The potential diagnostic utility of coexpression of Ki-67 and P53 in the renal biopsy in pediatric lupus nephritis

BACKGROUND: The proliferative activity as well as apoptosis has been suggested to play a role in the pathogenesis of lupus nephritis (LN). The aim of the study was to investigate the coexpression of Ki-67-triggered marked proliferation and P53-induced apoptosis in renal biopsy of childhood lupus nephritis (cLN) and to compare the coexpression of proliferative and apoptotic indices between different subgroups and clinicopathologic patterns of renal disease. METHODS: Renal biopsy specimens of 33 children with lupus nephritis (LN) and 10 healthy subjects were retrospectively evaluated. The type of LN and activity and chronicity indices were determined. Ki-67 and P53 immunostaining were performed. The coexpression of Ki-67 and P53 was compared among different subgroups of LN and correlated with disease activity index, serum creatinine, proteinuria, anticardiolipin antibodies, and complement levels. Histopathological examination of LN was classified based on the International Society of Nephrology/Renal Pathology. Histological LN activity was measured by the National Institutes of Health activity index (NIH-AI). RESULTS: In comparison with the healthy control group, the coexpression of Ki-67and P53 was greater in cLN (particularly in classes II, III, and IV) than in normal renal tissue. The coexpression of Ki-67and P53 shows a positive correlation with subclasses II, III, and IV of LN (P<0.02) and LN activity index (P<0.03). Moreover, the positive correlation was found between the coexpression of Ki-67 and P53 with erythrocyte sedimentation rate (P<0.02), D-dimer (P<0.03), serum creatinine (P<0.03), proteinuria (P<0.04), and anticardiolipin antibodies (P<0.05) significantly. Unexpectedly, adverse correlation between the coexpression of Ki-67 and P53 with serum C3 (P<0.02) and C4 complement (P<0.03) was significant. CONCLUSION: Our data showed that the coexpression of Ki-67-induced marked proliferation and P53-induced apoptosis in proliferative and active phases of cLN could reflect a valuable marker for treatment and remission in cLN patients before reaching the end stage of renal disease.