Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0268596 (EMA)
 2,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Epithelial membrane antigen was detected in normal glomeruli by a polyclonal antiserum to the antigen and by the monoclonal antibodies Ca 1, DAKO-EMA and HMFG 2, but not HMFG 1, using an indirect immunoperoxidase method. The antigen was in the form of a thin ring or collar at the junction of glomerulus and tubule. In a series of 47 renal biopsies from patients with proteinuria, the antigen could still be seen in glomeruli, provided that there were adequate numbers of glomeruli in the sections. The main object of study was the glomerular tip lesion, in which tip adhesions were seen to be just adjacent to the patch of epithelial membrane antigen. This suggested that the antigen may be important in pathogenesis of the lesion. Normal proximal tubules did not express epithelial membrane antigen but it was detected on the luminal border of acutely damaged proximal tubules. Thus the distribution of epithelial membrane antigen in the kidney is more complex than was previously thought.
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PMID:Epithelial membrane antigen in normal and proteinuric glomeruli and in damaged proximal tubules. 351 Dec 1

The finding of increased levels of immunoglobulin A (IgA) against food antigens in patients with IgA nephropathy prompted the hypothesis of an association between IgA nephropathy and celiac disease (CD). Attention was initially directed to antigliadin antibodies, then to IgA antiendomysial antibodies (IgA-EMA). IgG1-EMA have been found in patients with CD with IgA-EMA-negative results. The presence of IgA- and IgG1-EMA was investigated in 36 patients with IgA nephropathy, 15 patients with other primary glomerulonephritis, and 15 patients with lupus nephritis. IgA-EMA and IgG1-EMA were detected by indirect immunofluorescence analysis. At the time of renal biopsy, the following factors were evaluated: history of macroscopic hematuria, serum creatinine level, urinalysis, 24-hour proteinuria, blood pressure, and histological classification of IgA nephropathy. Sixteen of 36 patients with IgA nephropathy (44.4%) showed EMA positivity. Among patients with positive EMA, 12 patients (75%) were IgG1-EMA positive, 2 patients (12.5%) were IgA-EMA positive, and 2 patients (12.5%) were positive for both isotypes. No significant differences were observed between the two groups (EMA positive versus EMA negative) concerning age, serum creatinine level, macroscopic hematuria, blood pressure, 24-hour proteinuria, or degree of renal histological involvement. IgA- and IgG1-EMA were not detected in patients with other primary nephropathies or lupus nephritis. These results, based on the finding of IgG1-EMA, suggest a common pathogenetic pathway for CD and IgA nephropathy. On this basis, the presence of IgG1-EMA and/or IgA-EMA should be investigated in patients with IgA nephropathy. Furthermore, the role of a gluten-free diet in the natural history of IgA nephropathy, at least in EMA-positive patients, needs to be ascertained.
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PMID:Antiendomysial antibodies in Berger's disease. 1204 28