Pathophysiology of obstructive nephropathy

Obstruction of the urinary tract is a common and potentially reversible cause of acute and chronic renal failure. Although the clinical features of obstructive nephropathy have been generally recognized for many years, recently our understanding of the pathophysiology of the disturbed renal function has been enhanced by the detailed study of experimental models of this disorder.The effects of urinary tract obstruction on renal function must be considered both during and after relief of obstruction and are greatly influenced by whether the obstruction is unilateral or bilateral, acute or chronic, partial or complete. Striking changes in renal function occur during the first 24 hours of complete unilateral (UUO) or bilateral ureteral obstruction (BUO) in experimental animals. After relief of BUO, there is marked increase in sodium and water excretion despite the severe reduction in glomerular filtration rate (GFR), a natriuretic state referred to as postobstructive diuresis (POD). After relief of UUO, in contrast, there is no absolute increase in sodium and water excretion, although fractional excretion is greater from the post-obstructive kidney. Acute partial ureteral obstruction causes a decrease, not an increase, in sodium and water excretion, but the characteristic functional change in chronic hydronephrosis is an inability to conserve sodium and water. The purpose of this review is to examine the experimental data that clarifies selected aspects of the pathophysiology of obstructive nephropathy