Mechanism of Renovascular Backflow

Abstract

PYELOVASCULAR backflow has been observed since the earliest days of urography. Little understood, it has been the basis for much controversy. Little clinical significance has been attributed to it. We have repeated and added to earlier work done in the investigation of pyelovascular backflow. We have been able to quantitate the levels at which pyelovascular vs. pyelotubular backflow occurs, and we have demonstrated that pyelorenal backflow may have considerable clinical significance. The mechanism of pyelovascular backflow has not been determined. We have demonstrated such a mechanism by correlating the histopathology and intrapelvic pressure with microradiology. Review of Literature Hinman and Lee-Brown in 1924 reported a series of studies relating pyelotubular and pyelovascular backflow to pressure (2, 3). They measured the secretory pressure of a dog kidney at 70–90 mm Hg. With Bird and Moist they noted pyelotubular backflow with gradual increase in pressure. Bird and Moist were unable to produce pyelovenous backflow in dogs with pressures up to 120 mm Hg, but Hinman and Lee-Brown did so in cadaver kidneys with pressures as low as 40 mm mercury. Both were able to demonstrate backflow in hydronephrotic kidneys with pressures as low as 15 mm Hg. Elkin et at. reported backflow with intrapelvic pressures varying from 50 to 125 mm Hg following acute ureteral obstruction in humans (15). Some investigators have found the rate of increase in pressure an important factor (5, 7, 8), and others have determined an immediate rise in intrapelintrapelvic pressure followed by a drop at the onset of renovascular backflow (9). Over the years many observers have reported pyelovascular backflow during retrograde urography. Studies have correlated the degree of backflow with pressure. Renovascular backflow was also described in intravenous urography studies during abdominal compression and following acute ureteral obstruction (1, 10–12). Pyelovenous backflow is an important phenomenon since it may be one of the natural mechanisms of pelvic decompression in ureteral obstruction. It also may be an avenue for the bacteremia following ureteral reflux (16). Moist and Bird concluded that pyelovenous backflow was due to rupture of tubules in the straight and arcuate vein. Narath in 1940 noted that pyelovenous backflow occurred in the sinus renalis, the closed space adjacent to and extending from the fornix containing arteries, veins, lymphatics, and nerves (4). He was unable to demonstrate any mucosal perforation in pyelovenous backflow; therefore, he concluded that backflow was due either to absorption from the overdistended pelvis or minute calyceal mucosal tears and ruptures of the fornix with extravasation of the contrast medium into the arcuate vein. Histologic changes in the renal pelvis and fornix of the normal kidney and kidney sub ject to varying periods of ureteral obstruction from hours to weeks have been amply described (13).