L C Fung1, A Atala. 1. Department of Urology, Children's Hospital, Boston, Massachusetts 02115, USA.
Abstract
PURPOSE: To clarify the physiological significance of renal pelvic pressure elevations encountered in the evaluation of hydronephrotic kidney we examined the effects of different levels of renal pelvic pressure on the induction of renal injury. MATERIALS AND METHODS: A nonobstructive porcine model was created in which the urine drained against a constant predetermined pressure gradient. Renal pelvic pressure of 10, 20 and 40 cm. was created in 2, 2 and 4 animals, respectively. During 18 to 23 hours serial urinary N-acetyl-beta-D-glucosaminidase levels were determined as an indicator of renal tubular injury. Tissue specimens were examined histologically and renal arterial blood flow was monitored. RESULTS: Urinary N-acetyl-beta-D-glucosaminidase levels in the kidneys subjected to 10 cm. water remained essentially unchanged. However, at 20 and 40 cm. water statistically significant increases were observed. Similarly, renal arterial blood flow was unchanged at 10 cm. water but it became significantly lower than in controls at 20 and 40 cm. water. Histological evaluation revealed mild to moderate tubular dilatation in the kidneys subjected to 20 and 40 cm. water. CONCLUSIONS: Excessively high collecting system pressure induced renal cellular injury, as reflected by an increase in urinary N-acetyl-beta-D-glucosaminidase levels. While renal pelvic pressure up to 10 cm. water appeared to be innocuous, renal cellular injury was evident within as little as 1 hour at renal pelvic pressures 20 cm. water or greater. The degree of N-acetyl-beta-D-glucosaminidase in the urine also correlated with a decrease in renal arterial blood flow.
PURPOSE: To clarify the physiological significance of renal pelvic pressure elevations encountered in the evaluation of hydronephrotic kidney we examined the effects of different levels of renal pelvic pressure on the induction of renal injury. MATERIALS AND METHODS: A nonobstructive porcine model was created in which the urine drained against a constant predetermined pressure gradient. Renal pelvic pressure of 10, 20 and 40 cm. was created in 2, 2 and 4 animals, respectively. During 18 to 23 hours serial urinary N-acetyl-beta-D-glucosaminidase levels were determined as an indicator of renal tubular injury. Tissue specimens were examined histologically and renal arterial blood flow was monitored. RESULTS: Urinary N-acetyl-beta-D-glucosaminidase levels in the kidneys subjected to 10 cm. water remained essentially unchanged. However, at 20 and 40 cm. water statistically significant increases were observed. Similarly, renal arterial blood flow was unchanged at 10 cm. water but it became significantly lower than in controls at 20 and 40 cm. water. Histological evaluation revealed mild to moderate tubular dilatation in the kidneys subjected to 20 and 40 cm. water. CONCLUSIONS: Excessively high collecting system pressure induced renal cellular injury, as reflected by an increase in urinary N-acetyl-beta-D-glucosaminidase levels. While renal pelvic pressure up to 10 cm. water appeared to be innocuous, renal cellular injury was evident within as little as 1 hour at renal pelvic pressures 20 cm. water or greater. The degree of N-acetyl-beta-D-glucosaminidase in the urine also correlated with a decrease in renal arterial blood flow.