Lupus nephritis (LN) is a significant complication of systemic lupus erythematosus (SLE), increasing morbidity and mortality. Despite advancements in survival rates for severe LN, only half of patients achieve complete clinical remission with immunosuppressive therapy. Timely detection of LN is crucial for prompt intervention and improved patient outcomes. Biomarkers have emerged as valuable tools for LN detection and monitoring, but their role in LN pathogenesis remains unclear. Renal biopsy is the gold standard for identifying histological phenotypes, but the molecular pathophysiology of specific renal lesions is poorly understood. This review provides an up-to-date overview of recent developments in LN biomarkers. **Keywords:** biomarker; systemic lupus erythematosus; lupus nephritis SLE is a chronic autoimmune disease characterized by autoantibodies, autoreactive B and T cells, and cytokine dysregulation, leading to inflammation and organ damage. LN is the most common complication, affecting the kidney and contributing to high morbidity and mortality. LN is classified into six histological types, each with distinct responses to treatment and kidney function preservation. The pathogenesis involves complex interactions between innate and adaptive immune responses and the kidney parenchyma. Genetic, epigenetic, and environmental factors contribute to LN, but its precise etiology remains unclear. The onset and progression of LN vary among patients, highlighting the need for biomarkers to assess these diverse aspects. **LN Biomarkers** 1. **Serum AutoAbs:** AutoAbs, such as anti-dsDNA and anti-C1q, are valuable biomarkers for LN. They are associated with distinct histological classifications and predict disease activity and outcomes. 2. **Cytokines/Chemokines:** Cytokines like BAFF, APRIL, IP-10, IL-6, IL-10, IL-16, Ang2, and TWEAK are crucial in regulating immune responses and predicting LN activity. Urinary levels of these molecules can distinguish between active and inactive LN. 3. **Cell Adhesion Molecules (CAMs):** CAMs, including ALCAM, ICAM-1, VCAM-1, NCAM-1, and L-selectin, guide leukocyte movement and are potential biomarkers for LN. Urinary CAMs have shown high precision in distinguishing active and inactive LN. 4. **Other Protein/Lipid Molecules:** Proteins and lipids, such as CD163, EGF, ceramides, and complement components, are emerging as potential biomarkers for LN. 5. **Genetics:** Genetic variants in genes like TNFAIP3, FCGR, STAT4, BANK1, MERTK, and APOL1 contribute to LN susceptibility and severity. 6. **Epigenetics:** Epigenetic processes, including DNA methylation and histone modifications, play crucial roles in LN development. **Lupus nephritis (LN) is a significant complication of systemic lupus erythematosus (SLE), increasing morbidity and mortality. Despite advancements in survival rates for severe LN, only half of patients achieve complete clinical remission with immunosuppressive therapy. Timely detection of LN is crucial for prompt intervention and improved patient outcomes. Biomarkers have emerged as valuable tools for LN detection and monitoring, but their role in LN pathogenesis remains unclear. Renal biopsy is the gold standard for identifying histological phenotypes, but the molecular pathophysiology of specific renal lesions is poorly understood. This review provides an up-to-date overview of recent developments in LN biomarkers. **Keywords:** biomarker; systemic lupus erythematosus; lupus nephritis SLE is a chronic autoimmune disease characterized by autoantibodies, autoreactive B and T cells, and cytokine dysregulation, leading to inflammation and organ damage. LN is the most common complication, affecting the kidney and contributing to high morbidity and mortality. LN is classified into six histological types, each with distinct responses to treatment and kidney function preservation. The pathogenesis involves complex interactions between innate and adaptive immune responses and the kidney parenchyma. Genetic, epigenetic, and environmental factors contribute to LN, but its precise etiology remains unclear. The onset and progression of LN vary among patients, highlighting the need for biomarkers to assess these diverse aspects. **LN Biomarkers** 1. **Serum AutoAbs:** AutoAbs, such as anti-dsDNA and anti-C1q, are valuable biomarkers for LN. They are associated with distinct histological classifications and predict disease activity and outcomes. 2. **Cytokines/Chemokines:** Cytokines like BAFF, APRIL, IP-10, IL-6, IL-10, IL-16, Ang2, and TWEAK are crucial in regulating immune responses and predicting LN activity. Urinary levels of these molecules can distinguish between active and inactive LN. 3. **Cell Adhesion Molecules (CAMs):** CAMs, including ALCAM, ICAM-1, VCAM-1, NCAM-1, and L-selectin, guide leukocyte movement and are potential biomarkers for LN. Urinary CAMs have shown high precision in distinguishing active and inactive LN. 4. **Other Protein/Lipid Molecules:** Proteins and lipids, such as CD163, EGF, ceramides, and complement components, are emerging as potential biomarkers for LN. 5. **Genetics:** Genetic variants in genes like TNFAIP3, FCGR, STAT4, BANK1, MERTK, and APOL1 contribute to LN susceptibility and severity. 6. **Epigenetics:** Epigenetic processes, including DNA methylation and histone modifications, play crucial roles in LN development. **