C-reactive protein as a potential effector molecule in the pathogenesis of acute post-streptococcal glomerulonephritis: a narrative review.

C-reactive protein (CRP) is an acute-phase protein elevated in inflammatory and infection processes. Acute post-streptococcal glomerulonephritis (APSGN) is an infectious and inflammatory process characterized by the formation of immune complexes and renal injury. Although increased CRP levels have been reported in APSGN, whether CRP acts only a systemic biomarker or also contributes to disease mechanisms remain unclear. Therefore, the objective of this review is to highlight data that could reveal a role for CRP in the pathogenesis of APSGN. PubMed/Medline, Embase, Cochrane, and Google Scholar databases were searched from 1970 to 2026 addressing CRP biology, APSGN pathogenesis, and renal inflammatory mechanisms. Current evidence indirectly supports the idea that CRP, particularly through complement-, coagulation- and IgγFc receptors-dependent pathways, could amplify the inflammatory process during APSGN. In this regard, CRP could activate the complement and coagulation systems, interact with streptococcal neuraminidase, induce angiotensin II, immune complexes, and IgγFc receptors, events that could lead to increased inflammation, pro-inflammatory cytokines production, apoptosis, opsonization, phagocytosis, and renal injury in APSGN. Further research is needed to define the expression of CRP in renal tissues and its contribution to glomerular inflammation and define whether the use of CRP blockers can reduce the inflammatory events in APSGN.