The pathogenesis of childhood primary nephrotic syndrome (PNS) is unclear. However, an immune mechanism has generally been accepted as a cause. Imbalance of T lymphocyte and a variety of inflammatory cytokines, chemotactic and transcription factors are involved in the pathophysiology and manifestations of PNS,~(1,2) (and nuclear) factor kappa B (NF-κB) transcriptionally regulates the expression of these factors.~3 Research has been focused on NF-κB and inflammatory regulated mediators of renal diseases, but seldom on different clinical manifestations and histopathological changes. In order to explore a potential mechanism for the pathogenesis of PNS in children and a basis for preventing its advance, we determined NF-κB activity in the kidney of children with PNS in vitro using immunohistochemical staining and the multimedia coloured pathological image analysis system and its relations to clinical manifestations, histopathological changes and 24-hour urinary protein excretion. The pathogenesis of childhood primary nephrotic syndrome (PNS) is unclear. However, an immune mechanism has been accepted as a cause. Imbalance of T lymphocyte and a variety of inflammatory cytokines, chemotactic and transcription factors are involved in the pathophysiology and manifestations of PNS ~ (1,2) (and nuclear) factor kappa B (NF-κB) transcriptionally regulates the expression of these factors. ~ 3 Research has been focused on NF-κB and inflammatory regulated mediators of renal diseases, but seldom on different clinical manifestations and histopathological changes. In order to explore a potential mechanism for the pathogenesis of PNS in children and a basis for preventing its advance, we determined NF-κB activity in the kidney of children with PNS in vitro using immunohistochemical staining and the multimedia colored pathological image analysis system and its relations to clinical manifestations, histopathological changes and 24-hour urinary protein excretion.