Journal of Pathology and Translational Medicine

Original Articles

Morphologic Comparisons of Focal Segmental Glomerulo-sclerosis between Human and 5/6 Nephrectomy Rat Model.: Yong Jin Kim, Yong Sun Kim, Chae Hong Suh; Korean J Pathol. 1997;31(2):100-111.

Abstract PDF: This study was conducted to set up a common mechanism for varying phases of focal segmental glomerulosclerosis(FSGS) by comparing the morphological differences between human FSGS and changes in 5/6 renal ablation animal model, which has been accepted as experimental prototype for hyperfiltration theory as pathogenesis of FSGS. Both the human and the experimental rats showed very similar changes such as segmental glomerulosclerosis, vacuole formations or inclusion of small granules of podocytes, appearance of foamy cells in the capillary lumina, eosinophilic deposits along the mesangial area, and focal atrophy of tubules with associated interstitial fibrosis. The halo, frequently seen in human FSGS, is due to detachment of visceral epithelium from basement membrane, however, did not appear in the experimental rat specimen. On the other hand, the foamy cells and hyalinization were more frequently noted in the rat series and even involved the arterioles. The mesangial proliferation never appeared in the rat series occasionally found in human FSGS. In conclusion, the pathogenesis of FSGS cannot depend solely on the hyperfiltration theory of hemodynamic derangement, but has complex impairment of visceral epithelium and cells forming the constituents of basement membrane.

Expression of Transforming Growth Factor-beta and Morphologic Changes of Glomerulosclerosis in FGS/NgaKist Mouse.: Hoon Kyu Oh, Yong Jin Kim, Mi Ok Park, Chul Ho Lee, Byung Hwa Hyun, In Soo Shu; Korean J Pathol. 1998;32(1):35-42.

Abstract PDF: Focal segmental glomerulosclerosis (FSGS) is presented as not only one of the primary glomerular diseases but also as a secondary phenomenon for chronic irreversible renal diseases. The main pathological feature of FSGS is the accumulation of extracellular matrix in the glomeruli, for which overexpression of transforming growth factor-beta (TGF-beta) may be responsible for the accumulation of pathological matrix. A new animal model (FGS/NgaKist mouse) of renal failure by spontaneously generating glomerulosclerosis was developed. To elucidate the role of TGF-beta for FSGS, authors observed glomeruli of FGS/NgaKist mouse periodically. FGS/NgaKist mouse strain showed progression of proteinuria and focal glomerular sclerosis with the aging. The glomeruli showed anti IgG, IgA, IgM and complement complex deposits and extracellular matrix accumulation in the mesangium. TGF-beta mRNA and beta2antibody expressions were increased with the advance of glomerular sclerosis. The results suggest the following; FSGS of FGS/NgaKist strain is immune mediated disease and this stimuli on mesangial or endothelial cells may activate TGF-beta gene in their nuclei. This activation, in turn, can cause sclerosis by increasing TGF-beta mRNA transcription followed by secretion of TGF-beta and its action as cytokine for making collagen fibrils.

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