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Staphylococcus aureus Infection-Related Glomerulonephritis with Dominant IgA Deposition

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MDPI
DOI: 10.3390/ijms23137482

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Staphylococcus aureus; rapidly progressive glomerulonephritis; IgA-dominant glomerulonephritis; Staphylococcus infection-associated glomerulonephritis; bacterial superantigen; T-cell receptor; cytokine; polyclonal activation

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Since 1995, numerous cases of MRSA infection-associated glomerulonephritis, also known as Staphylococcus infection-associated glomerulonephritis (SAGN) or IgA-IRGN, have been reported. This disease presents as rapidly progressive glomerulonephritis or acute kidney injury with proteinuria, hematuria, and ongoing infection.
Since 1995, when we reported the case of a patient with glomerulonephritis with IgA deposition that occurred after a methicillin-resistant Staphylococcus aureus (MRSA) infection, many reports of MRSA infection-associated glomerulonephritis have accumulated. This disease is being systematized as Staphylococcus infection-associated glomerulonephritis (SAGN) in light of the apparent cause of infection, and as immunoglobulin A-dominant deposition infection-related glomerulonephritis (IgA-IRGN) in light of its histopathology. This glomerulonephritis usually presents as rapidly progressive glomerulonephritis or acute kidney injury with various degrees of proteinuria and microscopic hematuria along with an ongoing infection. Its renal pathology has shown several types of mesangial and/or endocapillary proliferative glomerulonephritis with various degrees of crescent formation and tubulointerstitial nephritis. IgA, IgG, and C-3 staining in the mesangium and along the glomerular capillary walls have been observed on immunofluorescence examinations. A marked activation of T cells, an increase in specific variable regions of the T-cell receptor beta-chain-positive cells, hypercytokinemia, and increased polyclonal immune complexes have also been observed in this glomerulonephritis. In the development of this disease, staphylococcal enterotoxin may be involved as a superantigen, but further investigations are needed to clarify the mechanisms underlying this disease. Here, we review 336 cases of IgA-IRGN and 218 cases of SAGN.

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