| Description |
Recent advances in genetic research methods will allow for an understanding of the interactions among variables important in the progression of kidney (renal) disease. These variables, which control fibrotic responses in diseased kidneys, include the proteoglycan decorin and the cytokine transforming growth factor beta one (TGFp-l). But before genetic methods may be employed to elucidate these factors, a preliminary investigation of such components is necessary. One intriguing means of examining fibrotic variables is the unilateral ureteral obstruction model (UUO). Ureteral obstruction results in hydronephrosis, the distention of the kidney with urine, and ultimately the initiation of fibrotic responses. For this exploration, the UUO model was employed. The fibrosis caused by this stimulus was rapid and severe. The UUO disease model was appropriate to employ because it is believed that the disease response in mice is representative of the progression of renal fibrosis in humans. The results of the experiment reflect not only the roles of decorin, TGFp-l, and other variables in the course of the disease, but they also illuminate the benefits and drawbacks of the UU0 model. This investigation has shown that fibrotic disease responses are initiated quickly by the kidney after a mechanical stimulus (mesangial stretch) is administered. These responses reached maximum levels shortly after initiation and remained high for the remainder of the study. By using techniques to examine the genetic and histological pathologies associated with renal disease, this investigation has broadened the understanding of the kidney's response to experimental hydronephrosis induced by UUO. Because of the high success rate of disease induction and relative ease of employing this model, unilateral ureteral obstruction will undoubtedly be important in the discovery of new drugs used for the treatment of progressive renal disease. |
