FIGURE 1.

Podocytopathies result from the equilibrium between the nature of injury and the glomerular capacity of repair. When podocyte injury does not determine net cell loss, no changes are present on light microscopy and only foot process effacement is detectable, as in minimal changes (MC). In a setting of fast podocyte loss in kids younger than 5 years old, massive attempt of repair takes place. Immature podocytes are generated and are visible as a halo of hypertrophic podocytes overlying capillary loops as in diffuse mesangial sclerosis (DMS). When severity or chronicity of podocyte injury overcomes the capacity of PECs to replace detached or loss podocytes, glomerular basement membrane denudation triggers an injury cascade. This results in the segmental solidification of the tuft with accumulation of extracellular matrix characteristic of focal segmental glomerulosclerosis (FSGS). Finally, if fast podocyte loss occurs in individuals where the regenerative capacity is inadequate, generation of new podocytes is hampered and proliferating progenitors accumulate in Bowman space in the form of pseudocrescents resulting in collapsing glomerulopathy (CG) (Hematoxylin and eosin stains, magnifications 40x. Bars= 50 μm). (Abbreviations: MC= minimal changes, DMS= diffuse mesangial sclerosis, FSGS= focal segmental glomerulosclerosis, CG= collapsing glomerulopathy, PEC= parietal epithelial cell, FPE= foot process effacement).