Our understanding on the pathophysiology of glomerular diseases has largely relied on meticulous evaluation and strategic approaches to renal biopsy material using light microscopy (LM), immunofluorescence (IF), and electron microscopy (EM). Glomerular morphology has been categorized based on injury patterns indicated by changes in glomerular cellularity and cell types, and abnormal loop changes under LM, after which several primary glomerular diseases have been named, such as focal segmental glomerulosclerosis and diffuse proliferative or mesangioproliferative glomerulonephritis. Subtyping of glomerular morphology has been used as a therapeutic guide or prognostic parameter of immunoglobulin A (IgA) nephropathy, lupus nephritis, and antineutrophil cytoplasmic antibody-associated glomerulonephritis. IF can be used to identify IgA nephropathy and C3 glomerulopathy regardless glomerular histology, meanwhile diffuse glomerular basement membrane (GBM) thinning on EM characterizes thin GBM nephropathy. Recently, immunohistochemistry, mass spectrometry, and next-generation sequencing techniques have been included in the diagnosis of fibrillary glomerulonephritis, typing of amyloid fibrils, and exploring the etiology of hereditary nephropathy, respectively. We admit that correlations between renal morphology and clinical findings continue to fall short of our expectations, and we hope that further investigations into glomerular morphology and the discovery of new diagnostic/research tools will narrow this gap.