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fredag 22 april 2016

Bergerin tauti, gluteeniallergisen munuaisoireilu

Jos munuaisoireileva gluteeniallerginen  haluaa ajatella myös munuaistaan,dieetin pitää olla tarkka eikä saa tehdä dieettipoikkeuksia, vaikka  suolisto kestäisikin  sellaisen. Ei kannata käyttää kauraa eikä vehnätärkkelysperäisiä gluteenittomia valmisteita.  Siis  koetettava tosiaankin välttää gluteenia ja katsoa että verenpaine on normaali, virtsassa ei ole valkuaista ja turvotuksia ei tule jalkaan eikä yleistä pöhöttymistä kudoksiin. Kannattaa myös  juoda säännöllisesti puhdasta vettä, eikä odottele,   että selkä jomottaa  veden vajeesta ennenkuin juo vettä. Veden jano voi nimittäin olla keliaakikolla   epäsuhteessa veden tarpeeseen. 
Tämä gluteenittomalla ruoalla hoituva Bergerin tauti on IgA-nefropatia.

Gliadiini antigeenina ja munuainen

Schroeder C, Osman AA, Roggenbuck D, Mothes T.
Nephrol Dial Transplant. 1999 Aug;14(8):1875-80.
Brack M, Schroeder C, Fooke M, Schlumberger W.
Nephron. 1999;82(3):221-31.
Evidences of nutritional antigens in the renal tissues were inconclusive, although circulating IgG class antibodies against cereals, milk, and egg proteins were present in quite a number of sera. Particular consideration was paid to IgA-antigliadin antibodies, which were statistically significantly associated with nephropathy as were IgA rheumatoid factors. The findings are discussed in relation to human IgA and IgM nephropathies.
Barsoum R, Nabil M, Saady G, Genin C, Saleh E, Francis M, el-Kalioubi A, Iskander I, el-Garem A.
Kidney Int. 1996 Sep;50(3):920-8.
Those complicated with hepatosplenic involvement also had a significant increase in the mean IgG anti-gliadin antibodies, IgG rheumatoid factor and IgM anti-DNA activity. Cases further complicated by overt glomerular disease showed a distinct IgA predominance, mainly expressed in the serum anti-gliadin antibody pool and anti-DNA activity.Free Article
Coppo R, Amore A, Gianoglio B, Porcellini MG, Peruzzi L, Reyna A, Gusmano R, Giani M, Sereni F, Gianviti A, et al.
Minerva Urol Nefrol. 1994 Mar;46(1):49-54. Italian.
Mean levels of antigliadin IgA were significantly higher in IgAN than in controls (CD p < 0.01 and U p < 0.03) and similar data were found for IgA to mesangial matrix (laminin and fibronectin), which were significantly greater in IgAN than in CD and U (p < 0.01-p < 0.0002). Serum IgA in children with IgAN showed a greater affinity for both polycations and glycosylated molecules. Children affected by IgAN present abnormalities in serum IgA similar to those observed in adults with the same disease.(ABSTRACT TRUNCATED AT 250 WORDS)
O'Donoghue DJ, Jewkes F, Postlethwaite RJ, Ballardie FW.
Clin Sci (Lond). 1992 Sep;83(3):281-7.
Coppo R, Amore A, Roccatello D.
J Am Soc Nephrol. 1992 Apr;2(10 Suppl):S173-80. Review.
To investigate the role of dietary components in immunoglobulin A mesangial nephropathy (IgAGN), this study focused on gliadin, based on the reported association between coeliac disease and IgAGN as well as the pilot observation that a gluten-free diet was able to reduce the levels of circulating IgA immune complexes (IgAIC). IgA mesangial deposits in mice were induced by oral immunization with gliadin and in rats by inducing alcoholic liver cirrhosis, which increased the levels of IgA against dietary antigens (Ag). Gliadin was able to bind to cultured mesangial cells by a lectinic bond, which was reversed by competitive sugars. Binding increased mesangial cell tumor necrosis factor synthesis and decreased prostaglandin E2 production. Several gluten lectinic fractions modulate leukocyte oxidative metabolism, cytotoxicity, and chemotaxis. In IgAGN patients, serum IgA to dietary Ag were sporadically positive and IgAIC containing IgA to dietary components were significantly increased. The affinity of serum IgA to various lectins was increased in some patients. Conversely, no substantial deposition in renal tissue of dietary Ags was observed by immunofluorescence. A gluten-free diet, given to IgAGN patients with high levels of circulating IgAIC and positive antigliadin IgA, was followed by a decrease in the mean levels of both IgAIC and IgA to various dietary Ag, parallel to a reduction in proteinuria. These data suggest that dietary components, such as Ag or lectins, may play a role in IgAGN by promoting IgAIC formation and perhaps favoring mesangial localization via lectinic interactions.
Free Article
Emancipator SN, Rao CS, Amore A, Coppo R, Nedrud JG.
J Am Soc Nephrol. 1992 Apr;2(10 Suppl):S149-58. Review.
Montinaro V, Gesualdo L, Schena FP.
Nephron. 1992;62(4):373-81. Review.
Coppo R, Amore A, Roccatello D, Gianoglio B, Peruzzi L, Alessi D, Reyna A, Mesiti A, Piccoli G, Sena LM.
Minerva Urol Nefrol. 1991 Jul-Sep;43(3):171-4. Italian.
It is generally thought that antigens inducing the formation of IgA immune complexes in primary IgA nephropathy and responsible for mesangial immune deposits are of infectious and alimentary origin. To investigate the possible role of alimentary antigens in eliciting the IgA mucosal immune response we studied the reactivity and the formation of mesangial IgA deposits in rodents following different experimental conditions: a) on gluten-free diet and oral immunization with gliadin; b) on gluten and soya free diet and oral immunization with soya; c) on chronic alcoholic intoxication. We found that oral immunization with gliadin induced the formation of mesangial deposits of IgA similar to those observed in human primary IgA nephropathy. On the contrary, oral immunization with soya failed to induce the formation of similar immune deposits even though the lectin components in soya and in gliadin are similar. Chronic ethanol intoxication induced an increase in serum IgA against alimentary antigens suggesting an increase in intestinal permeability due to alcohol. Mean times we observed significant IgA mesangial deposits. Our experimental data suggest that alimentary antigens can play a significant role in inducing primary IgA nephropathy
Coppo R, Mazzucco G, Martina G, Roccatello D, Amore A, Novara R, Bargoni A, Piccoli G, Sena LM.
Lab Invest. 1989 Apr;60(4):499-506.
Fornasieri A, Sinico RA, Maldifassi P, Paterna L, Benuzzi S, Colasanti G, D'Amico G.
Nephrol Dial Transplant. 1988;3(6):738-43.