Focal segmental glomerulosclerosis (FSGS) represents a histopathologic pattern of injury defined by sclerosis to portions of some, but not all glomeruli. It is considered a primary clinical podocytopathy where direct injury to kidney podocytes, specialized terminally differentiated epithelial cells that wrap around glomerular capillaries and are crucial for the kidney's filtration barrier, drives proteinuria or nephrotic syndrome.1 The etiology of podocyte injury in FSGS is heterogeneous, ranging from immune-mediated mechanisms and maladaptive hemodynamic changes, to disease-causing gene mutations.