Effect of experimentally induced urethral obstruction and surgical decompression in utero on renal development and function in rabbits.

To investigate the effect of urethral obstruction during late fetal life on renal development and function, we developed a rabbit fetal model of obstructive nephropathy to examine the pathological and biochemical consequences of urethral obstruction and beneficial effects of early surgical decompression. Animals were divided into four groups, i.e., obstructed, early decompressed, late decompressed, and control. Fetal renal development was evaluated by histological examination and counting the number of glomeruli in the four groups. The number of renal glomeruli correlated with gestational age in the normal fetus (r = 0.90, P < 0.0001). Urethral ligation on gestational day 25 (full-term, 31 days) resulted in thinning of the renal cortex and significantly decreased the number of renal glomeruli. The concentration of urinary microalbumin was higher when urethral obstruction was maintained for 3 days than 1 day after urethral obstruction, although urinary beta2- microglobulin, Na, Cl, and osmotic pressure did not change during this period. Decompression of urethral obstruction 1 day after induction of urethral obstruction resulted in improvement in the severity glomerular hypoplasia compared with late decompression (P < 0.01). Our results suggest that the rabbit fetal model simulates fetal urethral obstruction in humans, and indicates that early surgical decompression may be effective in restoration of normal renal function.