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: PO1490

A Case of Rapid Progressive Glomerulonephritis Associated with Disseminated Gonococcal Infection

Session Information

Category: Glomerular Diseases

  • 1202 Glomerular Diseases: Immunology and Inflammation

Authors

  • Osman, Safa, The University of Mississippi Medical Center, Jackson, Mississippi, United States
  • Ali, Nihal M., The University of Mississippi Medical Center, Jackson, Mississippi, United States
  • Vaitla, Pradeep, The University of Mississippi Medical Center, Jackson, Mississippi, United States
  • Cabeza Rivera, Franco H., The University of Mississippi Medical Center, Jackson, Mississippi, United States
Introduction

Disseminated gonococcal infection (DGI) results from bacteremic spread of the sexually transmitted pathogen, Neisseria gonorrhoeae. Direct and immunological damage of multiple organs can be seen. We are reporting a case of sterile DGI with RPGN as part of the initial presentation.

Case Description

A 60-years old male with a 5-year history of seronegative spondyloarthropathy, hypertension, heart failure, poor dentition who presented to the hospital with shortness of breathing, diarrhea, joint pain, and palpable purpura ongoing for several weeks. Work-up revealed severe anemia and rapidly progressive acute renal failure (Baseline creatinine unknown, peaked at 7.2 mg/dl on admission), urine showed 9.3 g of proteinuria, hematuria, and pyuria. Serological w/up showed low C3 with normal C4, ASO, ANA, ANCA and anti GBM. Negative HIV, hepatitis B, C, syphilis serologies, monoclonals and cryoglobulins. Skin biopsy showed leukocytoclastic vasculitis which improved with steroids. Kidney biopsy showed crescentic glomerulonephritis (GN) with 10% IFTA likely due to infectious GN (RPGN). Patient completed 3-day course of solumedrol but left before cyclophosphamide could be initiated. A week later he presented with persistent hematuria and oliguria. Echocardiogram showed tricuspid endocarditis and leaflet perforation. Blood cultures were negative. Patient started on vancomycin and Rocephin for culture negative endocarditis. Extensive infectious disease workup, metagenomics test showed Neisseria gonorrhea as the cause of endocarditis. Kidney function improved. Due to disseminated GC and concern for complement deficiency, he was referred to Adult Immunology clinic.

Discussion

DGI is estimated to occur in up to 3 percent of patients infected with N. gonorrhoeae. The probability that a localized gonococcal infection will spread to joints and other tissues depends upon specific host, microbial, and possibly immune factors. RPGN is unusual presentation, the immunopathogenesis is uncertain but immunological and hypersensitivity damage is postulated based on the frequent lack of N. gonorrhoeae growth from blood, skin, and synovial fluid cultures during disseminated infection. Congenital or acquired complement deficiencies (C5, C6, C7, or C8) predispose to DGI as a result of decreased complement-mediated killing of N. gonorrhoeae.