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Elevation of urinary IL-1β levels during transplant associated nephropathy in rat model of the nephrotic syndrome

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Abstract.

A recurrence of nephrotic syndrome is a well-known phenomenon in patients who receive kidney transplantation. In this study, we attempt to establish a rat model of recurrent nephrotic change after renal transplantation using puromycin aminonucleoside (PA) induced nephrotic rats . We then examine the mechanism leading to recurrence. Female Sprague-Dawley rats (8 weeks) were divided into four groups: group A, allogenic renal transplantation of a normal kidney to PA-induced nephrotic rats; group B, PA injection only as a nephrotic control; group C, allogenic transplantation of a normal kidney to rats receiving a saline injection; group D, rats receiving only a saline injection. The serum and urinary levels of protein, tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-2 and interferon (IFN)-γ were measured. The cytokine levels were assessed by performing enzyme-linked immunosorbent assays. Six days after renal transplantation, the kidneys were excised, tissue sections were stained with hematoxylin-eosin and the specimens were studied for pathological alterations. The urinary protein levels and the histological results of protein casts in renal tubules of the autologous kidneys of the nephrotic rats and the transplanted kidneys confirmed the recurrence of nephrotic syndrome in the transplanted kidney. After renal transplantation, urinary protein and IL-1β levels were significantly elevated in recurrent transplanted kidney groups compared with those in the control groups, while the TNF-α, IL-2, and IFN-γ levels were not elevated. In addition, serum levels of TNFα and IL-1β were not elevated. These results suggested that IL-1β may relate to the recurrent nephropathy in the transplanted kidney in the nephrotic rat.

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Higuchi, A., Fujisawa, M., Ueno, K. et al. Elevation of urinary IL-1β levels during transplant associated nephropathy in rat model of the nephrotic syndrome. Urol Res 30, 159–163 (2002). https://doi.org/10.1007/s00240-002-0259-0

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  • DOI: https://doi.org/10.1007/s00240-002-0259-0

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