Postinflammatory glomerular recanalization is established under the accommodation of transformed mesangial cells

The relationship between mesangial cell proliferation and sclerosis has been studied using rat Thy-1.1 nephritis. The reconstruction of capillary lumina is essential for the repair of postinflammatory tissue damage in this type of glomerulonephritis.

We administered thalidomide or STI571 to Thy-1.1 nephritic rats. Thalidomide was intended to be a sup-pressor of capillary proliferation, and STI571, which is known to be a tyrosine kinase receptor inhibitor, was used for preventing mesangial proliferation.

The thalidomide-treated group showed a significant increase of urinary protein on day 3. ED-1-positive cells stagnated longer and the matrix increase was delayed. STI571 caused suppression of mesangial proliferation, and microaneurysm remained longer than in the other 2 groups, which resulted in delay of glomerular capillary reconstruction. The number of alfa-SMA-positive cells appeared to be smaller in both the thalidomide- and the STI571-treated groups.

Thalidomide had an effect in the early period of the experiment; however, there was no influence on the repair of glomerular capillary at the end. STI571 treatment, which inhibited proliferation of alfa-SMA-positive cells, seems to show that some degree of mesangial cell proliferation is necessary to reconstruct capillary structures and to regain glomerular function.