Article Sections

Introduction

Nephrotic syndrome is defined by heavy proteinuria (>3.5 g/day), hypoalbuminemia, and peripheral edema.  It results from increased permeability of the glomerular filtration barrier ( Figure 1), which is composed of capillary endothelial cells, the glomerular basement membrane (GBM), and specialized epithelial cells called podocytes.  The underlying injury in nephrotic syndrome is noninflammatory and involves podocytes and the GBM without significant involvement of other glomerular structures; this is in contrast to the diffuse inflammatory damage seen in nephritic syndrome (discussed in a separate article).

Pathophysiology

In nephrotic syndrome, glomerular injury primarily affects the podocytes and is isolated from the inflammatory mediators in the circulation (Bowman space); therefore, it is noninflammatory.  Podocytes play a crucial role in maintaining the selectivity of the glomerular filtration barrier, and their dysfunction allows proteins that are normally retained in the blood to pass through, resulting in significant

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