Glomerulonephritis in horses can cause protein-losing nephropathy, chronic renal failure, and weight loss. Glomerular injury is most commonly associated with immune complex deposition, initiating a self-sustaining disease process that results in end-stage loss of renal function. The initiation and propagation of glomerulonephritis are based not only on the complex interaction of several cellular and soluble mediators but also on the secondary effects of protein loss, including systemic and glomerular hypertension. This article summarizes the recent understanding of the pathophysiology of glomerulonephritis gathered from human and experimental studies and describes a case of glomerulonephritis in a horse.