Obstructive nephropathy: an update of the experimental research

Ureteral obstruction (UO) is one of the most common problems confronting th e urologist, Although large amounts of animal and clinical research have be en done, the pathophysiologic mechanisms accompanying UO are not fully eluc idated. Most of our knowledge on UO has been derived from experimental stud ies in a variety of animal models. Both antenatal and postnatal UO models h ave been developed mainly by ligation of the ureter or by burying the urete r into the psoas muscle. Most experimental studies have focused on short-te rm complete ureteral obstruction. The long-term effects of partial ureteral obstruction have been less intensively studied. It is now clear that obstr uctive nephropathy is not a simple result of mechanical impairment to urine flow but a complex syndrome resulting in alterations of both glomerular he modynamics and tubular function caused by the interaction of a variety of v asoactive factors and cytokines that are activated in response to UO. Leuko cyte infiltration appears to play an important role in obstructive nephropa thy suggesting that UO also has an immunological component. Growth factors such as platelet-derived growth factor, transforming growth factor-beta, ep idermal growth factor and insulin-like growth factor I may all play a role in the development and progression of fibrotic and sclerotic changes in the obstructed kidney. At present, the selection of patients with congenital h ydronephrosis for operative treatment is controversial. Studies in animals and patients have shown that partial unilateral UO does not always cause a loss of renal function or progression in urinary tract dilation during long -term follow-up. The implications of UO continue to raise many questions an d further work is necessary to achieve a better understanding of the pathog enesis in obstructive nephropathy.