A patient with well-controlled human immunodeficiency virus (HIV) infection achieved complete renal remission following immunosuppressive treatment for biopsy-confirmed class III lupus nephritis while maintaining stable viral control.
Researchers described a 50-year-old female patient with an 8-year history of HIV who was receiving antiretroviral therapy with tenofovir 300 mg, lamivudine 300 mg, and dolutegravir 50 mg daily. She presented with polyarthritis, alopecia, malar rash, and a 10-kg weight loss over 6 months. Laboratory evaluation revealed pancytopenia, elevated anti–double-stranded DNA (dsDNA) antibodies, reduced complement concentrations, and proteinuria. Her CD4 count was 600 cells/mm³, and HIV viral load was 120 copies/mL. Renal biopsy demonstrated focal mesangial and endocapillaryhypercellularity, with granular immunoglobulin G, C3, and C1q deposits on immunofluorescence, supporting a diagnosis of class III lupus nephritis.
The researchers evaluated renal response, lupus disease activity, and HIV control during immunosuppressive treatment, including 24-hour urinary protein excretion, urine protein-to-creatinine ratio, serum creatinine,anti-dsDNA antibodies, complement concentrations, CD4 counts, and HIV viral load. The patient received intravenous corticosteroids at 500 mg daily for 3 days followed by oral prednisolone 50 mg/day with gradual tapering, hydroxychloroquine 200 mg/day, and mycophenolatemofetil 1 g/day. Treatment also included enalapril 10 mg/day and cotrimoxazole prophylaxis, while antiretroviral therapy was continued.
Renal measures improved posttreatment. By day 120, 24-hour urinary protein excretion had decreased from 1,600 to 230 mg/day. The urine protein-to-creatinine ratio declined from 1.8 to 0.3, while serum creatinine remained at 0.6 mg/dL. The patient achieved complete renal remission by 6 months, with preserved renal function.
Anti-dsDNA antibody concentrations decreased from 477 to 40 IU/mL by day 120, while complement C3 and C4 concentrations normalized. Hemoglobin increased from 8.7 to 12.1 g/dL, and white blood cell counts rose from 2,870 to 7,100/µL. Joint symptoms improved by 2 months, followed by weight gain at 3 months and visible hair regrowth at 4 months.
HIV control remained stable throughout immunosuppressive treatment. At day 120, the CD4 count was 580 cells/mm³ compared with 600 cells/mm³ at baseline, while viral load remained low at 130 copies/mL vs. 120 copies/mL initially. Following remission, the patient continued maintenance treatment with prednisolone 5 mg/day, mycophenolatemofetil 1 g/day, hydroxychloroquine 200 mg/day, and antiretroviral therapy. The researchers reported sustained renal remission without lupus flares or opportunistic infections during the subsequent follow-up described in the report.
HIV-associated immune complex kidney disease can resemble lupus nephritis clinically and histologically. However, the patient's elevated anti-dsDNA antibodies, reduced complement concentrations, systemic autoimmune manifestations, and renal immunofluorescence findings supported lupus nephritis. The biopsy findings also differed from the collapsing glomerular and tubular abnormalities associated with HIV-related nephropathy and antiretroviral nephrotoxicity.
The report was limited by its single-patient design, which prevented statistical inference or generalization to broader populations of patients with HIV and lupus nephritis. Disease activity was assessed using serial laboratory and renal measures rather than a validated composite index. No repeat renal biopsy was performed to confirm histologic remission, and follow-up was relatively short for evaluating lupus relapse, opportunistic infections, or HIV virologic rebound. The patient also had preserved CD4 counts and low viral load prior to immunosuppressive treatment, limiting the applicability of the findings to patients with advanced immunodeficiency or uncontrolled HIV.
The case suggested that standard immunosuppressive treatment may achieve renal remission in selected patients with HIV and biopsy-confirmed lupus nephritis when immune function is preserved and viral control is maintained.
"Differentiation from HIV-associated renal disease is critical and relies on serological and histopathological confirmation," wrote lead study author Ashwant Kumar, of the Institute of Rheumatology at Madras Medical College and Rajiv Gandhi Government General Hospital in India, and colleagues.
The study authors reported no conflicts of interest.
