Professor of Urology, Pediatric Urology, Medical University Innsbruck, Anichstr. 35, 6020 Innsbruck, Austria.
Ther Adv Urol. 2009 Dec;1(5):243-50. doi: 10.1177/1756287209348985.
Concerning the ureterovesical junction - the region most important for the anti-reflux mechanism - there is still a lot of misunderstanding and misinterpretation with regard to normal fetal development. Data are scarce on possible causes of primary vesicoureteral reflux and on involved mechanisms of the so-called maturation process of refluxing ureteral endings. The ratio of the intravesical ureteral length to the ureteral diameter is obviously lower than assumed so far, as clearly revealed by some studies. Therefore it can be doubted that the length and course of the intravesical ureter is of sole importance in the prevention of reflux. Additionally refluxing intravesical ureteral endings present with dysplasia, atrophy, and architectural derangement of smooth muscle fibers. Besides, a pathologically increased matrix remodeling combined with deprivation of the intramural nerve supply has been confirmed. Consequently, symmetrical narrowing of the very distal ureteral smooth muscle coat creating the active valve mechanism to defend reflux is not achievable. It is apparent that primary congenital vesicoureteral reflux seems to be the result of an abnormality within the ureterovesical junction with an insufficient muscular wrap. Nature is believed to establish much more sophisticated mechanisms than the so-called passive anti-reflux mechanism. Remodeling processes within the ureterovesical junction of refluxing ureteral endings support that maturation itself is nothing else than wound or defect healing and not a restitution of a morphological normal ureterovesical junction. Lacking the nerve supply a restoration of any muscular structure can not be achieved.
关于输尿管膀胱连接部 - 抗反流机制最重要的区域 - 对于正常胎儿发育,仍然存在很多误解和曲解。关于原发性输尿管反流的可能原因以及所谓的反流输尿管末端成熟过程中涉及的机制,相关数据仍然很少。一些研究清楚地表明,输尿管在膀胱内的长度与输尿管直径的比例明显低于迄今为止的假设。因此,可以怀疑防止反流的唯一重要因素是输尿管在膀胱内的长度和路径。此外,反流性膀胱内输尿管末端存在发育不良、萎缩和平滑肌纤维结构紊乱。此外,已经证实存在病理性增加的基质重塑以及壁内神经供应的剥夺。因此,无法实现对称缩小非常远端输尿管平滑肌层,从而形成主动瓣膜机制来防止反流。显然,原发性先天性输尿管反流似乎是输尿管膀胱连接部异常的结果,其肌肉包裹不足。人们认为,大自然建立的机制远比所谓的被动抗反流机制复杂得多。反流输尿管末端输尿管膀胱连接部的重塑过程表明,成熟本身无非是伤口或缺陷愈合,而不是输尿管膀胱连接部形态正常的恢复。由于缺乏神经供应,任何肌肉结构的恢复都无法实现。