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Infective Endocarditis-Associated Glomerulonephritis

Alejandro Best, MD renal pathologist at arkana laboratories
By Alejandro Best, MD

Nov 07, 2017

focal and segmental necrotizing and crescentic lesions, Infective Endocarditis-Associated Glomerulonephritis

This renal biopsy was taken from a 35 year old male with history of intravenous drug abuse and MRSA tricuspid valve endocarditis, who developed acute kidney injury (Cr 4.7 mg/dl) and hematuria.  The biopsy shows focal and segmental necrotizing and crescentic lesions involving approximately 10% of the available glomeruli (Fig 1 and 2). Additionally, there is severe acute tubular injury with numerous red blood cell casts (Fig 3). Immunofluorescence (not shown) reveals weak immune complex deposition within the spectrum of pauci-immune disease (IgA= 1+; IgM= trace; C3= 1+; Kappa= trace; lambda= 1+), and no definitive deposits were evident by electron microscopy. ANCA-mediated disease is the most common pathogenic mechanisms in cases of pauci-immune, focal necrotizing and crescentic glomerulonephritis; however, within the context of this patient’s clinical history, the biopsy findings are strongly favored to represent an endocarditis-associated glomerulonephritis. A large clinicopathologic series of cases of infective endocarditis-associated glomerulonephritis showed that the most common pattern of glomerular injury (seen in up to 53% of cases) is in the form of  necrotizing and crescentic glomerulonephritis (See reference). Furthermore, 44% of the cases met criteria for pauci-immune disease. These results highlight the importance of including infective endocarditis-associated glomerulonephritis in the differential diagnosis of a pauci-immune necrotizing and crescentic glomerulonephritis and a transesophageal echocardiogram and infectious diseases consult may be warranted in patients at risk for infective endocarditis before implementation of aggressive immunosuppressive therapy.

 

Reference:

Boils CL, Nasr SH, Walker PD, et al.  Update on endocarditis-associated glomerulonephritis.  Kidney Int 2015; 87: 1241-1249.

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