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IgA Immune Responses Against Acetaldehyde Adducts and Biomarkers of Alcohol Consumption in Patients with IgA Glomerulonephritis
Author(s) -
Kaartinen Kati,
Niemelä Onni,
Syrjänen Jaana,
Alatalo Päivikki,
Pörsti Ilkka,
Harmoinen Aimo,
Pasternack Amos,
Huhtala Heini,
Mustonen Jukka
Publication year - 2009
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.2009.00947.x
Subject(s) - acetaldehyde , population , antibody , immunology , medicine , immune system , antigen , glomerulonephritis , mean corpuscular volume , pathogenesis , immunoglobulin a , endocrinology , kidney , ethanol , immunoglobulin g , chemistry , hematocrit , biochemistry , environmental health
Background: The pathogenesis of IgA glomerulonephritis (IgAGN) involves intense deposition of IgAs within the glomerulus. Although previous studies have shown that heavy drinking frequently leads to the generation of IgA antibodies against neo‐antigens induced by ethanol metabolites and tissue deposition of IgAs, the associations between alcohol consumption, IgA immune responses, and kidney disease have not been examined. Methods: A total of 158 IgAGN patients (96 men, 62 women) were classified as abstainers ( n = 38), moderate drinkers ( n = 114), and heavy drinkers ( n = 6) based on self‐reported alcohol consumption. The reference population included 143 individuals (99 men, 44 women) who were either apparently healthy abstainers ( n = 31), moderate drinkers ( n = 43), or heavy drinkers devoid of liver disease ( n = 69). The assessments included various biomarkers of alcohol consumption: carbohydrate‐deficient transferrin (CDT), glutamyl transferase, γ‐CDT (combination of GGR and CDT), mean corpuscular volume (MCV), tests for liver and kidney function, serum immunoglobulin A (IgA), and specific IgA antibodies against acetaldehyde–protein adducts. Results: In male IgAGN patients, drinking status was significantly associated with MCV, p < 0.001; CDT, p < 0.01; and γ ‐CDT, p < 0.05. In the reference population, all biomarkers and anti‐adduct IgA levels were found to vary according to drinking status. In IgAGN patients, anti‐adduct IgA levels were elevated in 63% of the cases but the titers did not associate with self‐reported ethanol intake. Conclusions: These data indicate high levels of IgA antibodies against acetaldehyde‐derived antigens in IgAGN patients, which may hamper the use of the immune responses as markers of alcohol consumption among such patients. Future studies on the pathogenic and prognostic significance of anti‐adduct immune responses in IgAGN patients are warranted.