Posterior Urethral Valves:
Theoretical Considerations on Embryological Development

Dh, Frohneberg; Jw, Thüroff; Riedmiller, H.

doi:10.1159/000473548

Cited by 11 publications

(4 citation statements)

References 7 publications

(13 reference statements)

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“…This finding is consistent with the recognized pathoembryology, since posterior urethral valves are primarily a disturbance of the lower urinary tract, involving the urethra, which is believed to reflect an incomplete rupture of the urogeni-tal membrane [27,28]. The mechanism by which the AT2 receptor contributes to normal ureteral formation and how disruption of the AT2 receptor leads to abnormal ureteral development may relate to the recent evidence that the AT2 receptor promotes tissue remodelling through apoptosis of cells [29].…”

Section: Discussionsupporting

confidence: 83%

Angiotensin type 2 receptor is important in the normal development of the ureter

Hohenfellner

Hunley

Schloemer³

et al. 1999

Pediatric Nephrology

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In humans, the actions of angiotensin II are transduced through the AT1 and AT2 receptors which have recently been implicated in renal organogenesis. Polymorphisms in the human angiotensin II receptor genes have been linked to cardiovascular and nephrological disorders. In this study we evaluated 35 patients with either primary obstructive megaureter or posterior urethral valves. Each was genotyped for the A1166 AT1 polymorphism and the recently described A-1332G AT2 transition. The incidence of these genetic variants was also evaluated in normal controls without any ultrasonographic urological abnormalities. Similar to our previous findings in congenital urological abnormalities, the AT1 receptor genotype distribution did not differ between patients with either primary obstructive megaureter or posterior urethral valves versus controls. In contrast, compared with normal controls, there was a dramatic increase in the occurrence of the AT2 A-1332G transition in patients with primary obstructive megaureter (75.0% vs. 41.9% in controls, P<0.025). In patients with posterior urethral valves, there was no difference in the occurrence of the transition versus controls (36.9%, P=NS).

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Section: Discussionsupporting

confidence: 83%

Angiotensin type 2 receptor is important in the normal development of the ureter

Hohenfellner

Hunley

Schloemer³

et al. 1999

Pediatric Nephrology

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“…The embryological disturbance is primarily the mis‐apposition of the ureteric bud from the Wolffian duct, such that subsequent migration of the ureteric bud and incorporation into the bladder is aberrant [28]. Compatible with this hypothesis is the previous finding of no association of the AT2 A‐1332G transition in patients with PUV, which is also not a primary disorder of the ureter per se [29]. These findings also reiterate the likely polygenic nature of VUR.…”

Section: Discussionmentioning

confidence: 96%

Angiotensin II, type 2 receptor in the development of vesico‐ureteric reflux

et al. 1999

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Objective To investigate if mutation of the angiotensin II (Ang II) receptors AT2 is involved in primary vesico‐ureteric reflux (VUR) in humans. Patients and methods Genetic polymorphisms in the AT1 and AT2 receptors was evaluated in 23 patients having the most common congenital urological abnormality, namely primary congenital VUR. The occurrence of the A1166C transition in the AT1 receptor gene and the A‐1332G transition in the AT2 receptor gene were evaluated and compared with the incidence in normal controls with no urological abnormalities. Result The distribution of the AT1 receptor genotypes was no different between patients with VUR and healthy controls. Furthermore, 10 of 23 (44%) patients with VUR and seven of 19 (42%) controls carried the AT2 receptor gene variation. These results contrast with our previous finding of an association between the A‐1332G transition in the AT2 receptor gene and primary obstructive megaureter, and pelvi‐ureteric junction obstruction. Conclusions We propose that while the AT2 receptor is crucial for the normal development of the ureter, it does not contribute to the processes which culminate in VUR, which is primarily an abnormality in the bladder trigone.

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“…The classic form of PUV is found in the prostatic urethra, below or proximal to the verumontanum. Although the precise embryologic mechanism of PUV remains unknown [21], four theories have been proposed to explain their development and include hypertrophy of the urethral mucosal folds, persistence and continuation of the urogenital membrane [22], abnormal development of the Wolffian or Mullerian duct [23], and fusion of the verumontanum or the posterior urethral roof epithelium [24].…”

Section: Pathophysiology Of Posterior Urethral Valvesmentioning

confidence: 99%