Abstract: SA-PO663
Injection Heroin Use and AA-Type Renal Amyloidosis: An Underrecognized Etiology?
Session Information
- Glomerular Diseases: IgA and Complement-Mediated GN
November 05, 2022 | Location: Exhibit Hall, Orange County Convention Center‚ West Building
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1302 Glomerular Diseases: Immunology and Inflammation
Authors
- Mann, Jaskiran, Valley Hospital Medical Center, Las Vegas, Nevada, United States
- Chuapoco, Roberto Lorenzo, Touro College & University System, Las Vegas, Nevada, United States
- Nguyen, Hoang Anh, Valley Hospital Medical Center, Las Vegas, Nevada, United States
- Wallace, David C., Valley Hospital Medical Center, Las Vegas, Nevada, United States
- Yu, Kevin, Valley Hospital Medical Center, Las Vegas, Nevada, United States
Group or Team Name
- Valley Hospital Medical Center
Introduction
Serum amyloid A (SAA) renal amyloidosis is characterized by the deposition of serum amyloid A protein into renal glomeruli, tubules, and vessels. The AA amyloid proteins are misfolded aggregates derived from acute-phase reactant serum amyloid A protein. Regular injection heroin use has been linked to increased risk of secondary amyloidosis, possibly due to recurrent skin and soft tissue infections.
Case Description
Patient is a 40 year-old Caucasian male with history of untreated hepatitis C and daily injection heroin use who presented to the emergency department with cellulitis of bilateral hands, and was found to be septic and bacteremic with Streptococcus pyogenes. Patient was started on broad spectrum antibiotics. Transesophageal echocardiogram was negative for vegetations/endocarditis. Nephrology was consulted for worsening non-oliguric acute kidney injury with uptrending creatinine. Urine studies notable for protein 176 mg/dL with microalbumin 110.2mg/dL. Workup included renal ultrasound showing echogenic kidneys bilaterally; SPEP and UPEP with no M-spike, but elevated free kappa and lambda chains with normal kappa/lambda ratio; negative immunofixation; and repeat urine studies showing 20,840mg protein per day and UPC 16.4g/dL. Renal biopsy showed mild interstitial fibrosis and tubular atrophy (IFTA) and acute tubular injury, proteinaceous material in gloms and tubules that stained positive with congo red and demonstrated apple green birefringence; no evidence of kappa or lambda light chains on immunofluorescence. Renal function stabilized and patient was advised to follow up outpatient to initiate ACE inhibitor for proteinuria in likely AA renal amyloidosis.
Discussion
AA amyloidosis is an under-recognized cause of acute kidney injury. The pathophysiology may be due to inflammation associated with recurrent skin and soft tissue infections associated with injecting heroin, versus local inflammation due to injection heroin use. Case series have demonstrated rapid progression to dialysis-dependent renal failure and death in these patients. Greater awareness of renal amyloidosis and its complications may help reduce incidence of disease and/or slow its progression.