Abstract
Acute glomerulonephritis is a severe kidney disease that develops as a result of streptococcal skin and upper respiratory infections most commonly caused by M serotypes of the group A b-hemolytic streptococci (GAS). Most often this process is acute, but can have a tendency to the chronisation which often leads to renal dysfunction with the development of secondary renal hypertension that can be fatal. In spite of the numerous clinical and experimental studies data on the pathogenesis of the post streptococcal glomerulonephritis remain limited and come to several approaches:
1) cross-reactive antigenes of GAS and renal tissue;
2) streptokinase of GAS, some allele variants of which can transform plasmin to plasminogen that leads to complement activation and deposition of the C3 complement fraction in glomeruli;
3) cysteine protease or pyrogenic exotoxin B of GAS that bind plasmin and laminin as well as break up fibronectin and vitronectin;
4) increased serum concentration of different highly active oxygen-containing substances;
5) IgG Fc-receptors of GAS. All of above hypothesis have arguments "pro" and "contra", so, further experimental studies is necessary for more detail understanding of pathogenesis of the post streptococcal glomerulonephritis.
-
1.
Silva F.G. Acute postinfectious glomerulonephritis and glomerulonephritis complicating persistent bacterial infection. In: Jennette J.C., Olson J.L., Schwartz M.M., Silva F.G., editors. Hepinstall’s pathology of the kidney. 5th ed. Philadelphia: Lippincott-Raven Publishers; 1998. p.389-453.
-
2.
Stollerman G.H. Rheumatic fever and streptococcal infection. In: Stollerman G.H., editor. Clinical cardiology monographs. New York: Grune and Stratton; 1975. p. 1-303.
-
3.
Cunningham M.W. Pathogenesis of group A streptococcal infections. Clin Microbiol Rev 2000; 13:470-511.
-
4.
Kefalides N.A., Pegg N.T., Ohno N., Poon-King T., Zabriskie J.B., Fillit H. Antibodies to basement membrane collagen and to laminin are present in sera from patients with poststreptococcal glomerulonephritis. J Exp Med 1986; 163:588.
-
5.
Markowitz M.M., Lange C.F. Streptococcal related glomerulonephritis. J Immunology 1964; 92:65.
-
6.
Lange C.F. Chemistry of cross-reactive fragments of streptococcal cell membrane and human glomerular basement membrane. Transplant Proc 1969; 1:959-63.
-
7.
Kraus W., Beachey E.H. Renal autoimmune epitope of group A streptococci specified by M protein tetrapeptide: Ile-Arg-Leu-Arg. Proc Nat Acad Sci USA 1988; 85:4516-20.
-
8.
Goroncy-Bermes P., Dale J.B., Beachey E.H., Opferkuch W. Monoclonal antibody to human renal glomeruli cross-reacts with streptococcal M protein. Infect Immun 1987; 55:2416-9.
-
9.
Lindberg L.H., Vosti K.L. Elution of glomerular bound antibodies in experimental streptococcal glomerulonephritis. Science 1969; 166:1032-3.
-
10.
Burova L.A., Koroleva I.V., Ogurtzov R.P., Murashov S.V., Svensson M.-L., Schalen C. Role of streptococcal IgG Fc-receptor in tissue deposition of IgG in rabbits immunized with Streptococcus pyogenes. APMIS 1992; 100:567-74.
-
11.
Yoshizawa N., Treser G., McClung J.A., Sagel I., Takahashi K. Circulating immune complexes in patients with uncomplicated group A streptococcal pharyngitis and patients with acute poststreptococcal glomerulonephritis. Am J Nephrol 1983; 3:23-9.
-
12.
Seligson G., Lange K., Majeed H.A., Deol H.L., Cronin W., Boyle R. Significance of endostreptosin antibody titers in poststreptococcal glomerulonephritis. Clin Nephrol 1985; 24:69-75.
-
13.
Nordstrand A., Norgren M., Ferretti J.J., Holm S.E. Streptokinase as a mediator of APSGN in an experimental mouse model. Infect Immun 1998; 66:315-21.
-
14.
Nordstrand A., Norgren M., Holm S.E. An experimental model for acute glomerulonephritis in mice. APMIS 1996; 104:805-16.
-
15.
Tewodros W., Nordstrand A., Kronvall G., Holm S.E., Norgren M. Streptokinase gene polymorphism in group A streptococci isolated from Ethiopian children with various disease manifestations. Microb Pathog 1993; 15:303-11.
-
16.
Cu G.A., Mezzano S., Bannan J.D., Zabriskie J.B. Immunohistochemical and serological evidence for the role of streptococcal proteinase in APSGN. Kidney Int 1998; 54:819-26.
-
17.
Nordstrand A., Norgren M., Holm S.E. Pathogenic mechanism of acute poststreptococcal glomerulonephritis. Scand J Infec Dis 1999; 31:523-37.
-
18.
Holm S.E., Ferretti J.J., Simon D., Johnston K. Deletion of a streptokinase gene eliminates the nephritogenic capacity of a type 49 strain. In: Orefici G., editor. New properties on streptococci and streptococcal infections. Proceedings of the XI Lancefield International Symposium. Zentralbl. Bakteriol. New York: Gustav Fischer-Verlag; 1992. Suppl. 22. p. 261-3.
-
19.
Saetre T., Hoiby E.A., Kahler H., Lyberg T. Changed expression of leukocyte adhesion molecules and increased production of reactive oxygen species caused by Streptococcus pyogenes in human whole blood. APMIS 2000; 108:573-80.
-
20.
Ginsburg I., Ward P.A., Varani J. Can we learn from the pathogenic strategies of group A hemolytic streptococci how tissues are injured and organs fail in post-infectious and inflammatory sequelae? FEMS Immunol Med Microbiol 1999; 25:325-38.
-
21.
Norrby-Teglund A., Pauksens K., Holm S.E., Norgren M. The relation between low capacity of human sera to inhibit streptococcal mitogens and serious manifestation of disease. J Infect Dis 1996; 170:585-91.
-
22.
Haanes E.J., Heath D.G., Cleary P.P. Architecture of the vir regulons of group A streptococci parallels opacity factor phenotype and M protein class. J Bacteriol 1992; 174:4967-76.
-
23.
Бурова Л.А., Тотолян А.А., Кристенсен П., Шален К. Иммуноглобулиновая Fc-рецепция стрептококков и ее участие в постстрептококковых осложнениях. Журн микробиол 1984; 10:12-20
-
24.
Бурова Л.А., Тотолян А.А. Роль стрептококковых Fc-рецепторов для IgG в формировании микробного очага и развитии иммунопатологических состояний. Ревматология 1988;3:9-12.
-
25.
Burova L.A., Nagornev V.A., Pigarevsky P.V., Gladilina M.M., Seliverstova V.G., Schalen C., et al. Triggering of renal tissue damage in the rabbit by IgG Fc-receptor positive group A streptococci. APMIS 1998; 106:277-87.
-
26.
Rodrigues Iturbe B., Carr R.I., Garcia R., Rabideau D., Rubio L., McIntosh R.M. Circulating immune complexes and serum immunoglobulins in acute poststreptococal glomerulonephritis. Clin Nephrol 1980; 13:1-4.
-
27.
Бурова Л.А., Нагорнев В.А., Пигаревский П.В., Гладилина М.М., Молчанова И.В., Селиверстова В.Г. и др. Стрептококковые IgG Fc-связывающие белки – факторы инициации экспериментального гломерулонефрита. Бюл экспер биол мед 1999; 128 (11):548-52.
-
28.
Burova L., Thern A., Gladilina M., Molchanova I., Pigarevsky P., Seliverstova V., et al. Streptococcal IgG binding proteins are a triggering factor of experimental glomerulonephritis on rabbits. In: Martin D.R., Tagg J.R., editors. Streptococci and Streptococcal Diseases Entering the New Millenium. New Zealand; 2000. p.717-9.
-
29.
Бурова Л.А., Пигаревский П.В., Гладилина М.М., Нагорнев В.А., Тотолян А.А. Роль стрептококковых IgG Fc-связывающих белков в патогенезе экспериментального гломерулонефрита. Мед иммунол 2001; 3 (2):213-4.
-
30.
Burova L., Molchanova I., Gladilina M., Pigarevsky P., Nagornev V., Schalen C. Selective affinity for immune complexes in group A streptococci type M12 and development of experimental glomerulonephritis in rabbits. In: Martin D.R., Tagg J.R., editors. Streptococci and Streptococcal Diseases Entering the New Millenium. New Zealand; 2000. p.713-6.
-
31.
Gomez Guerrero C., Duque N., Casado M.T., Pastor C., Blanco J., Mampaso F., et al. Administration of IgG Fc-fragments prevents glomerular injury in experimental immune complex nephritis. J Immunol 2000; 164:2092-101.