course of plasmapheresis and two months of treatment with corticosteroids and cyclophosphamide (grade B and C). Treatment for pauci-immune crescentic GN should be pulse methylprednisolone, followed by oral corticosteroids and cyclophosphamide for 6 to 12 months (grade B). Recurrences can be managed similarly (grade B), along with appropriate supportive therapy. In patients who develop ESRD, successful transplantation can be performed. Diffuse endocapillary proliferative GN is classically postinfectious. It generally has a good prognosis when no crescent formation occurs. Adult patients with persistent proteinuria, hypertension, and renal function impairment need careful follow-up and management to modify progressive hemodynamic injury.
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PMID:Management of idiopathic crescentic and diffuse proliferative glomerulonephritis: evidence-based recommendations. 1036 93

Crescentic glomerulonephritis can be induced in rodents by injection of heterologous antibodies against the glomerular basement membrane. There is evidence that glomerular inflammation in that model represents a delayed-type hypersensitivity response to the heterologous immunoglobulin, whereas the antibody response is not important. The aim of the present study was to test this hypothesis. Delayed-type hypersensitivity is mediated by T cells with the Th1 phenotype. We compared mice immunized with rabbit immunoglobulin G in complete Freund's adjuvant or in incomplete Freund's adjuvant, producing, respectively, Th1- or Th2-biased responses to the antigen. Intravenous injection of rabbit antimouse glomerular basement membrane serum provoked proteinuria, infiltration with T cells and macrophages, as well as profound histological damage in the group treated with complete Freund's adjuvant. There was no evidence of glomerulonephritis in the group which received incomplete Freund's adjuvant. Deposits of mouse IgG along the glomerular basement membrane were similar in both groups. Thus, a Th1 response appears to be essential for the induction of glomerulonephritis in this model.
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PMID:A Th1 response is essential for induction of crescentic glomerulonephritis in mice. 1039 12

Crescentic glomerulonephritis shows active and progressive glomerular changes with rapid deterioration in kidney function. A large dose of glucocorticoid (pulse therapy) is clinically used for the treatment, but its efficacy has not been fully estimated. In this study we assessed the therapeutic effect of a large dose of methyl-prednisolone (MP) on a rat model of crescentic glomerulonephritis that had been induced in WKY rats by an injection of anti-glomerular basement membrane antibody. The infiltration of CD8+ cells and monocytes was manifest by day 3, proteinuria appeared on days 4 and 5, and cellular crescents were diffusely formed by day 7. The gene expression of MCP-1, a chemokine for monocytes and T lymphocytes, was enhanced within 4 hours and peaked on day 3. Daily administration of MP (30 mg/kg/d) from day 3 through day 6 reduced the gene expression of MCP-1 and the numbers of glomerular leukocytes and largely prevented both crescent formation and proteinuria. When daily MP treatment started on day 7, the numbers of glomerular CD8+ cells and monocytes, crescents, and urinary protein were significantly reduced by day 11. In addition, continuing treatment with a small dose of MP (3 mg/kg/d) begun on day 11 completely prevented the increase in blood urea nitrogen and serum creatinine levels. These results indicate that treatment with a large dose of MP histologically and clinically ameliorates crescentic glomerulonephritis in a rat model, supporting the efficacy of pulse MP therapy for the treatment of the disease in human subjects.
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PMID:Therapeutic effect of glucocorticoid on experimental crescentic glomerulonephritis. 1052 Oct 89

A 66-year-old female was admitted to our hospital in January, 1998, complaining of low grade fever and muscle weakness of her legs. Physical examination revealed muscle weakness of her neck (4/5) and proximal skeletal muscles of her bilateral legs (3/5-4/5). She showed proteinuria and microhematuria. Her serum levels of ureanitrogen, creatinine, aspartate aminotransferase, alanine aminotransferase, creatinekinase, aldolase and myoglobin were all within the normal ranges. Antinuclear antibodies were negative, but her serum levels of pANCA (743 EU) and C reactive protein (18.0 mg/dl) were elevated. Neuroconduction velocity of her left common peroneal nerve was decreased to 40.8 m/sec and electric myograph showed neurogenic changes. Magnetic resonance images (MRI) of her bilateral thigh depicted high signal intensity in quadriceps by T 2 weighed images, but the signals were not enhanced by gadolinium injection. Muscle and renal biopsies revealed necrotizing vasculitis of the small arteries. Crescentic glomerulonephritis was also observed by renal biopsy. These findings supported the diagnosis of microscopic PN. On 16 th admission day, she developed acute cardiac and respiratory failures due to cardiac and respiratory muscle involvements with PN, and was assisted by mechanical ventilation. She was treated with methylprednisolone pulse therapy (500 mg/day, three consecutive days) on 18 th admission day, followed by 40 mg of oral prednisolone daily. However, her symptoms deteriorated, and herserum creatinine levels increased to 2.4 mg/dl. On 24 th admission day, intravenous cyclophosphamide pulse therapy (500 mg/day) was instituted. Her cardiac wall motion on echocardiography and serum creatinine levels gradually improved, but her skeletal and respiratory muscle weakness did not improve. On 38 th admission day, she was complicated with respiratory infection by methicillin resistant Staphylococcus aures. On 62 th admission day, she died of endotoxic shock. This is the first report describing respiratory muscle involvement with PN, and the second report describing MRI findings of muscle involvement by PN. Therefore, our case provides important clinical information for the diagnosis and treatment of the disease.
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PMID:[A case of microscopic polyangiitis with severe cardiac and respiratory muscle involvement]. 1061 70

Glomerular expression of cytokines, interleukin-1 (IL-1), and tumor necrosis factor-alpha (TNF-alpha), together with leukocytic infiltration, are prominent features in crescentic glomerulonephritis. Because these cytokines are targets for nuclear transcription factor-kappaB (NF-kappaB), the use of NF-kappaB decoy oligodeoxynucleotide (ODN) treatment was evaluated in an experimental disease model. Crescentic glomerulonephritis was induced in primed Wistar rats by injection of sheep antiglomerular basement membrane serum. Thirty minutes after injection, rats were anesthetized and the left kidney was perfused with NF-kappaB decoy ODN or scrambled ODN control mixed with a virus-liposome complex, and then killed 7 d later. Animals given the scrambled control ODN developed severe glomerulonephritis by day 7 with heavy proteinuria, glomerular crescents and interstitial lesions, marked leukocytic infiltration, and upregulated renal expression of cytokines (IL-1 and TNF-alpha) and adhesion molecules (intercellular adhesion molecule-1). In contrast, NF-kappaB decoy ODN treatment substantially inhibited the disease with a 50% reduction in proteinuria, a threefold reduction in histologic damage, a 50% reduction in leukocytic infiltration, and a 50 to 80% reduction in the renal expression of cytokines and leukocyte adhesion molecules. In conclusion, this study has demonstrated that NF-kappaB plays a key role in cytokine-mediated renal injury and that NF-kappaB decoy ODN treatment has clear therapeutic potential in rapidly progressive glomerulonephritis.
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PMID:In vivo administration of a nuclear transcription factor-kappaB decoy suppresses experimental crescentic glomerulonephritis. 1086 80

Leucocytes infiltrate into renal tissue and are involved in the pathogenesis of crescentic glomerulonephritis. The initial event in the process of leucocyte infiltration is characterized by selectin-mediated leucocyte rolling on endothelial surface. Role of selectins in pathogenesis of glomerulonephritis has still been controversial. Sulphated glycolipids and sulphated polysaccharides interfere with the binding of P- and L-selectin with carbohydrate ligands on endothelial cells or on leucocytes. Here we evaluated the role of selectins and the preventive effects of sulphated colominic acid (SCA), a synthetic sulphated polysaccharide, on experimental crescentic glomerulonephritis in Wistar-Kyoto (WKY) rats. Crescentic glomerulonephritis was induced by injection of nephrotoxic serum (NTS) in WKY rats. Rats subsequently received intraperitoneal injection of saline, neutralizing or non-neutralizing monoclonal antibody (mAb) to rat P-selectin and L-selectin, SCA (5 or 10mg/kg/day) or nonsulphated colominic acid (CA) (10mg/kg/day) for 2 weeks. Localization of P-, E-selectin, ligands for L-selectin and intraglomerular leucocytes was examined by immunohistochemistry. Gene expression of platelet-derived growth factor (PDGF) B chain in glomeruli was quantified using real-time RT-PCR. P-selectin was highly expressed on glomerular endothelial cells after injection of NTS, whereas E-selectin and L-selectin ligands were not detected. Anti-P-selectin mAb, but not anti-L-selectin mAb, significantly reduced glomerular infiltration of macrophages, crescent formation, and proteinuria. SCA also reduced proteinuria, macrophage infiltration, and crescent formation in a dose-dependent manner. Furthermore, SCA suppressed gene expression of PDGF B chain in glomeruli. Our results indicate that P-selectin partially mediates glomerular infiltration of macrophage in experimental crescentic glomerulonephritis. Moreover, SCA may inhibit intraglomerular infiltration of macrophages by interfering with P-selectin-dependent adhesion pathway, and progression of experimental crescentic glomerulonephritis.
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PMID:Preventive effect of sulphated colominic acid on P-selectin-dependent infiltration of macrophages in experimentally induced crescentic glomerulonephritis. 1210 15


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