anti-glomerular basement membrane disease/creatinine

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[The heterogeneity of anti-GBM autoantibodies in sera from patients with anti-GBM disease and its clinical correlation].

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OBJECTIVE To investigate the heterogeneity of epitopes recognized by anti-GBM autoantibodies in sera from a large cohort of Chinese patients with anti-GBM disease and its clinical significance. METHODS The present study included 108 patients with anti-GBM disease who were diagnosed in our hospital,

Autoantibodies against Linear Epitopes of Myeloperoxidase in Anti-Glomerular Basement Membrane Disease.

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OBJECTIVE Approximately 20%-30% of patients with anti-glomerular basement membrane disease present coexisting anti-myeloperoxidase (MPO) autoantibodies. We previously showed the recognition of a linear fragment of the MPO heavy chain N-terminus ((1)H, MPO279-409) in plasma from most double-positive

Anti-glomerular basement membrane disease: outcomes of different therapeutic regimens in a large single-center Chinese cohort study.

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Anti-glomerular basement membrane (GBM) disease usually presents with rapidly progressive glomerulonephritis accompanied by pulmonary hemorrhage. The low incidence and fulminant course of disease preclude a large randomized controlled study to define the benefits of any given therapy. We conducted a

Antigenic heterogeneity of IgA anti-GBM disease: new renal targets of IgA autoantibodies.

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Anti-glomerular basement membrane (anti-GBM) disease is an aggressive form of glomerulonephritis, usually mediated by immunoglobulin G (IgG) autoantibodies to the noncollagenous (NC1) domain of alpha 3(IV) collagen. Less is known about the target antigen(s) in patients with atypical anti-GBM disease

Glomerular C1q deposition and serum anti-C1q antibodies in anti-glomerular basement membrane disease.

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BACKGROUND Anti-glomerular basement membrane (GBM) disease is a well-known antibody-induced autoimmune disease. A few patients have glomerular C1q deposition, but it is usually absent on renal histopathology. The role of C1q deposition in kidney injury is unclear. Recently, anti-C1q antibodies are

AP-VAS 2012 case report: anti-glomerular basement membrane disease with high titer of myeloperoxidase anti-neutrophil cytoplasmic antibody-an autopsy case report.

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It has been reported that patients who are positive for both myeloperoxidase anti-neutrophil cytoplasmic antibody (MPO-ANCA) and anti-glomerular basement membrane (GBM) antibody have a poor prognosis. We present an autopsy case of anti-GBM disease with a high titer of MPO-ANCA. The patient was a

Renal biopsy collagen I mRNA predicts scarring in rabbit anti-GBM disease: comparison with conventional measures.

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Progressive loss of normal structure associated with scarring is the hallmark of chronic diseases of most organs. To test the hypothesis that measurement of interstitial collagen mRNA levels would be a useful index to predict future scarring, we developed an assay to quantitate alpha 1(I)

The Clinical and Immunologic Features of Patients With Combined Anti-GBM Disease and Castleman Disease.

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Patients with both anti-glomerular basement membrane (anti-GBM) disease and Castleman disease have been rarely reported. In this study, we report 3 patients with this combination. They had immunologic features similar to patients with classic anti-GBM disease. Sera from the 3 patients recognized the

Characteristics and prognosis of Chinese patients with anti-glomerular basement membrane disease.

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BACKGROUND Patients with anti-glomerular basement membrane (GBM) disease were predominantly reported in Caucasian population and reports from Chinese were lacking. The general picture of Chinese patients with anti-GBM disease was still unclear. This study is to investigate the characteristics and

The clinical and immunological features of patients with combined anti-glomerular basement membrane disease and membranous nephropathy.

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The association of anti-glomerular basement membrane (GBM) disease, also known as Goodpasture's disease, with membranous nephropathy (MN) has been well documented. However, little is known about the clinical and immunological features of patients with such a combination. This study was designed to

Plasma from patients with anti-glomerular basement membrane disease could recognize microbial peptides.

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Infection has long been suspected as a trigger of autoimmune diseases, and molecular mimicry mechanism was hypothesized in this study. Microbe originated peptides were searched from the Uniprot database based on a previous defined critical amino acid motif within α3129-150, isoleucine137,

Mesangial IgA deposits indicate pathogenesis of anti-glomerular basement membrane disease.

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Anti-glomerular basement membrane (anti-GBM) disease is characterized by crescentic glomerulonephritis with immunoglobulin G (IgG) autoantibodies to the non-collagenous (NC1) domain of α3(IV) collagen presenting along the GBM. The patient clinically manifests with rapidly progressive

Anti-GBM disease with a mild relapsing course and low levels of anti-GBM autoantibodies.

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Anti-glomerular basement membrane disease (anti-GBM) is usually characterized by rapidly progressive glomerulonephritis, and when autoantibody production has ceased, relapses are rare. Here, we report a 71-year-old women diagnosed at a stage of mild renal insufficiency. Over a period of 10 years,

Prognostic Factors in Anti-glomerular Basement Membrane Disease: A Multicenter Study of 119 Patients.

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We report the overall and renal outcome in a French nationwide multicenter cohort of 119 patients with anti-glomerular basement membrane (anti-GBM) disease. Sixty-four patients (54%) had an exclusive renal involvement, 7 (6%) an isolated alveolar hemorrhage and 48 (40%) a combined renal and

Levels of epitope-specific autoantibodies correlate with renal damage in anti-GBM disease.

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BACKGROUND Although the clinical importance of demonstrating the presence of anti-glomerular basement membrane (anti-GBM) antibodies is well established, less is known concerning the clinical utility of measuring the levels of autoantibodies. Two conformational epitopes of anti-GBM antibodies have

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