Abstract: PUB366
C3 Glomerulonephritis in Intravenous (IV) Drug Use
Session Information
Category: Glomerular Diseases
- 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics
Author
- Ravi, Divya, Unity Hospital, Rochester, New York, United States
Introduction
C3 glomerulopathy includes a group of disorders where there is dysregulation and overactive stimulation of the alternative pathway of the complement system. The common triggers are monoclonal antibodies, autoimmune diseases and infections. We present a case of C3 glomerulonephritis in a patient with IV drug use.
Case Description
A 30 year old male patient with past medical history of asthma, GERD, anxiety and IV fentanyl and cocaine use presented with complaints of intermittent fever, chills and dark urine since 3 months. He was found to be febrile with mild left sided CVA tenderness.He had AKI with creatinine elevated to 2.4 from baseline of 1.0-1.2. Urinalysis showed RBC casts along with moderate proteinuria. Patient was started on vancomycin and cefepime while awaiting cultures. Glomerulonephritis workup was sent and revealed elevated C3 and CRP but negative auto-immune panel. Protein-creatinine ratio was 9310 mg/day. Blood cultures were negative and TEE was negative for vegetations. He was started on suboxone for opiate use disorder. Patient underwent a kidney biopsy which showed diffuse active intracapillary proliferation glomerulonephritis with C3 containing immune complex deposits. The patient was started on lisinopril and offered immunosuppressive therapy but wanted to complete COVID19 vaccination first. On follow up, he was found to have improvement of proteinuria (97 mg/day) and creatinine returned back to his baseline (1.0-1.2)
Discussion
Previous cases of C3 glomerunephritis have been associated in other pro-inflammatory states like auto-immune flares and infections. In our patient, while infection and autoimmune disease was ruled out, we found presence of C3 deposits and glomerular disease which improved with cessation of IV drug use. This raises an important question of whether transient bacteremia or an inflammatory state brought on by IV drug use can induce C3 glomerulopathy.