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Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
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Group A β-hemolytic Streptococcus (GAS) infection classically causes acute poststreptococcal glomerulonephritis (APSGN), a glomerulus-dominant lesion.However, infection-related acute tubulointerstitial nephritis (AIN) secondary to GAS is rarely reported.We present a case of dialysis-requiring AIN without glomerular involvement, in which Nephritis-Associated Plasmin Receptor (NAPlr) and Streptococcal Pyrogenic Exotoxin B(SPEB) localized mainly within the interstitium. This case highlights a distinct immunopathologic pattern of streptococcal infection-related kidney injury that differs from classic APSGN.
A 54-year-old woman with hypertension and no prior kidney disease was admitted with septic shock and acute kidney injury (AKI) due to cervical cellulitis caused by GAS. Rapid antigen and culture tests were positive, and ASO titer was elevated (1331 IU/mL) with normal complement (C3, C4). Despite antibiotic therapy, anuria persisted, requiring hemodialysis. A renal biopsy performed on day 34 showed no glomerular lesions but demonstrated diffuse plasma cell-, neutrophil-, and eosinophil-rich tubulointerstitial inflammation with tubulitis and basement membrane disruption. Drug lymphocyte stimulation tests (DLSTs) for suspected agents were negative, and no allergic manifestations (such as rash or eosinophilia) were observed. Immunostaining revealed positivity for NAPlr, plasmin activity, and SPEB in the interstitium but negativity in glomeruli.Urine output increased afterward, and dialysis was discontinued on day 37; serum creatinine stabilized at 1.22 mg/dL without corticosteroid therapy.
This case illustrates infection-related AIN induced by GAS in the absence of glomerular involvement, contrasting with the classical APSGN pattern. The lack of glomerular NAPlr deposition may reflect altered glomerular charge selectivity during septic shock, impeding adherence of cationic streptococcal antigens to the basement membrane. SPEB, a small cationic exotoxin, likely passed through the glomerular filtration barrier and accumulated in the interstitium, directly promoting inflammation and tissue injury. Similar mechanisms were proposed by Chang et al. (Nephrol Dial Transplant, 2011) and Okunaga et al. (CEN Case Rep, 2023), who reported NAPlr-positive infection-related AIN. Our patient demonstrated spontaneous renal recovery after infection control, suggesting that this form of AIN is self-limited and may not require immunosuppression.
Streptococcal infection can induce AIN without glomerular involvement when streptococcal antigens such as SPEB and NAPlr localize predominantly in the interstitium. Recognition of this pattern is critical for differentiating infection-related AIN from drug-induced AIN and for avoiding unnecessary corticosteroid therapy. Effective infection control alone can lead to complete renal recovery even in dialysis-requiring cases.
