Rollino Cristiana, D'Urso Leonardo, Beltrame Giulietta, Ferro Michela, Quattrocchio Giacomo, Quarello Francesco
Divisione di Nefrologia e Dialisi, Ospedale S. Giovanni Bosco, Torino, Italy.
G Ital Nefrol. 2011 Nov-Dec;28(6):599-611.
Vesicoureteral reflux (VUR) may be congenital or acquired. The most frequent form of congenital VUR is primary VUR. Its prevalence in adults is not exactly known, but it is higher in women, whose greater propensity for urinary tract infections increases the likelihood of an instrumental examination leading to the diagnosis of less severe cases. In men, even severe VUR may go undiagnosed for a long time. Primary VUR is due to a defect in the valve mechanism of the ureterovesical junction. In physiological conditions, the terminal ureter enters the bladder wall obliquely and bladder contraction leads to compression of this intravesical portion. Abnormal length of the intravesical portion of the ureter due to a genetic mutation (whose location is yet to be established) leads to VUR. In its less severe forms VUR may be asymptomatic, but in 50-70% of cases it manifests with recurrent cystitis or pyelonephritis. The manifestations leading to a diagnosis of VUR in adults, besides urinary tract infections, are proteinuria, renal failure and hypertension. The gold-standard diagnostic examination is a micturating cystourethrogram. Reflux nephropathy develops as a result of a pathogenetic mechanism unrelated to high cavity pressure or urinary tract infections but due to reduced formation of the normal renal parenchyma (hypoplasia or dysplasia). Abnormal renal parenchyma development is attributable to the same genes that control the development of the ureters and ureterovesical junction. VUR is considered only a marker of this abnormal development, playing no role in scar formation. There is no conclusive evidence regarding the indications for VUR correction. However, the risk that VUR leads to recurrent pyelonephritis and reflux nephropathy must be kept in mind. VUR certainly has to be corrected in women who contemplate pregnancy.
膀胱输尿管反流(VUR)可分为先天性或后天性。先天性VUR最常见的形式是原发性VUR。其在成年人中的患病率尚不完全清楚,但在女性中更高,女性患尿路感染的倾向更大,这增加了通过器械检查诊断出较轻病例的可能性。在男性中,即使是严重的VUR也可能长期未被诊断出来。原发性VUR是由于输尿管膀胱连接部瓣膜机制缺陷所致。在生理情况下,输尿管末端斜行进入膀胱壁,膀胱收缩导致膀胱内这部分输尿管受压。由于基因突变(其位置尚未确定)导致输尿管膀胱内部分长度异常,从而引发VUR。在较轻的形式中,VUR可能无症状,但在50%-70%的病例中,它表现为复发性膀胱炎或肾盂肾炎。除尿路感染外,导致成年人VUR诊断的表现还有蛋白尿、肾衰竭和高血压。金标准诊断检查是排尿性膀胱尿道造影。反流性肾病是由一种与高腔内压力或尿路感染无关的发病机制引起的,而是由于正常肾实质形成减少(发育不全或发育异常)。肾实质发育异常归因于控制输尿管和输尿管膀胱连接部发育的相同基因。VUR仅被视为这种异常发育的一个标志,在瘢痕形成中不起作用。关于VUR矫正的指征尚无确凿证据。然而,必须牢记VUR导致复发性肾盂肾炎和反流性肾病的风险。对于计划怀孕的女性,VUR肯定必须予以矫正。