Background: Glomerular diseases are commonly classified based on immune complex and complement deposition patterns. While classical and alternative complement pathways are well studied, the role of the lectin pathway (LP) in glomerular disease pathogenesis remains underexplored. Previous observations at our institute revealed C4d deposition in 20% of C3 glomerulonephritis (C3GN) and 50% of dense deposit disease (DDD), prompting further investigation into LP activation across various glomerular pathologies. Methods: In this prospective study (2020–2021), 39 consecutive kidney biopsies (native and transplant) with glomerular pathology were analyzed. Light microscopy (LM), IF, and electron microscopy (EM) were used for diagnosis. Routine immunofluorescence (IF) findings guided selection for additional immunofluorescent staining with C5b-9, C4d, MASP, MBL, and ficolin on OCT blocks stored at –80°C. Results: Lectin pathway activation was observed in 75% of membranous nephropathy (MN) cases, with higher prevalence in primary MN (72%). Early-stage MN showed stronger LP activation (80%) compared to late-stage disease. IgG4 predominance (16%) and co-dominance (58%) were frequently associated with LP activation. No correlation was found between LP activation and anti-PLA2R status. C3 tissue deposition was present in 75% of secondary and 28% of primary MN cases. In secondary MN, C3 tissue positivity correlated with low serum C3 in 75% of cases; this correlation was absent in primary MN. IgA nephropathy (IgAN) showed no deposition of lectin pathway markers, although all cases exhibited strong C5b-9 deposition. C3 was deposited in 50% of IgAN cases without correlation to serum C3 levels. C4d was positive in 25% of IgAN. In complement-mediated MPGN, strong C3 and C5b-9 deposits were observed along capillary walls and mesangium, but no lectin pathway proteins were detected. Other glomerular diseases including MPGN, FSGS, non-proliferative glomerulopathies, diabetic nephropathy, amyloidosis, chronic active antibody-mediated rejection (AMR), acute tubular injury (ATI), and thrombotic microangiopathy (TMA) showed no evidence of complement activation via the lectin pathway. Conclusion: Our study demonstrates consistent activation of the lectin pathway in primary membranous nephropathy, particularly in early stages, and links it to IgG4 deposition. LP activation is variable in secondary MN and lupus nephritis, but absent in IgAN, MPGN, FSGS, and other glomerulopathies. These findings suggest a potential pathogenic role for the lectin pathway in MN and underscore the therapeutic potential of complement-targeted interventions tailored to specific pathways.