Long-Term Outcome of Boys With Posterior Urethral Valves

Parkhouse, Helen; Barratt, T. M.; Dillon, Michael; Duffy, PG; Fay, J.; Ransley, P. G.; Woodhouse, Christopher; Williams, D I

doi:10.1016/s0022-5347(17)40678-1

Cited by 45 publications

(80 citation statements)

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“…1 The specific diseases associated with BOO include posterior urethral valves (PUV) 2 and prune belly syndrome (PBS) 3 which is associated with a mechanically or functionally obstructed fetal bladder. The renal histological lesion which accompanies severe BOO comprises congenital dysplasia and subcortical cysts.…”

mentioning

confidence: 99%

Urinary Outflow Obstruction Increases Apoptosis and Deregulates Bcl-2 and Bax Expression in the Fetal Ovine Bladder

Thiruchelvam

Nyírády

Peebles

et al. 2003

The American Journal of Pathology

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During organogenesis, net growth of tissues is determined by a balance between proliferation, hypertrophy, and apoptotic death. Human fetal bladder outflow obstruction is a major cause of end-stage renal failure in children and is associated with complex pathology in the kidney and lower urinary tract. Experimental manipulation of the fetal sheep urinary tract has proved informative in understanding the pathobiology of congenital obstructive uropathy. In this study we used an ovine model of fetal bladder outflow obstruction to examine effects on apoptotic cell death in the developing urinary bladder. While 30 days of obstruction in utero between 75 and 105 days gestation resulted in overall growth of the fetal bladder as assessed by weight, protein, and DNA measurements, we found that apoptosis, as assessed by in situ end-labeling, was up-regulated in fetal bladder detrusor muscle and lamina propria cells and that this was accompanied by a down-regulation of the anti-death protein Bcl-2 and an up-regulation of the pro-death protein Bax. Moreover, activated caspase-3, an effector of apoptotic death, was increased in obstructed bladders. This is the first study to define altered death in an experimental fetal model of bladder dysmorphogenesis. We speculate that enhanced apoptosis in detrusor smooth muscle cells is part of a remodeling response during compensatory hyperplasia and hypertrophy. Conversely, in the lamina propria, an imbalance between death and proliferation leads to a relative depletion of cells.

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mentioning

confidence: 99%

Urinary Outflow Obstruction Increases Apoptosis and Deregulates Bcl-2 and Bax Expression in the Fetal Ovine Bladder

Thiruchelvam

Nyírády

Peebles

et al. 2003

The American Journal of Pathology

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“…In a review of 21 adults by Parkhouse and Woodhouse, 41 4 of 9 men provided normal semen, and 2 were able to father children. Therefore, patients should be carefully counseled regarding their potential to father children.…”

mentioning

confidence: 99%

Current trends in the management of posterior urethral valves in the pediatric population

Yohannes¹,

Hanna²

2002

Urology

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“…Male mgb-/-mice can be rescued from the complications of renal failure and early demise by cutaneous vesicostomy, but of the vesicostomized animals that survive the perioperative period, approximately 40% die within the first two weeks despite a patent stoma and no apparent surgical complications. This result is reminiscent of the fact that 27% to 70% of children with PUV will have progressive CKD despite surgery (Ansari, et al, 2010;Kousidis, et al, 2008;Parkhouse, et al, 1988;Roth, et al, 2001;Sanna-Cherchi, et al, 2009). Finally, mgb-/-mice possess no extrarenal features to complicate their utilization as a functional model of congenital obstructive nephropathy.…”

Section: Megabladder Mousementioning

confidence: 99%

“…The profound changes that can result are outlined in Figure 6. As many as 70% of boys with PUV develop advanced chronic or end-stage kidney disease (CKD Stage 3-5; Parkhouse et al, 1988;Reinberg et al, 1992;Roth et al, 2001;Sanna-Cherchi, et al, 2009). Those with ultrasound findings at or before 24 weeks' gestation are significantly more likely to have a poor renal outcome than children with PUV detected later in pregnancy after a normal second trimester scan (Hutton, et al, 1994).…”

Section: Natural History Of Lower Urinary Tract Obstructionmentioning

confidence: 99%