Renal diseases are in many cases associated with the presence of increased numbers of apoptotic cells in the kidney. Apoptosis has been proposed as an important mechanism involved in the resolution of a proliferative response. Furthermore, recent studies indicate its possible involvement in progression of renal disease, leading to sclerosis. Moreover, in an experimental model of acute mesangioproliferative glomerulonephritis in the rat, induced via antibodies directed to Thy-1, evidence was obtained for the occurrence of apoptosis coinciding with the very early induction of mesangial injury. The present review is focused on apoptosis in relation to this model, and discusses recent findings concerning direct involvement of triggering of Thy-1 as well as deposition of terminal complement complexes in the induction of mesangial cell apoptosis.