Lynda Chowdhury, BS, MD
Resident Physician
n/a
Dallas, Texas, United States
Disclosure information not submitted.
Ahmed Alobaidi, MD
Attending Physician
Methodist Health System, United States
Disclosure information not submitted.
Amit Mann, MD
Attending Physician
Methodist Health System, United States
Disclosure information not submitted.
Title: Endocarditis-Associated C3-Dominant Glomerulonephritis in a Renal Donor
Introduction: Infective endocarditis (IE) is prevalent globally with acute kidney injuries (AKI) occurring commonly as a complication of the disease. Histological specimens typically demonstrate either diffuse or focal endocapillary proliferation, crescentic or necrotizing glomerulonephritis, or interstitial nephritis in endocarditis-related renal disease. A patient presenting with IE-associated C3-dominant glomerulonephritis without hypocomplementemia will be outlined here. He is unique in presenting with an absence of the most commonplace injury patterns save subepithelial and mesangial electron-dense deposits.
Description: A 27 year-old Hispanic man with a past medical history of nephrectomy for renal donation presented to a community hospital in Dallas with a high fever and declining alertness. He had a serum creatinine of 6.98 mg/dL with unknown baseline, minimal hematuria, nephrotic-range proteinuria, and pyuria on initial laboratory studies. Blood cultures grew methicillin-sensitive Staphylococcus aureus (MSSA) from admission. A transesophageal echocardiogram showed a hypermobile vegetation along the anterior mitral valve leaflet confirming suspected infective endocarditis. His non-oliguric AKI was evaluated. His serum C3 and C4 complement levels, antinuclear, myeloperoxidase (MPO), and proteinase-3 (PR-3) antibody titers were all within normal limits. A renal biopsy was obtained and revealed minimal segmental endocapillary proliferation, a single subepithelial electron-dense deposit, and granular immunofluorescent C3 staining in peripheral mesangial segments.
Discussion: Bacterial infection-related glomerulonephritis portends a guarded prognosis of renal recovery among adult patients. Dominant C3 deposition without associated immunoglobulins can result from in situ localization of bacterial antigens promoting plasmin activation to recruit neutrophils and monocytes to initiate leukocyte-mediated damage. Immunosuppressive therapies for C3 glomerulopathy triggering antibody-independent activation of the alternative or lectin complement pathways may be merited where disease remission becomes difficulty to achieve.