Kidney Week

Abstract: PUB048

HIV-Associated Immune Complex Kidney Disease in a Patient with Normal Complement Levels

Session Information

• Publication Only

Category: Acute Kidney Injury

• 102 AKI: Clinical, Outcomes, and Trials

Authors

• Markoja, Kaitlin, MedStar Georgetown University Hospital, Washington, District of Columbia, United States

Kaitlin Markoja, MD

• Iyer, Karishma, MedStar Georgetown University Hospital, Washington, District of Columbia, United States

Karishma Iyer, MD

• Cheraghvandi, Lukman, MedStar Georgetown University Hospital, Washington, District of Columbia, United States

Lukman Cheraghvandi, MD

• Kwon, Donghyang, MedStar Georgetown University Hospital, Washington, District of Columbia, United States

Donghyang Kwon, MD

• Pourafshar, Negiin, MedStar Georgetown University Hospital, Washington, District of Columbia, United States

Negiin Pourafshar, MD, FASN

Introduction

HIV infection is frequently complicated by renal dysfunction. There is a variety of renal pathology associated with HIV.

Case Description

A 35-year-old male with a medical history including HIV (CD4 257 cells/mm³, viral load 36 copies/mL) not on antiretroviral therapy (ART) and schizophrenia presented with shortness of breath. He was treated for community acquired pneumonia at another facility three months prior, where his serum creatinine (SCr) was 4.5-5 mg/dL. At our institution, he was afebrile, not hypoxic, and hypertensive with systolic blood pressure 160-180 mmHg. Laboratory results showed elevated blood urea nitrogen at 84 mg/dL and SCr at 10.76 mg/dL. Urinalysis had moderate proteinuria and 5 red blood cells per high-power field, with a urine protein to creatinine ratio of 2.0 g/g. CT of the chest, abdomen, and pelvis revealed dense left lower lobe pneumonia, and blood cultures later confirmed Streptococcus pneumoniae infection. He was treated with ceftriaxone, yet SCr remained elevated. Serologic investigation was unremarkable.

Renal biopsy revealed interstitial edema with a lymphoplasmacytic infiltrate with occasional eosinophils in the interstitium. Tubules showed epithelial flattening and cellular debris, tubular loss, interstitial fibrosis, and vascular wall thickening. Immunofluorescence revealed 1+ IgG granular positivity, while electron microscopy detected occasional immune-complex deposits in the mesangium, accompanied by mesangial matrix expansion, concerning for HIV-associated immune complex kidney disease (HIVICK).

With blood pressure reduction and treatment for infection, SCr decreased to 6 mg/dL. SCr remained stable two months later and after ART initiation.

Discussion

HIVICK involves immune complex deposition, which can occur in situ or via secondary deposition. Proposed viral antigens include p24 and gp120. Previous studies suggest that HIVICK is more prevalent in patients with higher viral loads, hepatitis co-infection, and low complement levels. However, our patient had low HIV viremia, no hepatitis, and normal complement levels. Renal biopsy is crucial to discern HIV-associated renal pathologies accurately. Treatment strategies for HIVICK warrant further exploration, particularly considering the overall higher risk for immunosuppression in this population and each patient's unique clinical profile.