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[A case of interstitial nephritis induced by a super antigen produced by methicillin-resistant Staphylococcus aureus
1Department of Nephrology, Kasukabe Shuwa Hospital, Saitama, Japan.
Abstract:
We report the case of a 21-year-old man who had been developing acute renal failure with Methicillin-resistant Staphylococcus aureus (MRSA) colitis and sepsis. He was admitted for consciousness disturbance, nausea, vomiting, and diarrhea. Oliguria was also observed and his serum creatinine level was elevated to 10 mg/dl. Urinary protein was positive and an abundance of hyaline cast were seen in urinary sedimentation. Diarrhea and pyrexia were prolonged and serum C-reactive proteins were elevated, but lymphocyte and leukocyte counts temporarily decreased from the 3rd to the 6th hospital day and remained low until normalizing after the 14th day. His clinical symptoms improved with hemodialysis (HD) and effective antibiotic therapies. An MRSA strain producing toxic shock syndrome toxin-1 (TSST-1), a super antigen which specifically stimulates human V beta 2-positive T cells, was separated from his feces and blood. To ascertain the cause of his renal dysfunction, a renal biopsy was performed on the 8th day. His renal histology revealed acute interstitial nephritis with severe inflammatory cell infiltration around the medullary areas without glomerular changes. Most of the infiltrated cells were small monocytes, and lymphoid cells were rich in the interstitium. With immunohistochemical staining, over 70% of T-cells were V beta 2-positive. TSST-1-producing MRSA was detected in his blood specimen. Furthermore, V beta 2-positive T cells were accumulated in the renal intersititium, and transient lymphocytopenia was observed. These data suggested the following possible pathogenesis for interstitial nephritis: TSST-1 acts as a super antigen in the renal interstitium where major histocompatibility complex (MHC) is class-2-positive, thereby resulting in interstitial nephritis with T cell migration.
Insights
A young man developed acute renal failure due to Methicillin-resistant Staphylococcus aureus (MRSA) sepsis. Toxic shock syndrome toxin-1 (TSST-1) from MRSA triggered T-cell activation, leading to interstitial nephritis and renal dysfunction.
Area of Science:
- Nephrology
- Infectious Diseases
- Immunology
Background:
- Acute renal failure (ARF) in sepsis can have complex etiologies.
- Methicillin-resistant Staphylococcus aureus (MRSA) is a significant pathogen causing severe infections.
- Superantigens, like toxic shock syndrome toxin-1 (TSST-1), can dysregulate the immune system.
Observation:
- A 21-year-old male presented with ARF, MRSA colitis, and sepsis, including consciousness disturbance and elevated creatinine.
- Renal biopsy revealed acute interstitial nephritis with significant T-cell infiltration, predominantly V beta 2-positive.
- MRSA producing TSST-1 was identified in blood and stool, correlating with transient lymphocytopenia.
Findings:
- TSST-1, a superantigen, was implicated in the pathogenesis of interstitial nephritis.
- The superantigen likely activated V beta 2-positive T cells within the renal interstitium.
- This T-cell activation, in the context of MHC class-2 expression, led to inflammatory cell infiltration and renal dysfunction.
Implications:
- This case highlights a novel mechanism of MRSA-induced acute interstitial nephritis.
- Understanding superantigen-mediated renal injury is crucial for managing sepsis-related ARF.
- Targeting T-cell activation pathways may offer therapeutic strategies for similar conditions.