What is the role of M and T proteins in the etiology of acute poststreptococcal glomerulonephritis (APSGN)?

Updated: Dec 05, 2018
  • Author: Rajendra Bhimma, MBChB, MD, PhD, DCH (SA), FCP(Paeds)(SA), MMed(Natal); Chief Editor: Craig B Langman, MD  more...
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The M and T proteins in the bacterial wall have been used for characterizing streptococci. Nephritogenicity is mainly restricted to certain M protein serotypes (ie, 1, 2, 4, 12, 18, 25, 49, 55, 57, and 60) that have shown nephritogenic potential. These may cause skin or throat infections, but specific M types, such as 49, 55, 57, and 60, are most commonly associated with skin infections. However, not all strains of a nephritis-associated M protein serotype are nephritogenic. [7] In addition, many M protein serotypes do not confer lifetime immunity. Group C streptococci have been responsible for recent epidemics of APSGN (eg, Streptococcus zooepidemicus). Thus, it is possible that nephritogenic antigens are present and possibly shared by streptococci from several groups. [2]

In addition, nontypeable group A streptococci are frequently isolated from the skin or throat of patients with glomerulonephritis, representing presumably unclassified nephritogenic strains. [7] The overall risk of developing acute poststreptococcal glomerulonephritis after infection by these nephritogenic strains is about 15%. The risk of nephritis may also be related to the M type protein and the site of infection. The risk of developing nephritis infection by M type protein 49 is 5% if it is present in the throat. This risk increases to 25% if infection by the same organism in the skin is present.

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