Renal glomerular endothelial cells (GEC) are a specialized microvascular cell type involved in the regulation of glomerular ultrafiltration. They form the inner part of the filtration barrier and are involved in pathophysiological processes in the glomerulum. They constitutively synthesize bio-active molecules, to which this basal activity can be chronically augmented by various inflammatory and thrombotic agents. GEC injury exerts significant influences on the progression and repair process of glomerular disease. When the glomerular lesion is severe, angiogenesis is prevented due to endothelial cell injury, with subsequent sclerosis taking place in the impaired region. These glomerular endothelial cell injuries inevitably affect mesangial and epithelial cells and presumably modify the progression of renal disease by reciprocally interacting with them. Because of difficulties associated with the culture, cloning and propagation, the biological properties of these cells remain largely u