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Streptococcal and staphylococcal related glomerulonephritis
There has been considerable effort to reclassify glomerular diseases that occur as a result of an infection. PIGN describes a unique clinical and pathogenic sequence of events that lead to an immune complex–mediated glomerulonephritis after resolution of an acute infection. Specifically, the acute glomerulonephritis develops after (post) a latent period of variable duration from the time the infection has completely cleared. Since the infection has completely resolved, antibiotic therapy is ineffective for treating the kidney disease. The only infection known to cause this scenario of events is streptococcal disease. Therefore the category of PIGN is better termed poststreptococcal glomerulonephritis (PSGN), as no other microorganism leads to this pathologic phenomenon.
Compared with PSGN, all other infections (viral, bacterial, and fungal) can be “associated” with the development of glomerulonephritis through a separate pathogenic pathway. For these infections, the onset of glomerulonephritis is almost synchronous with the presence of active infection, and the immune complexes are completely dependent on the availability of ongoing antigenemia generated from the infection. In this circumstance as opposed to PSGN, eradication of the infection through antibiotic therapy will halt the ongoing immune complex deposition in the kidney. Staphylococcal-associated acute glomerulonephritis (SAAG) is now as common as PSGN in adults and represents the classic example of this paradigm of infection-associated glomerulonephritis. It is essential to understand the differences between PSGN and SAAG not only in regard to pathophysiology but more importantly in regard to therapeutic intervention. Key points in differentiating PSGN from SAAG and other glomerular diseases are shown in the below table
Clinical and Pathologic Features of Infection-Related Glomerular Diseases
PSGN | SAAG | IgA Nephropathy | C3 Glomerulopathy | |
|---|---|---|---|---|
| Location of infection | Pharyngitis Skin | Skin Lung Urinary tract | Pharyngitis | Pharyngitis |
| Latent period | Pharyngitis: 7–14 days Skin: 14–21 days | None | None | None |
| Primary histology on kidney biopsy | Diffuse proliferative and exudative glomerulonephritis | Diffuse proliferative and exudative glomerulonephritis | Mesangial proliferative glomerulonephritis | Membranoproliferative glomerulonephritis |
| Site of immune deposits | Subepithelial Some subendothelial and mesangial | Subepithelial Some subendothelial and mesangial | Mesangial | Subendothelial Mesangial Intramembranous Subepithelial |
| Serum complement | Low C3 | Primarily low C3 but often with both low C3 and C4 | Normal | Low C3 |
| Immunofluorescence | IgG and C3 “Starry sky” or “garland” pattern | IgA dominant C3 and IgG in lower intensity | IgA and C3 | C3 |
| Treatment | None—spontaneous resolution | Antibiotics | Variable protocols of immunosuppression | Variable—centered on immunosuppression—complement inhibition |
PSGN , Poststreptococcal glomerulonephritis; SAAG , staphylococcal-associated acute glomerulonephritis; URI , upper respiratory illness.
