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Abstract: SA-PO864

Renal Riddles: Acute Interstitial Nephritis in Newly Diagnosed HIV

Session Information

Category: Glomerular Diseases

  • 1401 Glomerular Diseases: From Inflammation to Fibrosis

Authors

  • Rajagopal, Amulya, Henry Ford Hospital, Detroit, Michigan, United States
  • Sahota, Ruchi Jalota, Henry Ford Hospital, Detroit, Michigan, United States
  • Hanna, James, Henry Ford Hospital, Detroit, Michigan, United States
  • Soi, Vivek, Henry Ford Hospital, Detroit, Michigan, United States
  • Faber, Mark D., Henry Ford Hospital, Detroit, Michigan, United States
  • Kumbar, Lalathaksha Murthy, Henry Ford Hospital, Detroit, Michigan, United States
Introduction

Acute interstitial nephritis (AIN) is an inflammatory process often triggered by medications, infections, autoimmune diseases, or idiopathic factors. Interstitial nephritis can occur as a direct consequence of HIV infection, but cases demonstrating this through exclusion of other etiologies are rare. We present a case of acute interstitial nephritis overlying non-collapsing focal segmental glomerulosclerosis (FSGS) in a patient with newly diagnosed HIV.

Case Description

A 51 year old African American male presented with hypertensive emergency along with 3 days of lower extremity edema, cough, dyspnea, and fatigue. Significant labs included: Cr 4.80 mg/dl (unclear baseline), UA with blood and > 500 protein, UPCR 9.9 g/g. Serology workup of nephrotic syndrome revealed ANA 1:640, ds-DNA 1:20, C3 low. Hepatitis panel was negative. HIV-1 positive, with viral load < 30 copies/mL, CD4 547, and Treponemal IgG with nonreactive RPR. Renal ultrasound showed bilateral increased renal echogenicity. Renal biopsy revealed primary FSGS non-collapsing variant and AIN with plasma cell rich infiltrate. Treatment with highly active antiretroviral therapy (HAART) was initiated. One month later, patient was readmitted with right cranial nerve (CN) III and VI palsy. MRI brain revealed possible new meningioma or inflammatory process. Repeat serology showed C3 improved, elevated IgG4, normal SSA/Ro and SSB/La, elevated rheumatoid factor, cerebrospinal fluid pleocytosis of mononuclear cells, and elevated IgG index and oligoclonal bands. Restaining of prior renal biopsy was negative for IgG4-related disease. Patient was started on corticosteroids for possible inflammatory neurologic process. Follow-up visits noted improvement in Cr < 1.0 mg/dl with continued nephrotic range proteinuria despite treatment.

Discussion

This case underscores the complexity of diagnosis in the presence of, autoimmune markers, HIV infection, and overlapping clinical features. The diagnosis of AIN occurred prior to initiation of HAART or any other medications. The patient's renal function showed initial improvement with HAART, but a more significant improvement was observed upon the initiation of corticosteroid treatment. The recommended treatment for HIV-associated interstitial nephritis involves initiating HAART, while the efficacy of corticosteroids in this condition remains uncertain.