Glomerulonephritis induced by methicillin-sensitive Staphylococcus aureus infection

• Published in: Clinical and experimental nephrology Vol. 7; no. 3; pp. 247 - 249
• Main Authors: Handa, Tomohiro, Ono, Takahiko, Watanabe, Hitomi, Takeda, Toshiya, Muso, Eri, Kita, Toru
• Format: Journal Article
• Language: English
• Published: Japan Springer Nature B.V 01.09.2003
• Subjects: Anti-Bacterial Agents - therapeutic use; Female; Glomerulonephritis - microbiology; Glomerulonephritis - pathology; Humans; Methicillin - therapeutic use; Methicillin Resistance; Middle Aged; Staphylococcal Infections - complications; Staphylococcal Infections - drug therapy; Staphylococcus aureus - drug effects; Superantigens
• ISSN: 1342-1751; 1437-7799
• DOI: 10.1007/s10157-003-0240-4

A 57-year-old woman developed exacerbation of atopic dermatitis, fever, and nephrotic syndrome with microscopic hematuria. By bacteriological study, methicillin-sensitive Staphylococcus aureus (MSSA) was detected from each culture of pharyngeal mucus, stool, and blood samples. Renal biopsy specimens showed endocapillary proliferative glomerulonephritis with massive IgA deposition in the mesangium and along the capillary loops. After antistaphylococcal therapy with antibiotics, MSSA was negative for each culture and urinary protein decreased. Nine months after the first renal biopsy, a re-biopsy was performed, which revealed apparent disappearance of both endocapillary cell proliferation and IgA deposition. It is known that methicillin-resistant S. aureus (MRSA) infection causes glomerulonephritis through T-cell stimulation by superantigen presented by MRSA. The present results suggest that not only MRSA but also MSSA can cause this type of glomerulonephritis.