Background: Glomerulopathies are the main cause of ESRD. Primary or secondary causes of glomerular diseases com prise more than 70% of cases that end up in renal replace ment therapies. Summary: The total glomerular mass that each individual contains is key to maintaining normal kidney function. Diabetes, hypertension, and any primary or sec ondary glomerulopathy may threaten the normal glomeru lar function. In fact, any glomerular insult may alter the glo merular filtration barrier, which in turn is composed by the podocyte, the glomerular basement membrane, and the capillary endothelial cell. Deposition of immune complexes, antibodies, or complement components at the subepitheli al, intramembranous, or subendothelial space, and muta tions in podocyte, slit diaphragm, or glomerular basement membrane proteins or enzymes are the main etiologies of glomerular alterations. Podocytes are glomerular cells that do not divide under normal circumstances. In this respect, maintenance of the absolute podocyte number per glomer ulus is critical for normal glomerular function. As the insult progresses, podocytes start to detach from the glomerular basement membrane. When the podocyte loss is over 40% in a glomerulus, glomerulosclerosis develops, and oblitera tion of the glomerulus is the rule. In clinical grounds, this phenomenon is diagnosed mainly by proteinuria and a de cline in glomerular filtration rate. Key messages: In this re view article, the impact of podocyturia in glomerular diseas es and the main mechanisms of podocyte detachment are discussed. Finally, potential targets of therapeutic approach are suggested.