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Secretory immunoglobulin A in urinary tract infection, chronic glomerulonephritis, and renal transplantation
M Marx1, M Weber, D Schafranek
11st Department of Internal Medicine, University of Mainz, Federal Republic of Germany.
An enzyme-linked immunoassay (ELISA) for the quantitation of secretory IgA (S-IgA) in the urine is described. The assay is sensitive (linear down to 0.02 microgram/ml), specific, and reproducible (intraassay variation 7.8%, interassay variation 18.9%). The assay was used to determine the urinary excretion rates of S-IgA in patients with bladder catheter (n = 12), cystotomy and urinary tract infection (n = 13), urosepsis (n = 5), chronic glomerulonephritis, including IgA-nephritis (n = 31), in renal allograft recipients (n = 30), and in healthy controls (n = 46). An elevated S-IgA urinary excretion (P less than 0.01) was found in all patient groups studied. The highest values were observed in urosepsis. No significant differences between S-IgA levels in IgA-nephritis and other forms of chronic glomerulonephritis were detected. The elevated S-IgA excretion in renal allograft recipients indicates that immunosuppressive therapy does not influence the local S-IgA production in the urinary tract. The susceptibility of these patients to urinary tract infections is therefore not due to a S-IgA deficiency.
An enzyme-linked immunoassay (ELISA) for the quantitation of secretory IgA (S-IgA) in the urine is described. The assay is sensitive (linear down to 0.02 microgram/ml), specific, and reproducible (intraassay variation 7.8%, interassay variation 18.9%). The assay was used to determine the urinary excretion rates of S-IgA in patients with bladder catheter (n = 12), cystotomy and urinary tract infection (n = 13), urosepsis (n = 5), chronic glomerulonephritis, including IgA-nephritis (n = 31), in renal allograft recipients (n = 30), and in healthy controls (n = 46). An elevated S-IgA urinary excretion (P less than 0.01) was found in all patient groups studied. The highest values were observed in urosepsis. No significant differences between S-IgA levels in IgA-nephritis and other forms of chronic glomerulonephritis were detected. The elevated S-IgA excretion in renal allograft recipients indicates that immunosuppressive therapy does not influence the local S-IgA production in the urinary tract. The susceptibility of these patients to urinary tract infections is therefore not due to a S-IgA deficiency.