Monocyte chemoattractant protein-1 expression in renal tissue is associated with monocyte recruitment and tubulo-interstitial lesions in patients with lupus nephritis

Objective To investigate the pattern of monocyte chemoattractant prolein-1 (MCP-1) distr ibution in the renal interstitium and evaluate its pathogenic role in tubulo-in terstitial lesions in patients with lupus nephritis, the distribution of MCP-1 in renal tissue was observed. Methods Eighteen female patients with biopsy-proven lupus nephritis were enrolled in th is study. No intensive immunosuppresive therapy was used in these patients duri ng the 3 months prior to renal biopsy. The distribution of MCP-1, infiltra tion of CD68(+) (macrophage/monocyte), CD4(+) and CD8(+) cells in the tubulo-in terstitium of patients with lupus nephritis was detected using immunohistochemic al staining with specific antibodies. Renal specimens from patients with minima l change glomerulonephritis were used as controls. Results MCP-1 protein was widely distributed in the renal tissue of patients with lupus nephritis, mainly located at the baso-lateral surface of tubular epithelial ce lls (16/18 biopsies), and on the wall of interstitial blood vessels (9/18 biopsi es). In contrast, tubular MCP-1 staining was weak and rare in renal tissue fro m controls (7.4±6.2% vs 26.7±22.8%, P<0.01). Tubulo-interstitial in filtration of CD68(+) , CD4(+) and CD8(+) cells was markedly increased in patient s with lupus nephritis as compared to controls. The tubular expression of MCP- 1 was strongly associated with the amount of CD68(+) cell infiltration in the in terstitium (r=0.5420, P<0.05) and the extent of interstitial fib ro sis. There was no correlation between MCP-1 production in tubules and the degr ee of urinary protein excretion in patients with lupus nephritis (r=0.054 7, P>0.05).Conclusions The expression of MCP-1 in the renal tubules and vascular wall was markedly inc reased in patients with lupus nephritis. The overproduction of MCP-1 in renal tissue may contribute to monocyte recruitment in the interstitium and thus resul t in tubulo-interstitial damage in lupus nephritis.