» Articles » PMID: 33460013

Atypical Anti-glomerular Basement Membrane Disease Complicated by Methicillin-susceptible Staphylococcus Aureus Infection-related Rapidly Progressive Glomerulonephritis: a Case Report and Literature Review

Overview
Journal CEN Case Rep
Specialty Nephrology
Date 2021 Jan 18
PMID 33460013
Citations 1
Authors
Affiliations
Soon will be listed here.
Abstract

Atypical anti-glomerular basement membrane (GBM) disease, which is characterized by low levels of or negativity for anti-GBM antibodies in circulation but positivity in the kidney, has been recognized in this decade. However, a therapeutic strategy has not been established to date because its outcome is better than that of classic anti-GBM disease. This case report and literature review highlight atypical anti-GBM disease in infection-related rapidly progressive glomerulonephritis. A 72-year-old Japanese man diagnosed with methicillin-susceptible Staphylococcus aureus (MSSA)-induced vertebral osteomyelitis experienced for 2 months was referred to our hospital because of renal insufficiency. He developed rapidly progressive glomerulonephritis with a serum creatinine level of 6.8 mg/dL, C-reactive protein level of 9.7 mg/dL, urinary protein-to-creatinine ratio of 3.37 g/gCr, and gross hematuria. The serum anti-GBM antibody concentration was 3.5 U/mL, which was slightly above the normal range (< 3.0 U/mL). Conservative treatment, mainly with antibiotics, improved the symptoms and renal function. The serum anti-GBM antibody concentration peaked at 4.0 U/mL on day 7 and decreased to an undetectable range at the end of eight-week antibiotic therapy. This is the first case report describing the presentation and disappearance of serum anti-GBM antibody in a patient with MSSA infection. Conservative treatment may be effective for patients with atypical anti-GBM disease complicated by infectious diseases.

Citing Articles

A case report of atypical anti-glomerular basement membrane nephritis associated with Mycobacterium Avium.

Bech Jensen J, Gravesen E, Jensen S, Bressendorff I Clin Nephrol Case Stud. 2024; 12:12-16.

PMID: 38239388 PMC: 10795487. DOI: 10.5414/CNCS111254.

References
1.
Ossman R, Buob D, Hellmark T, Brocheriou I, Peltier J, Tamouza R . Factors Associated With Pathogenicity of Anti-Glomerular Basal Membrane Antibodies: A Case Report. Medicine (Baltimore). 2016; 95(19):e3654. PMC: 4902534. DOI: 10.1097/MD.0000000000003654. View

2.
Zhao J, Yan Y, Cui Z, Yang R, Zhao M . The immunoglobulin G subclass distribution of anti-GBM autoantibodies against rHalpha3(IV)NC1 is associated with disease severity. Hum Immunol. 2009; 70(6):425-9. DOI: 10.1016/j.humimm.2009.04.004. View

3.
Arimura Y, Muso E, Fujimoto S, Hasegawa M, Kaname S, Usui J . Evidence-based clinical practice guidelines for rapidly progressive glomerulonephritis 2014. Clin Exp Nephrol. 2016; 20(3):322-41. PMC: 4891375. DOI: 10.1007/s10157-015-1218-8. View

4.
Levy J, Turner A, Rees A, Pusey C . Long-term outcome of anti-glomerular basement membrane antibody disease treated with plasma exchange and immunosuppression. Ann Intern Med. 2001; 134(11):1033-42. DOI: 10.7326/0003-4819-134-11-200106050-00009. View

5.
Gu Q, Xie L, Jia X, Ma R, Liao Y, Cui Z . Fever and prodromal infections in anti-glomerular basement membrane disease. Nephrology (Carlton). 2017; 23(5):476-482. DOI: 10.1111/nep.13040. View