ASN's Mission

ASN leads the fight to prevent, treat, and cure kidney diseases throughout the world by educating health professionals and scientists, advancing research and innovation, communicating new knowledge, and advocating for the highest quality care for patients.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on Twitter

Kidney Week

Abstract: PO0240

Cat Scratch Kidney

Session Information

  • AKI Mechanisms - 3
    October 22, 2020 | Location: On-Demand
    Abstract Time: 10:00 AM - 12:00 PM

Category: Trainee Case Report

  • 103 AKI: Mechanisms

Authors

  • Rajan, Roy, Dartmouth-Hitchcock Health GraniteOne, Lebanon, New Hampshire, United States
  • Pettus, Jason R., Dartmouth-Hitchcock Health GraniteOne, Lebanon, New Hampshire, United States
  • Hopley, Charles W., Dartmouth-Hitchcock Health GraniteOne, Lebanon, New Hampshire, United States
Introduction

A case of anuric RPGN secondary to post infectious glomerulonephritis in setting of bartonella infection

Case Description

An 84-year-old female presented with creatinine of 7.85mg/dl (baseline 0.81mg/dl) during a workup for painless hematuria. She developed progressive hypoxia and blood-tinged sputum concerning for pulmonary/renal syndrome and was treated with immunosuppression and plasma exchange.

Serologic tests including ANA/ENA, anti-GBM, C-ANCA, P-ANCA, and MPO Ab were negative. However, PR3 Ab was elevated at 29.3 Units. Complement C3 and C4 levels were normal. Blood/urine cultures, assays for hepatitis B/C, HIV and Respiratory panel were negative. Renal biopsy showed an MPGN-pattern proliferative glomerulonephritis with necrotizing crescents. IF displayed global 3+ granular staining for both IgG and C3 as well as trace granular C1q. EM confirmed mixed mesangial (dominant), subendothelial, and a few distinct subepithelial hump-like deposits by EM, suggestive of an infection related glomerulonephritis.With a biopsy suggesting an infectious process and BAL without evidence of alveolar hemorrhage, immunosuppression and PLEX were discontinued. Broader infectious workup was negative for ASO titers, Borrelia antibody, Quantiferon/AFB cultures, and BAL for fungal organisms. However, Bartonella IgG was positive at 1:1024 (normal <1:128). Bartonella PCR was negative. Both TTE and TEE were negative for valvular lesions. Additional patient history elucidated recent acquisition of a pet cat and multiple scratches. Treatment focus shifted from immunosuppression to antibiosis.

Discussion

Our case highlights an underappreciated entity associated with GN, particularly in the absence of overt clinical endocarditis. There has been a crossover association reported with ANCAs, particularly anti-PR3, which can demonstrate either a pauci-immune or immune complex pattern as with our patient. The case demonstrates how renal biopsy and social history remain vital diagnostic tools in patients presenting with non-specific systemic illness.