Abstract: TH-PO564
HIV Infection Associated with Plasma Cell-Rich Acute Interstitial Nephritis: A Case Report
Session Information
- Trainee Case Reports - I
October 25, 2018 | Location: Exhibit Hall, San Diego Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Trainee Case Reports
- 103 AKI: Mechanisms
Authors
- Elabd, Hatem, Albert Einstein College of Medicine/Jacobi, New York, United States
- Rashid, Tarek, Albert Einstein College of Medicine/Jacobi, New York, New York, United States
- Elkholi, Mennallah, University of Alexandria , Alexandria, Egypt
- Stokes, Michael Barry, Columbia University Medical Center, New York, New York, United States
Introduction
Acute interstitial nephritis (AIN) in HIV infected patients is usually attributable to drugs, opportunistic infections, and immune syndromes (e.g. immune reconstitution syndrome and diffuse infiltrative lymphocytosis syndrome). Whether HIV itself causes AIN is uncertain.
Case Description
A 59-year-old African female with a past history of hypertension was admitted with generalized weakness. Medications included lisinopril and nifedepine, and she denied NSAID, herbal, or illicit drugs. Physical exam disclosed no evidence of sicca syndrome. Laboratory evaluation was remarkable for serum creatinine of 12.9 mg/dl and blood urea nitrogen 149 mg/dl (baseline 3 months prior was 1.1mg/dl and 23 mg/dl respectively), hemoglobin 8.2g/dl, platelets 67 cells/mm3, 2+ schistocytes in peripheral smear, and LDH of 365 U/L. Urine microscopy showed innumerable WBCs/hpf, but no RBCs or casts. Spot urine protein–to-creatinine ratio was 1.7g/g. Given the suspicion for microangiopathic hemolytic anemia, she received empirical plasma exchange for 8 sessions, with no improvement of hematological parameters. Subsequent HIV-1 antibody test was positive, with viral load of >715,000 copies/ml, and CD4+ count of 20 cells/mm3. ADAMTS-13 activity was normal.
Renal biopsy showed normal appearing glomeruli and tubulointerstitial nephritis with numerous CD138+ plasma cells. No granulomas or features of thrombotic microangiopathy were seen. Immunofluorescence exam was negative, and no electron dense deposits or endothelial cell tubuloreticular inclusions were seen. Extensive infectious disease work up was negative. Bone marrow biopsy revealed hypercellular marrow, polyclonal plasmacytosis with CD138+ plasma cells (20%), and no evidence for malignancy or infections. Antiretroviral therapy (ART) regimen was started, with subsequent improvement in hematological parameters. Serum creatinine improved to 2.5mg/dl and proteinuria resolved.
Discussion
To our knowledge, there are only 2 previous case reports where AIN was thought to be a direct complication of HIV infection, both of which also showed a plasma cell-rich tubulointerstitial infiltrate. The exclusion of common causes of AIN and response to ART therapy in our case suggest that HIV infection itself may occasionally present with acute kidney injury and AIN.