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Altered primate glomerular development due to in utero urinary tract obstruction
Douglas G Matsell1, Amy Mok, Alice F Tarantal
1Department of Pediatrics, Anatomy and Cell Biology, and Child Health Research Institute, University of Western Ontario, London, Ontario, Canada. doug.matsell@lhsc.on.ca
Kidney International
|March 29, 2002
Summary
In utero urinary tract obstruction impairs kidney development, causing renal dysplasia. This obstruction leads to abnormal ureteric branching, reduced glomeruli, and podocyte loss, impacting newborn kidney function.
Area of Science:
- Developmental Biology
- Nephrology
- Pediatric Urology
Background:
- In utero urinary tract obstruction causes renal failure in newborns and children.
- Obstruction during nephrogenesis leads to cystic renal dysplasia, with severity correlating to obstruction timing and duration.
- A non-human primate model accurately mimics human obstructive renal dysplasia, highlighting effects on glomerular development and podocyte survival.
Purpose of the Study:
- To investigate the impact of urinary obstruction on glomerular development in a fetal model.
- To analyze the histopathological and developmental changes in kidneys affected by in utero ureteric obstruction.
Main Methods:
- Ultrasound-guided injection of alginate beads to induce unilateral ureteric obstruction in fetal primates as early as 75 days gestation.
- Histochemistry, histomorphometry, and immunocytochemistry were employed to analyze kidney development.
Main Results:
- Kidneys exhibited features of human obstructive cystic dysplasia, including reduced weight and deficient ureteric duct branching.
- Demonstrated deficient cortical ureteric duct development and branching.
- Observed reduced glomerular number and altered glomerular basement membrane formation.
Conclusions:
- Urinary tract obstruction during active nephrogenesis disrupts ureteric duct branching and glomerular vascularization.
- This leads to podocyte loss and decreased glomerular number, mirroring human renal dysplasia.
- These findings predict compromised postnatal renal function and outcomes in affected infants.