Polyclonal activation of an IgA subclass against Staphylococcus aureus cell membrane antigen in post-methicillin-resistant S.aureus infection glomerulonephritis

Acute poststaphylococcal glomerulonephritis superimposed on diabetic glomerulosclerosis

“…13 Because most cases of IgA-dominant poststaphylococcal glomerulonephritis have been described in nondiabetic patients, this selective glomerular IgA deposition is more likely related to the Staphylococcus bacterium itself. Arakawa et al 14 found that serum IgA titers against S. aureus cell membrane antigen are elevated. This group speculated that postmethicillinresistant S. aureus-associated glomerulonephritis might be mediated by staphylococcal enterotoxin, which acts as a superantigen.…”

“…The superantigen/ major histocompatibility class II complex then interacts with the variable portion of the beta chain (Vb) of the T cell without major histocompatibility restriction, causing massive T-cell activation and production of high amounts of cytokines, including those with IgA class-switching functions. 3,14,15 Unknown staphylococcal cell surface antigens may also be implicated in mounting an IgA-dominant immune response as some of the reported cases of IgAdominant APIGN were associated with S. epidermidis, which does not produce enterotoxin. 5,7 Interestingly, the same Japanese group recently detected S. aureus envelope antigen designated 'probable adhesin' on the glomeruli of 68% patients with IgA nephropathy and IgA-dominant methicillin-resistant S. aureus-associated glomerulonephritis.…”

IgA-dominant post-infectious glomerulonephritis presenting as a fatal pulmonary-renal syndrome

“…Fifty-one percentage of the cases (in which an infection site was identified) were due to cellulitis, and Staphylococcus is the most commonly associated pathogen, but there are also reports indicating occurrence in patients with urinary tract infections. [1][2][3][4][5][6]8,9 The clinical manifestations include acute nephritic syndrome with severe renal failure (acute or rapidly progressive), new onset of gross hematuria with or without RBC casts (25% of the cases), nephrotic and non-nephrotic range proteinuria, edema, and hypertension (∼75% at presentation). Extrarenal manifestations rarely occur in adults with IRGN.…”

“…The IgA-rich environment in diabetics coupled with IgA-specific responses to the proposed staphylococcal superantigen may precipitate a unique variant of PIGN with glomerular IgA deposition and explain the predilection for more severe IgA dominant IRGN in diabetic patients. 3,5,8,9…”