FSGS

FSGS results from podocyte injury and effacement of foot processes, leading to increased glomerular permeability. It can be primary (idiopathic, often due to circulating permeability factors) or secondary to conditions such as HIV infection (collapsing variant), heroin use, obesity, sickle cell disease, reflux nephropathy, or APOL1 gene variants (common in patients of African descent). Light microscopy shows segmental sclerosis and hyalinosis affecting some glomeruli, while others appear normal; electron microscopy reveals diffuse podocyte foot process effacement similar to minimal change disease, but FSGS is typically steroid-resistant. Clinically, patients present with nephrotic syndrome (proteinuria >3.5 g/day, hypoalbuminemia, edema, hyperlipidemia) and may have hypertension and microscopic hematuria, distinguishing it from minimal change disease. Diagnosis requires renal biopsy since light microscopy findings can be patchy and missed on limited sampling. Treatment involves corticosteroids (variable response), calcineurin inhibitors, ACE inhibitors/ARBs for proteinuria reduction, and management of underlying secondary causes. Prognosis is guarded, with many patients progressing to end-stage renal disease, especially with collapsing variant or steroid resistance. FSGS is a major indication for kidney transplantation, though it can recur in the transplanted kidney.