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)

This report describes a 50-year-old female with necrotizing crescentic glomerulonephritis (NCGN), associated with antineutrophil cytoplasmic antibodies (ANCA) recognizing various neutrophil cytoplasmic constituents. The patient was admitted to our hospital because of proteinuria. She had been well until seven months before admission, when she experienced fever and arthralgia. Tests for ANCA showed a p-ANCA pattern in indirect immunofluorescence, and high positivity for ANCA against myeloperoxidase (MPO) and lactoferrin in ELISAs. The renal biopsy on admission revealed crescentic glomerulonephritis with segmental necrosis. Therefore, we made the diagnosis of NCGN secondary to ANCA-associated renal disease. The second renal biopsy obtained after a period of 70 days with prednisolone and cyclophosphamide therapy displayed marked improvement indicating the disappearance of cellular crescents and necrosis lesions. Moreover, the levels of MPO-ANCA were correlated with the disease activity. We considered this patient to be a rare case of NCGN with ANCA recognizing various antigens. MPO-ANCA in this case might have been directly associated with the pathogenesis of NCGN.
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PMID:[A case of necrotizing crescentic glomerulonephritis in which myeloperoxidase antineutrophil cytoplasmic antibodies (ANCA) reflect the disease activity and recognize various neutrophil cytoplasmic constituents]. 913 36

A 39-year-old Japanese woman had been receiving propylthiouracil for 5 years for hyperthyroidism when she developed myalgia, scleritis, proteinuria, fever, and inflammation of the nose. Examination of a renal biopsy specimen showed focal segmental necrotizing glomerulonephritis. Indirect immunofluorescent staining showed a highly positive perinuclear pattern of anti-neutrophil cytoplasmic antibody (ANCA) in her serum. Enzyme-linked immunosorbent assay (ELISA) of the ANCA showed positivity for anti-proteinase 3, anti-myeloperoxidase, anti-leukocyte elastase, and anti-lactoferrin, but anti-cathepsin G and anti-lysozyme were negative. Because ELISA showed the titer of anti-leukocyte elastase antibody to be markedly elevated, we challenged this data by performing dot blot analysis. The patient's serum reacted with the native form, but not with denatured leukocyte elastase. Propylthiouracil-induced vasculitis was suspected. Symptoms abated within 2 weeks and all values of ANCA were reduced after the drug was withdrawn. Vasculitis is a rare side-effect of propylthiouracil therapy. Recently it was reported in association with ANCA. We present the findings of this patient and compare them with those described in 19 published cases of propylthiouracil-induced vasculitis associated with ANCA.
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PMID:Case of propylthiouracil-induced vasculitis associated with anti-neutrophil cytoplasmic antibody (ANCA); review of literature. 918 Dec 82

We have experienced a case of myeloperoxidase-antineutrophil cytoplasmic antibody (MPO-ANCA)-related glomerulonephritis induced by propylthiouracil (PTU). A 45-year-old female had been treated with PTU for 4 years after the diagnosis of hyperthyroidism. She was referred to out hospital because of abrupt macroscopic hematuria and moderate proteinuria after several days of upper respiratory tract infection. On admission, her laboratory findings showed deterioration of renal function. Renal biopsy revealed crescentic glomerulonephritis without deposition of immune complexes. Her serology was found to be MPO-ANCA-positive and cytoplasmic-ANCA-negative. Based of these findings, we diagnosed idiopathic crescentic glomerulonephritis. Following the initiation of steroid pulse therapy, her urinary protein excretion and renal function gradually improved in parallel with a decrease in the MPO-ANCA titer. Although steroid therapy effectively responded to their renal function without the withdrawal of PTU, it seems that PTU may be closely associated with the development of (MPO-ANCA)-related glomerulonephritis in this case. Therefore, hyperthyroidism patients treated with PTU should be paced under vigilant observation by monitoring their urinalysis and serum creatinine level.
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PMID:[A case of myeloperoxidase-antineutrophil cytoplasmic antibody (ANCA)-positive crescentic glomerulonephritis induced by propylthiouracil (PTU)]. 928 19

A 74-year-old man was admitted to our hospital because of edema of the lower legs, fever, and increasing fatigue. Laboratory evaluation revealed proteinuria, microhematuria, leukocytosis, thrombocytosis, anemia, a high level of C-reactive protein. A test for myeloperoxidase-antineutrophil cytoplasmic antibodies was highly positive. Microscopic polyarteritis nodosa was diagnosed and therapy with prednisolone was begun. Examination of a renal biopsy sample showed necrotizing crescentic glomerulonephritis. A chest roentgenogram and CT scan disclosed bilateral basilar interstitial changes. Six months later, the patient was admitted again because of disturbance of consciousness, malnutrition, and hyponatremia. After admission, alveolar infiltrates developed in the right lung and the patient died on the 5th hospital day as a result of respiratory failure. An autopsy revealed Candida pneumonia of the right lung and massive intra-alveolar hemorrhage, which was believed to have caused the respiratory failure. Other findings were usual interstitial pneumonia, cellular small-vessel angiitis in the lungs, and healed angiitis in the kidneys and liver. In this case of microscopic polyangiitis and chronic interstitial pneumonia, steroid therapy was effective against the angiitis, but the patient died of an opportunistic infection and alveolar hemorrhage.
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PMID:[Microscopic polyangiitis and pulmonary fibrosis in a patient who died of Candida pneumonia and intra-alveolar hemorrhage]. 936 70

A 45-year-old man with a long history of bronchial asthma was admitted to the National Cardiovascular Center with complaints of severe pain, swelling, and ecchymoses of the lower extremities. A diagnosis of Churg-Strauss syndrome was made because of marked eosinophilia, vasculitis, and a history of asthma. Urinalysis revealed severe proteinuria and microscopic hematuria. A renal biopsy demonstrated extensively crescentic glomerulonephritis. The antineutrophil cytoplasmic antibody against myeloperoxidase (MPO-ANCA) level, determined by enzyme-linked immunosorbent assay (ELISA), was 494 ELISA units. Under treatment with prednisolone, the symptoms and eosinophilia improved within 3 days. The MPO-ANCA level decreased to its lowest value, and renal function was ameliorated within 3 months. The patient has been followed regularly on an ambulatory basis with a regimen of prednisolone.
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PMID:Crescentic glomerulonephritis and elevated antimyeloperoxidase antibody in a patient with Churg-Strauss syndrome. 938 Feb 24

A 47-year-old woman developed pulmonary hemorrhage and an increase in proteinuria during remission of membranous nephropathy. Renal biopsy revealed crescentic glomerulonephritis. She also had a high perinuclear antineutrophil cytoplasmic antibody level, so a diagnosis of myeloperoxidase-antineutrophil cytoplasmic antibody-associated glomerulonephritis was made. After immunosuppressive therapy was started, the pulmonary hemorrhage resolved and her proteinuria decreased. Renal biopsy was repeated after treatment and showed histological improvement. This case suggests that there may be a relationship between membranous nephropathy and myeloperoxidase-antineutrophil cytoplasmic antibody-associated glomerulonephritis.
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PMID:Myeloperoxidase-antineutrophil cytoplasmic antibody-associated glomerulonephritis with membranous nephropathy in remission. 939 63

Here we report a case of microscopic polyangitis (MPA) with anti-neutrophil cytoplasmic antibodies against myeloperoxidase (MPO-ANCA) accompanied by perceptive dominant hearing loss as the initial sign of the disease. A 52-year-old woman was admitted to Tokyo Metropolitan Ohtsuka Hospital in April 1996 because of bilateral progressive hearing loss. On admission, she had presented bilateral perceptive hearing loss, fever, myalgia, and weight loss. Laboratory data showed accelerated erythrocyte sedimentation rate, proteinuria, microscopic hematuria, leukocytosis, hypoproteinemia, and elevated creatinine level. Serum level of MPO-ANCA was elevated. Chest X-ray and computed tomography showed mild pleural effusion and interstitial shadow in bilateral lung fields. The biopsy findings detected that focal glomerulonephritis, and necrotizing angitis of small artery in kidney. The diagnosis of MPA was made with clinical course, laboratory findings, radiographic findings, and biopsy finding. Treatment was initiated with 45 mg of prednisolone, followed by marked improvement of hearing loss and decreased titer of serum MPO-ANCA. There are only seven reports showing hearing loss as the initial sign of the disease occurred in polyarteritis nodosa and MPA. The present case suggests the possibility that hearing loss may be the symptom of MPO-ANCA associated vasculitis.
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PMID:[A case of microscopic polyangitis accompanied by hearing loss as the initial sign of the disease]. 949 68

Although glomerular disease remains the most common cause of end-stage renal disease worldwide, major advances have been made recently in understanding the cellular and molecular mechanisms which mediate these disorders. Nephrotic syndrome in non-inflammatory lesions such as minimal change/focal sclerosis and membranous nephropathy results from disorders of the GEC which can be simulated in animal models by antibodies to various GEC membrane epitopes. Clarification of how these antibodies effect the GEC to induce a loss of glomerular barrier function should substantially improve understanding of the pathogenesis of minimal change/focal sclerosis. In MN, proteinuria is mediated primarily by C5b-9 through similar mechanisms that also involve the GEC as a target and GEC production of oxidants, proteases and TGF beta in response to sublytic C5b-9 attack. C5b-9 also mediates mesangial proliferative glomerulonephritis induced by anti-measangial cell antibodies and thrombotic microangiopathy induced by antibodies to the glomerular endothelial cell. In all of these lesions induced by antibodies to glomerular cells, cell-bound complement regulatory proteins are important in modulating the injury observed. Upregulation of complement regulatory proteins may prove an effective therapeutic manoeuver in the future. Inflammatory glomerular lesions are induced by circulating inflammatory cells or proliferating resident glomerular cells. Understanding of how these cells induce tissue injury has also evolved considerably over the past decade. Neutrophil-induced disease involves leukocyte adhesion molecules in regulating neutrophil localization; proteases, oxidants and MPO in mediating injury and platelets in augmenting these processes. The activated mesangial cell following immune injury exhibits altered phenotype and proliferation with release of oxidants and proteases. Mesangial cell proliferation may be initiated by bFGF and is maintained by an autocrine mechanism involving PDGF. TGF beta is important in the subsequent development of sclerosis. Finally, recent studies establish the nephritogenic potential of cell-mediated mechanisms alone without humoral immunity, and these mechanisms may be important in glomerulonephritis which occurs in the absence of antibody deposits. As understanding of these areas evolves, numerous new therapeutic strategies can now be devised including agents which selectively block or inhibit complement effects, leukocyte adhesion molecules, oxidants, proteases, growth factors and other cytokines and activated T cells. Appreciation of the role of several natural inhibitors of these mechanisms may also allow therapeutic manipulations that upregulate regulatory proteins with a consequent therapeutic benefit. Thus, these changes in basic understanding of the mechanisms of glomerular disease are likely to translate into new and more specific and effective forms of therapy in the next decade.
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PMID:Pathogenesis of glomerular damage in glomerulonephritis. 950 91

A 12-year-old girl with a main complaint of sever pain on the both knees was admitted to our hospital in October, 1995. She gave a three year history of recurrent arthralgia and purpuric rashes, and persistent microhematuria and proteinuria. She developed vesicles and purpuric rashes on the hands and auricles, morning stiffness, fever, uveitis and pericarditis. Laboratory findings showed an elevated level of erythrocyte sedimentation rate and iron-deficiency anemia. Serum perinuclear pattern ANCA with antimyeloperioxidase specificity (MPO-ANCA) was positive. A renal biopsy specimen disclosed a focal and segmental necrotizing glomerulonephritis with crescents. Our case fulfills the both diagnostic criteria for polyarteritis nodosa and juvenile rheumatoid arthritis. This is a rare case of MPO-ANCA associated vasculitis in children.
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PMID:[A case of juvenile rheumatoid arthritis with MPO-ANCA associated nephritis]. 956 75

Transplantation of MHC-compatible, T-cell-depleted, bone marrow cells has successfully treated autoimmunities, immunodeficiencies, malignancies, and developmental deficiencies of the hematopoietic system. Recombinant inbred SCG/Kj mice develop spontaneous crescentic glomerulonephritis, systemic vasculitis, and a lymphoproliferative disorder early in life. To determine whether the precipitous autoimmune disease of SCG/Kj mice could be treated by bone marrow transplantation, 30 SCG/Kj mice were engrafted with T-cell-depleted, bone marrow (TCDM) from allogeneic, MHC-compatible, autoimmune-resistant C3H/He donors, and 30 SCG/Kj mice served as controls and received TCDM from syngeneic, SCG/Kj donors. A significant survival advantage was evident from SCG/Kj mice engrafted with C3H/He TCDM (p < 0.005), and an 89% extension of median survival compared to recipients of SCG/Kj TCDM. Within 28 weeks post-transplantation, 62% of mice engrafted with SCG/Kj TCDM had died with clinical signs of fatal crescentic glomerulonephritis. This result compared with only 10% of mice engrafted with C3H/He TCDM. Mice engrafted with SCG/Kj TCDM developed significantly greater titers of autoantibodies to ss-DNA, ds-DNA, and myeloperoxidase (ANCA) (p < 0.001), had shorter latencies to the development of, and a greater incidence of proteinuria, hematuria, and peripheral lymphadenopathy, and a greater mean grade of glomerular lesion (p < 0.001), than mice engrafted with C3H/He TCDM. These findings indicate that the genetic defect of the SCG/Kj strain of mice resides within the hematopoietic stem cells and provokes the speculation that bone marrow transplantation might be a useful means of treating progressive crescentic glomerulonephritis in humans.
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PMID:Prevention of crescentic glomerulonephritis in SCG/Kj mice by bone marrow transplantation. 964 40


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