Acute post streptococcal glomerulonephritis (APSGN) results from a recent infection caused by nephritogenic strains of group a beta-hemolytic streptococci. On the other hand, there is a strong link between streptococcal tonsillitis and IgA nephropathy. Methods: We report the case of a female patient who developed IgA nephropathy 2 years after an episode of acute post-streptococcal glomerulonephritis. We wonder if IgA nephropathy is the chronic form of post streptococcal glomerulonephritis. Results: A 39 year-old female with no medical past history was hospitalized in nephrology department in 2013 for acute nephritic syndrome 15 days after tonsillitis. Laboratory data revealed kidney injury (creatinine level at 171mmol/l), hypocomplementemia (C3= 0.14g/l), biologic inflammatory syndrome, nephrotic proteinuria (8g/d), countless red blood cells on the cytobacteriological urine examination, and elevated ASLO level (400UI/). Renal biopsy showed malignant postinfectious glomerulonephritis. The stomatological examination before corticosteroid therapy revealed the presence of 2 dental abscesses.The patient received 3 boli Solumédrol 1g/day X 3 days switched by oral relay (1mg/Kg/day) after dental treatment (Antibiotherapy (Augmentin 1gx2/day x 10 days) +dental extractions + scaling).We obtained an improvement in renal function: creatinine =101mmol/l at the 9th day of corticotherapy. Unfortunately, the patient has been lost to sight. Two years later, she consulted us for macroscopic hematuria evolving for 2 weeks and concomitant with a tonsillitis. Laboratory data showed correct renal function, normal level of C3 (1g/l), proteinuria at 0.6g/d, correct protidemia and albuminemia, with countless red blood cells on the cytobacteriological urine examination. The stomatological examination was redone and once again showed dental abscesses which were treated. Kidney biopsy was performed and showed IgA nephropathy. She was put under nephroprotective treatment (ACE inhibitor). In front of this presentation, we discussed first of all a diagnostic error that was eliminated by re-reading the first biopsy. We then evoked an AGN added to IgA nephropathy. In this case, the absence of IgA could be explained by the intense inflammatory reaction in the glomeruli which can be responsible for the mesangial clearance of IgA. These IgA could also be phagocytized by macrophages and neutrophils. On the other hand, complement activation during AGN could dissociate immune complexes. Therefore, the finding of presumed streptococcal dental abscesses (elevation of ASLO) accompanying the 2 nephropathies presented by the patient, led us to believe that acute glomerulonephritis was an acute consequence of a streptococcal infection and that IgA nephropathy was the consequence of the chronic carriage of this germ. Conclusions: Both AGN and IgA nephropathy are 2 post-streptococcal glomerulonephritis.The first is an acute complication whereas the IgA nephropathy is secondary to the chronic carriage of nephritogenic strains of group A Streptococci.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.