Glomerulonephritis causing acute renal failure during the course of bacterial infections. Histological varieties, potential pathogenetic pathways and treatment
- PMID: 18247152
- DOI: 10.1007/s11255-007-9323-6
Glomerulonephritis causing acute renal failure during the course of bacterial infections. Histological varieties, potential pathogenetic pathways and treatment
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.
Similar articles
-
ANCA-associated crescentic glomerulonephritis with mesangial IgA deposits.Am J Kidney Dis. 2000 Oct;36(4):709-18. doi: 10.1053/ajkd.2000.17615. Am J Kidney Dis. 2000. PMID: 11007672
-
Latency, Anti-Bacterial Resistance Pattern, and Bacterial Infection-Related Glomerulonephritis.Clin J Am Soc Nephrol. 2021 Aug;16(8):1210-1220. doi: 10.2215/CJN.18631120. Epub 2021 Jun 7. Clin J Am Soc Nephrol. 2021. PMID: 34099500 Free PMC article.
-
PR3-ANCA-positive crescentic necrotizing glomerulonephritis accompanied by isolated pulmonic valve infective endocarditis, with reference to previous reports of renal pathology.Clin Nephrol. 2006 Sep;66(3):202-9. doi: 10.5414/cnp66202. Clin Nephrol. 2006. PMID: 16995343
-
[Instructions and implementations for percutaneous renal biopsy. Guidelines for the therapy of glomerular nephropaties].G Ital Nefrol. 2003 Sep-Oct;20 Suppl 24:S3-47. G Ital Nefrol. 2003. PMID: 14666502 Review. Italian.
-
New trends of an old disease: the acute post infectious glomerulonephritis at the beginning of the new millenium.J Nephrol. 2014 Jun;27(3):229-39. doi: 10.1007/s40620-013-0018-z. Epub 2014 Jan 31. J Nephrol. 2014. PMID: 24777751 Review.
Cited by
-
Antineutrophil Cytoplasmic Antibody Induction due to Infection: A Patient with Infective Endocarditis and Chronic Hepatitis C.Can J Infect Dis Med Microbiol. 2016;2016:3585860. doi: 10.1155/2016/3585860. Epub 2016 Mar 21. Can J Infect Dis Med Microbiol. 2016. PMID: 27366166 Free PMC article.
-
Febrile-range hyperthermia augments lipopolysaccharide-induced lung injury by a mechanism of enhanced alveolar epithelial apoptosis.J Immunol. 2010 Apr 1;184(7):3801-13. doi: 10.4049/jimmunol.0903191. Epub 2010 Mar 3. J Immunol. 2010. PMID: 20200273 Free PMC article.
-
Antineutrophil cytoplasmic antibodies in infective endocarditis: a case report and systematic review of the literature.Clin Rheumatol. 2022 Oct;41(10):2949-2960. doi: 10.1007/s10067-022-06240-w. Epub 2022 Jun 23. Clin Rheumatol. 2022. PMID: 35732985 Free PMC article.
-
IgA-dominant Staphylococcus infection-associated glomerulonephritis: case reports and review of the literature.NDT Plus. 2011 Jun;4(3):181-5. doi: 10.1093/ndtplus/sfr017. Epub 2011 Mar 8. NDT Plus. 2011. PMID: 25984152 Free PMC article.
-
Proteinase 3-antineutrophil cytoplasmic antibody-positive necrotizing crescentic glomerulonephritis complicated by infectious endocarditis: a case report.J Med Case Rep. 2019 Dec 5;13(1):356. doi: 10.1186/s13256-019-2287-1. J Med Case Rep. 2019. PMID: 31801609 Free PMC article.
References
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Medical
Miscellaneous