An Overview on Nephrotic Syndrome

Abstract

Nephrotic syndrome is a clinical disorder characterized by heavy proteinuria, hypoalbuminemia, hyperlipidemia, and varying degrees of edema. It results from structural or functional disruption of the glomerular filtration barrier, particularly at the level of podocytes and the slit diaphragm. Nephrotic syndrome can be classified into primary (idiopathic) forms, such as minimal change disease (MCD) and focal segmental glomerulosclerosis (FSGS), and secondary forms associated with systemic diseases including diabetes mellitus, lupus nephritis, infections, drugs, and malignancies.

In pediatric populations, minimal change disease is the most common and is typically steroid-responsive, whereas FSGS is more frequently associated with steroid resistance and higher risk of renal function decline. The pathophysiology involves immune dysregulation, podocyte injury, genetic susceptibility, and altered glomerular permeability. Persistent or poorly controlled disease can lead to complications such as infection, thrombosis, acute kidney injury, and progression to chronic kidney disease or end-stage renal disease (ESRD).

Management strategies depend on the underlying cause and treatment response, ranging from corticosteroids and immunosuppressive therapy to supportive measures such as diuretics, antiproteinuric agents, and lipid control. Recent advances in molecular and genetic studies have improved understanding of disease mechanisms, particularly in cases of steroid-resistant nephrotic syndrome (SRNS).