Renal Tubulointerstitial Lesions in Mercuric Chloride-Treated Brown Norway Rats.

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Abstract
Renal tubulointerstitial lesions in mercuric chloride-treated Brown Norway rats were investigated focusing on the relationship between the development of lesions and kinetics of infiltrating cells and α-smooth muscle actin (SMA)-positive myofibroblasts. Fifteen rats were injected with 1 mg/kg b.w. of mercuric chloride at day 0, and 5 rats were killed at days 2, 4, and 6, respectively. Another 20 rats were injected with the same dose of mercuric chloride at days 0, 2 and 4, and 5 rats were killed at days 6, 8, 10, and 20, respectively. No additional changes were detected in glomeruli, whereas, mainly in the proximal tubules, necrosis was prominent at day 2, regenerative changes were obvious at day 4, and dilatation of the affected tubules with peritubular fibrosis developed at and after day 6. Following the renal epithelial damage, mononuclear cell infiltration developed in the renal interstitium at and after day 6, and among the infiltrating cells, ED1-positive macrophages were most predominant and CD8-positive T cells were next throughout the experimental period. They began to increases prominently at 2 days after 3 injections of mercuric chloride, i.e. at day 6. In addition, the number of α-SMA-positive myofibroblasts also increased at and after day 6, and the kinetics of ED1-positive macrophages corresponded well with that of α-SMA-positive myofibroblasts. Renal interstitial fibrosis developed along with the increase in numbers of these two cell populations. As to other infiltrating cells, although the absolute number was very small, CD45RA-positive B cells significantly increased at and after day 10. A few CD4-positive T cells and ED2-positive cells were also observed but their numbers did not show significant changes. The present results indicate that ED1-positive macrophages and α-SMA-positive myofibroblasts participate in renal fibrosis in Brown Norway rats following mercuric chloride-treatment, although the role of lymphocytes in renal fibrosis is still obscure.