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Objectives Lupus nephritis (LN) is a major cause of renal failure in SLE. HIgh 24-hour proteinuria is a biomarker for LN flare, but potential confounders, like comorbidities or nephrotoxic exposure, should be ruled out. Nephropathy is also a complication in HIV patients. The kidney acts as a viral reservoir despite effective antiretroviral therapy. HIV-associated nephropathy (HIVAN) is the usual involvement; ‘lupus-like’ immune complex glomerulonephritis can occur with histological findings that mimic LN. There is limited literature data regarding patients presenting with both conditions. We report the case of a SLE patient with HIV and nephropathy.Methods A 24-aged female patient was diagnosed with HIV in 2011 and treated with antiretroviral therapy achieving sustained virological suppression. In 2013 arthritis, serositis, hematological cytopenias, high-titer ANA and anti-dsDNA led to SLE diagnosis so hydroxychloroquine and glucocorticoid were started. In 2014, due to high proteinuria levels (2 g/24h), a renal biopsy was perform and it showed Class III-IV LN. A satisfactory response to mycophenolate mofetile (MMF) was observed until 2017 when proteinuria rose to 1.5g/24h and Euro-Lupus protocol cyclophosphamide became necessary followed by maintenance with MMF. Transient remission was achieved, although proteinuria levels fluctuated between 0.3g/24h to 0.8g/24h and slowly the estimated glomerular filtration rate (eGFR) declines over the years.Results In August 2025 the patient was referred to the multidisciplinary nephro-rheumatology clinic for persistent proteinuria (> 0.5g/24h) and rising serum creatinine up to 1.7 mg/dL (eGFR 35 ml/min/1.73m2). A renal re-biopsy was reccomended. Hystological findings were characterized by segmental glomerulosclerosis, focal tubular atrophy, moderate epithelial cytoplasmic vacuolization, and interstitial fibrosis with moderate arteriolosclerosis without immune deposits ruling out active LN.Abstract LBA:01:11 Figure 1Conclusions The decline in kidney function was ascribed to HIVAN. MMF was continued, leveraging its documented antireplicative properties observed in HIV-positive transplant recipients. To optimize nephroprotection and mitigate proteinuria, dual renin-angiotensin-aldosterone system blockade was initiated. Electron microscopy is currently pending to identify intrarenal viral particles. The peculiarity of this case lies in the association between HIVAN and LN. Rheumatologists should consider that an increase in proteinuria in SLE patients is not always indicative of a flare; renal biopsy remains the gold standard for differential diagnosis.