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[A comparative study of manchurian Dutchmanspipe and antibiotics induced acute tubular necrosis in renal cellular biological features].

OBJECTIVE
To explore the possible cell biological mechanisms of the difference in prognosis between the acute tubular necrosis (ATN) induced by Manchurian Dutchmanspipe (MD-ATN) and that by antibiotics (A-ATN), by means of comparing their renal tubular mesenchymal cell phenotype characteristics and extra-cellular stroma secretion.


METHODS
The expression of proliferative cell nuclear antigen (PCNA), epithelial cell growth factor (EGF), alpha-smooth muscle actin (alpha-SMA), fibronectin (FN), collagen type III and IV, transforming growth factor beta 1 (TGF beta 1) and connective tissue growth factor in renal biopsy samples of patients with MD-ATN (4 patients) and A-ATN(5 patients) were compared with immunohistochemical SP method. The analysis of above-mentioned parameters on repairing of injury and development of fibrosis was stressed for the obvious difference in clinical prognosis between the two groups.


RESULTS
(1) The PCNA positive rate of renal tubular epithelial cell (RTEC) and EGF expression in the MD-ATN group were significantly lower than those in the A-ATN group respectively (P < 0.01); (2) Renal tubular mesenchymal alpha-SMA level increased in both groups with no significant difference; (3) TGF beta 1 positive cell infiltration and obvious CTGF expression revealed in renal mesenchyma of both groups with insignificant difference; (4) FN, collagen III and IV levels were significantly higher in the MD-ATN group than that in the A-ATN group (P < 0.05).


CONCLUSION
(1) As compared with A-ATN group, the RTEC auto-repairing ability was lower in the DM-ATN group, lower expression of EGF might be one of the mechanisms of its poor repair; (2) High expression of alpha-SMA, TGF beta 1 and CTGF presented in all patients with ATN, but extra-cellular stromal deposit appeared only in the renal stroma of patients with MD-ATN, suggesting that its chronical trend might be related with the reducing of extra-cellular stromal degradation factor and/or endogenous anti-fibrosis factor.