Although the pathogenesis is not fully understood, current evidence supports that most cases of glomerulonephritis (GN) are due to an immunologic response to a variety of different etiologic agents. The immunologic response, in turn, activates a number of biological processes (eg, complement activation, leukocyte recruitment, and release of growth factors and cytokines) that result in glomerular inflammation and injury [1,2]. GN may be isolated to the kidney (primary glomerulonephritis) or be a component of a systemic disorder (secondary glomerulonephritis