The notion that the Ang/Tie system contributes to disease pathogenesis is supported by clinical studies and studies in animal models, and by the relation between symptoms of critical illness and disturbances in this system. In mice, Ang-2 over-expression in glomeruli causes proteinuria and apoptosis of glomerular ECs [19] . In a rat model of glomerulonephritis, Tie2 is over-expressed by ECs, and Ang-1 and Ang-2 are over-expressed by podocytes in a time-dependent manner during the repair phase [20] . Therefore, Ang/Tie might be involved in renal failure and repair.