Nephrotic Syndrome: An Overview

Nephrotic syndrome (NS) is a clinical entity characterized by massive proteinuria (>3.5 g/day), hypoalbuminemia, edema, and hyperlipidemia, reflecting glomerular filtration barrier injury rather than a single disease. The condition is classified as either primary, due to intrinsic glomerular disease such as focal segmental glomerulosclerosis (FSGS), membranous nephropathy, and minimal change disease, or secondary, resulting from systemic disorders such as diabetes mellitus. Idiopathic nephrotic syndrome is increasingly understood as an immune-mediated process, with both T-cell and B- cell dysregulation contributing to podocyte injury and proteinuria. Complications include infection, thromboembolic events, and progressive renal dysfunction, with incidence rates varying between children (1.15–16.9/100,000) and adults (≈3/100,000 annually). Diagnosis is established through protein quantification (spot urine protein/creatinine ratio or 24-hour urine collection) and supported by biochemical findings including hypoalbuminemia and hyperlipidemia. Management is multifaceted, targeting reduction of proteinuria, control of edema, prevention of complications, and achievement of remission. Treatment strategies include sodium and fluid restriction, diuretics, immunosuppressive therapy, and renin– angiotensin system inhibitors. Evidence supporting routine use of ACE inhibitors or ARBs for improved clinical outcomes remains mixed, though their antiproteinuric effect is well recognized. Supportive care, including infection prevention, anticoagulation in high-risk patients, and management of dyslipidemia, is critical. Despite its rarity, NS poses significant morbidity and risk for progression to chronic kidney disease or end-stage kidney disease, highlighting the need for early diagnosis, individualized therapy, and long-term follow-up to optimize patient outcomes.