Abstract: FR-PO952
Long-Term Resolution of HIV-Associated Nephropathy (HIVAN) after Treatment with Highly Active Antiretroviral Therapy (HAART)
Session Information
- Glomerular Diseases: Potpourri
October 25, 2024 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics
Authors
- Elkhodary, Mohamed Tarek, The University of Tennessee Health Science Center College of Medicine, Memphis, Tennessee, United States
- Wall, Barry M., Veterans Affairs Medical Center, Memphis, Tennessee, United States
Introduction
HIVAN is strongly associated with APOL1 homozygosity. There is usually a second hit, HIV infection being the prototype, which facilitates or precipitates the onset of collapsing focal segmental glomerulosclerosis (FSGS). Removal of this second hit could potentially allow renal recovery. We describe a patient who developed nephrotic range proteinuria and renal failure secondary to HIVAN, necessitating hemodialysis, who recovered renal function following HAART and has had long-term preservation of renal function with no opportunistic infections.
Case Description
47-year-old African American male with bipolar disorder and CKD 3a presented in 2010 with fever, diaphoresis, and a gluteal abscess. Serum creatinine was markedly elevated, 8.0 mg/dl. Urinalysis was positive for +2 proteinuria, but negative for RBCs, WBCs, or cellular casts. UPCR was 7.75 mg/g. On imaging, kidneys were enlarged with increased echogenicity. Serological investigations were negative and complement levels were normal. Tests for RPR and hepatitis C were negative. HBsAg was positive. HIV-1 / 2 western blot returned positive with reduced CD4 count, 52 cells/µL, and HIV viral load of 246,940 copies/ml. He required hemodialysis support. Renal biopsy demonstated collapsing FSGS. HAART was initiated with continued outpatient hemodialysis. CD4 count improved and HIV viral load markedly decreased within 5 months of starting HAART. Renal function gradually improved and hemodialysis was discontinued. Proteinuria markedly improved, and he has maintained a stable serum creatinine (2.1 mg/dl) for 14 years while continuing antiviral treatment with nondetectable HIV viral load, CD4 count remaining >250 cells/µL and no opportunistic infections.
Discussion
HIVAN is driven by direct infection of kidney epithelial cells with HIV and subsequent HIV gene expression, particularly in patients of African ancestry with APOL1 homozygosity. Histologically, HIVAN results in a collapsing form of FSGS with tubular dilation and interstitial inflammation. HIVAN typically presents with rapid decline in kidney function with nephrotic range proteinuria. The risk increases if the patient has CD4 < 200 cells/µL, and /or high viral load. Early initiation of HAART can be associated with improvement in CD4 counts and HIV viral load, and can lead to subsequent long term improvement in GFR and proteinuria.