Abstract
Characteristically, urinary tract obstruction in humans is associated with progressive hydronephrosis, parenchymal atrophy, and impairment of renal functions. At present, it is neither possible to predict the functional changes of a hydronephrotic kidney nor the changes in kidney function after surgical relief of an obstructed kidney. The question therefore arises whether kidney function would benefit from pharmacologic treatment as an adjunct to surgery in this complex disorder? In the unilateral ureteral obstruction (UUO) model of experimental hydronephrosis in rats the pathophysiology is characterized by profound changes in renal hemodynamics, tubular functions, and progressive interstitial fibrosis1. Many processes are involved in the renal tubulointerstitial reaction that occurs after unilateral ureteral obstruction. Importantly, there are tubular apoptosis and cellular inflammatory changes with macrophage infiltration and the presence of interstitial fibroblasts, preceded by increased tumor necrosis factor- expression, which stimulates production of chemoattractant factors, including monocyte chemoattractant protein-11. The macrophages are capable of releasing potent peptide growth factors, including transforming growth factor-1 (TGF-1), which plays a major role for matrix protein overproduction in obstructive nephropathy.
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