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Kidney Week

Abstract: FR-PO0724

From Headache to Hemodialysis: Undiagnosed HIV Presenting as APOL1-Associated Collapsing Glomerulopathy

Session Information

Category: Glomerular Diseases

  • 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics

Authors

  • Isidor, Marc H., HCA Florida Lawnwood Hospital, Fort Pierce, Florida, United States
  • Mirza, Sabbir, HCA Florida Lawnwood Hospital, Fort Pierce, Florida, United States
  • Kanu, Donald Orji, HCA Florida Lawnwood Hospital, Fort Pierce, Florida, United States
  • Khan, Rahil, HCA Florida Lawnwood Hospital, Fort Pierce, Florida, United States

Group or Team Name

  • Team Lawnwood
Introduction

HIV-associated nephropathy (HIVAN) classically presents as a glomerulopathy with rapidly progressive kidney failure. African Americans are at high risk due to APOL1 high-risk variants (G1/G2), carried in biallelic configuration seen in 13% of this population. Although HIVAN incidence has declined with antiretroviral therapy, it may be the initial manifestation of undiagnosed HIV.

Case Description

32-year-old AA man no significant PMHx presents with worsening headache. Patient arrived in ED in hypertensive crisis (188/106 mmHg). Labs notable for BUN 57 /Cr 8.4 mg/dL (eGFR 8), potassium 5.6, hgb 7.5 g/dL (MCV 72). Urinalysis showed proteinuria (200 mg/dL, total protein 358 mg) with microscopic hematuria. Inpatient workup was positieve for HIV : viral load 14,265 copies/mL, CD4 333 cells/μL. Treponemal antibody was positive with nonreactive RPR, consistent with latent syphilis.
Renal ultrasound showed bilaterally atrophic echogenic kidneys consistent with underlying CKD. Kidney biopsy revealed collapsing glomerulopathy with mild IgG immune complex deposition of uncertain significance. APOL1 genotyping was sent.
Creatinine remained 7.7–8.9 mg/dL throughout the 14-day admission. Hemodialysis was initiated on day 7 followed by ART therapy on day 8 (dolutegravir and TDF/emtricitabine). Latent syphilis was treated with benzathine penicillin G. The patient remained dialysis-dependent at discharge.

Discussion

This case illustrates HIVAN presenting as dialysis-dependent AKI on previously unrecognized CKD. Bilateral renal atrophy and microcytic anemia suggest subclinical disease progression prior to presentation. The CD4 count of 333 cells/μL is notably higher than the 200 threshold typically associated with HIVAN, supporting the concept that APOL1 high-risk genotype — rather than immunosuppression severity alone — drives collapsing glomerulopathy, with HIV acting as a "second hit" triggering podocyte injury in genetically susceptible individuals. Importantly, TDF/emtricitabine is not recommended when creatinine clearance is below 30 mL/min; transition to a TAF-based regimen should be considered. Viral suppression may mitigate APOL1-associated kidney decline, though patients with advanced disease often remain dialysis-dependent. Kidney biopsy is essential for diagnosis, and APOL1 genotyping provides prognostic value and may identify candidates for emerging targeted therapies such as inaxaplin.