The pathophysiology of secondary FSGS involves glomerular hypertrophy and hyperfiltration-induced podocyte stress, leading to progressive proteinuria and sclerosis.2 The management of secondary FSGS typically includes renin–angiotensin–aldosterone system blockade, blood pressure control, and weight optimization to reduce glomerular stress.4 This evidence concerns the gene REN and focal segmental glomerulosclerosis.