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Glomerulonephritis causing acute renal failure during the course of bacterial infections. Histological varieties, potential pathogenetic pathways and treatment

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Abstract

To illustrate diagnostic approaches, potential pathogenetic differences, epidemiological implications and therapeutic dilemmas posed by glomerulonephritis (GN) with acute renal failure (ARF) complicating bacterial infections, we analyzed the course of four male patients, aged 53–71 years, who developed GN and ARF following bacterial infections. The first two patients developed GN with immunoglobulin A (IgA) deposits after infections with hospital-acquired methicillin resistant Staphylococcus aureus (MRSA). Clinical, serologic and histological features, classification of GN and treatment differed between the two patients. In the first patient, serological features (transient hypocomplementemia, normal serum protein electrophoresis) and histological findings were consistent with typical post-infectious GN. Treatment with antibiotics alone resulted in normalization of the renal function despite the severity of ARF, which required temporary hemodialysis. In the second patient, serological features (normal serum complement, polyclonal elevation of gamma globulins) and histological picture of the kidneys were characteristic of IgA nephropathy with fibrocellular crescents, and skin histology was consistent with vasculitis. Cyclophosphamide and corticosteroids were added to the antibiotics, with partial improvement of the renal failure. The third patient developed simultaneous acute rheumatic fever and post-streptococcal GN causing severe ARF requiring hemodialysis. Complete recovery of ARF and migratory polyarthritis followed initiation of corticosteroids. The fourth patient developed ARF and cerebral vasculitis following a prolonged course of Streptococcus mutans endocarditis with delayed diagnosis. He also developed multiple serological abnormalities including elevated titers of antineutrophil cytoplasmic antibodies (ANCA), antinuclear antibodies (ANA), anti-phospholipid antibodies, rheumatoid factor, and modest hypocomplementemia. Kidney biopsy revealed ANCA-mediated focal GN with 10% crescents and acute interstitial nephritis. Treatment with cyclophosphamide plus corticosteroids, but not with antibiotics alone, resulted in resolution of both the ARF and the features of cerebral vasculitis. GN following bacterial infections may have various pathogenetic mechanisms, presents complex diagnostic challenges, may be preventable in the case of hospital-acquired MRSA, and, in addition to antibiotics, may require immunosuppressive therapy in carefully selected and monitored cases.

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Acknowledgement

This work was supported by the New Mexico, VA, Health Care System.

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Authors and Affiliations

  1. Section of Nephrology, Renal Section (111C), New Mexico Veterans Affairs Health Care System and University of New Mexico School of Medicine, 1501 San Pedro, SE, Albuquerque, NM, USA

    Jorge I. Zeledon, Karen S. Servilla, Yijuan Sun & Antonios H. Tzamaloukas

  2. Section of Infectious Diseases, New Mexico Veterans Affairs Health Care System and University of New Mexico School of Medicine, Albuquerque, NM, USA

    Robin L. McKelvey, Diedre Hofinger & Suzan Kellie

  3. Section of Rheumatology, New Mexico Veterans Affairs Health Care System and University of New Mexico School of Medicine, Albuquerque, NM, USA

    Konstantin N. Konstantinov

  4. Department of Pathology, New Mexico Veterans Affairs Health Care System and University of New Mexico School of Medicine, Albuquerque, NM, USA

    Larry W. Massie

  5. Department of Radiology, New Mexico Veterans Affairs Health Care System and University of New Mexico School of Medicine, Albuquerque, NM, USA

    Michael F. Hartshorne

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  1. Jorge I. Zeledon
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  2. Robin L. McKelvey
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  10. Antonios H. Tzamaloukas
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Correspondence to Antonios H. Tzamaloukas.

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Zeledon, J.I., McKelvey, R.L., Servilla, K.S. et al. Glomerulonephritis causing acute renal failure during the course of bacterial infections. Histological varieties, potential pathogenetic pathways and treatment. Int Urol Nephrol 40, 461–470 (2008). https://doi.org/10.1007/s11255-007-9323-6

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