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Abstract: SA-PO672

Bartonella Infection-Associated Glomerulonephritis and Recurrent Dense Deposit Disease in a Kidney Transplant

Session Information

Category: Glomerular Diseases

  • 1302 Glomerular Diseases: Immunology and Inflammation

Authors

  • Chen, Yuang, Vanderbilt University Medical Center, Nashville, Tennessee, United States
  • Velagapudi, Ramya Krishna, Vanderbilt University Medical Center, Nashville, Tennessee, United States
  • Fogo, Agnes B., Vanderbilt University Medical Center, Nashville, Tennessee, United States
  • Paueksakon, Paisit, Vanderbilt University Medical Center, Nashville, Tennessee, United States
  • Concepcion, Beatrice P., Vanderbilt University Medical Center, Nashville, Tennessee, United States
Introduction

Dense deposit disease (DDD) is caused by dysregulation of the alternative complement pathway, leading to excessive complement activation and complement deposition in the glomerular capillary walls and mesangium. Patients with DDD are at risk to have over-activation of the complement pathway in the setting of acute infection, and may present with initial features suggesting infection-associated glomerulonephritis (IAGN) that transform to DDD. We present a case of infection-associated trigger of recurrent DDD in a kidney transplant patient with acute bartonella infection.

Case Description

A 29 year old man with DDD and subsequent living unrelated kidney transplantation, maintained on tacrolimus, MMF, and prednisone, presented 1 year after transplant with headaches, fevers, diarrhea, and myalgias. He was diagnosed and treated for cat scratch disease (bartonella IgM 1:64). He was readmitted 11 days after initial presentation for neuroretinitis and non-oliguric AKI (Cr 3.5 mg/dL [baseline 1.4 mg/dL], low C3 and normal C4, UA with 89 RBC, 12 WBC, >500 protein, UPCR 1.48). Biopsy revealed diffuse endocapillary hypercellularity with neutrophils, diffuse global chunky mesangial and capillary loop staining for C3+++, IgM++, and EM with mesangial and subendothelial deposits of usual density without hump-type subepithelial deposits. There was ribbon-like staining for C3++ along tubular basement membranes with focal dense TBM transformation by EM, indicative of IAGN transforming to DDD. Factor H autoantibodies were then detected. He was treated with high-dose prednisone, doxycycline/rifabutin, and twice-weekly plasma exchange with FFP for 8 weeks. The bartonella infection resolved and kidney function returned to baseline with resolution of proteinuria and hypocomplementemia. Repeat biopsy 3 months later confirmed resolving IAGN-like features and early recurrent DDD.

Discussion

The inherent dysregulation of the alternative complement pathway in our patient likely put him at risk for overactivation of the complement system in the setting of an acute infection, leading to IAGN-like acute lesions and evolution to recurrent DDD in the kidney transplant. Prompt diagnosis and management led to clinical resolution but with persistent morphological changes. More research is needed to further characterize this association.