Premium
Segmental up‐regulation of transforming growth factor‐β in the pathogenesis of primary megaureter. An immunocytochemical study
Author(s) -
NICOTINA P.A.,
ROMEO C.,
ARENA F.,
ROMEO G.
Publication year - 1997
Publication title -
british journal of urology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.773
H-Index - 148
eISSN - 1464-410X
pISSN - 0007-1331
DOI - 10.1046/j.1464-410x.1997.00486.x
Subject(s) - megaureter , immunocytochemistry , ureter , fetus , medicine , gestation , transforming growth factor , pathogenesis , urinary system , pathology , urology , anatomy , pregnancy , biology , genetics
Objective To examine the maturational‐delay hypothesis of primary megaureter (PM), i.e. that the condition arises by a segmental maturational delay of the ureteric wall that can resolve spontaneously within the first year of life, using comparative immunocytochemistry of ureters resected from infants and from homologous pre‐natal ureters. Materials and methods Seventeen distal urinary tracts were obtained from children with PM who were referred for surgery (aged 6 months to 8 years, mean 2.1 years). These were compared with ureteric buds obtained from 11‐week‐old human and 11‐ to 38‐week‐old calf fetuses. The samples were immunostained using a monoclonal antibody specific for transforming growth factor β (TGF‐β). Results The histological appearances of the narrowed ureteric segments from patients under 18 months old were like the fetal ureteric buds at 26–38 weeks of gestation. Positive TGF‐β immunoreactions were detected in the longitudinal muscle layer in the ureter from patients 6–12 months old. Such reactions weakened progressively in those patients older than 1 year, becoming negative in all children older than 3 years. The TGF‐β immunolabelling in resected ureters was closely similar to that in fetal ureters from 20 to 26‐week old calves. Conclusions From these results, PM should be ascribed to a segmental developmental delay of the terminal ureter arising at about 20 weeks of gestation, with a possible pathogenetic involvement of autocrine TGF‐β overexpression.