Glomerulonephritis after Methicillin-resistant Staphylococcus aureus Infection Resulting in End-stage Renal Failure.

Yamashita, Yumi; Tanase, Takehito; Terada, Yoshio; Tamura, Hiroyuki; Akiba, Takashi; Inoue, Haruhiro; Ida, Takashi; Sasaki, Sei; Marumo, Fumiaki; Nakamoto, Yasushi

doi:10.2169/internalmedicine.40.424

Cited by 14 publications

(7 citation statements)

References 5 publications

(12 reference statements)

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“…In addition to the cases of MRSA-associated with glomerulonephritis described in our reports, other cases have been reported (9-1 2), including some in the present issue of the Journal (13).…”

supporting

confidence: 65%

Glomerulonephritis Associated with <i>Staphylococcus aureus </i>Infection

Kôyama

Hirayama

2001

Intern. Med.

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supporting

confidence: 65%

Glomerulonephritis Associated with <i>Staphylococcus aureus </i>Infection

Kôyama

Hirayama

2001

Intern. Med.

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“…This leads to release of lymphokines including interleukins 1, 2 and 6, tumor necrosis factor and interferon-c, and polyclonal increases of IgA and IgG with formation in the glomeruli and/or the circulation of immune complexes containing IgA and IgG. Subsequent reports confirmed the association between infections with MRSA or methicillin-sensitive Staphylococcus aureus (MSSA) and glomerulonephritis with IgA and IgG deposits [12][13][14][15][16]. Recently, Koyama and associates reported co-localization of a staphylococcal envelope antigen and the IgA glomerular deposits in 70% of the biopsies in patients with primary IgA nephropathy, suggesting that this staphylococcal antigen may play a role in the induction of the nephropathy [17,18].…”

Section: Discussionmentioning

confidence: 95%

“…The histological picture may influence the treatment and course of glomerulonephritis. Crescents signal a poor prognosis with end-stage renal disease occurring in some instances [9,12]. Treatment with corticosteroids seems to improve the clinical course in these instances [13,19].…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2008

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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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“…The association of MRSA infection with GN has been well documented in Japan (2)(3)(4)(5)(6)(7)(8)(9). Based primarily on these publications, it appears evident that S. aureus-associated GN is characterized by glomerular IgA deposits; therefore, the renal biopsy findings strongly resemble primary (idiopathic) IgA nephropathy.…”

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confidence: 99%

Staphylococcus Infection-Associated Glomerulonephritis Mimicking IgA Nephropathy

Satoskar

Nadasdy

Plaza

et al. 2006

Clinical Journal of the American Society of Nephrology

130

152

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The association of methicillin-resistant Staphylococcus aureus (MRSA) infection with glomerulonephritis (GN) has been well documented in Japan but not in North America. Recently, eight renal biopsies with IgA-predominant or -codominant GN from eight patients with underlying staphylococcal infection, but without endocarditis, were observed at a single institution in a 12-mo period. Renal biopsies were worked up by routinely used methodologies. Eight cases of primary IgA nephropathy were used as controls. Five patients had MRSA infection, one had methicillin-resistant S. epidermidis (MRSE) infection, and two had methicillin-sensitive S. aureus infection. Four patients became infected after surgery; two patients were diabetic and had infected leg ulcers. All patients developed acute renal failure, with active urine sediment and severe proteinuria. Most renal biopsies showed only mild glomerular hypercellularity. Two biopsies had prominent mesangial and intracapillary hypercellularity; one of them (the MRSE-associated case) had large glomerular hyalin thrombi. This patient also had a positive cryoglobulin test. Rare glomerular hyalin thrombi were noted in two other cases. Immunofluorescence showed IgA pre-or codominance in all biopsies. Electron microscopy revealed mesangial deposits in all cases. Five biopsies had rare glomerular capillary deposits as well. In the MRSE-associated GN, large subendothelial electron-dense deposits were present. These cases demonstrate that staphylococcal (especially MRSA) infection-associated GN occurs in the US as well, and a rising incidence is possible. It is important to differentiate a Staphylococcus infection-associated GN from primary IgA nephropathy to avoid erroneous treatment with immunosuppressive medications.Clin J Am Soc Nephrol 1: 1179 -1186, 2006. doi: 10.2215/CJN.01030306 S taphylococci are widespread pathogens and their frequent antibiotic resistance makes treatment difficult. Occasional episodes of glomerulonephritis (GN) after Staphylococcus epidermidis bacteremia in patients with ventriculoatrial or ventriculojugular shunts and after S. aureus bacteriemia secondary to endocarditis are well documented and are discussed in most nephrology and renal pathology textbooks. These Staphylococcus infection-related glomerulonephritides are associated with glomerular immune complex deposits, which contain complement (mainly C3) IgG and sometimes IgM. Much less is known about GN associated with methicillinresistant S. aureus (MRSA), and methicillin-resistant S. epidermidis (MRSE), which are now endemic in most hospitals. A growing number of community-acquired infections are also reported (1).The association of MRSA infection with GN has been well documented in Japan (2-9). Based primarily on these publications, it appears evident that S. aureus-associated GN is characterized by glomerular IgA deposits; therefore, the renal biopsy findings strongly resemble primary (idiopathic) IgA nephropathy. The IgA-containing immune complexes are mainly deposited in the mesangium, but they ...

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Glomerulonephritis after Methicillin-resistant Staphylococcus aureus Infection Resulting in End-stage Renal Failure.

Cited by 14 publications

References 5 publications

Glomerulonephritis Associated with <i>Staphylococcus aureus </i>Infection

Glomerulonephritis Associated with <i>Staphylococcus aureus </i>Infection

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

Staphylococcus Infection-Associated Glomerulonephritis Mimicking IgA Nephropathy

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