ArticleAmerican journal of physiology. Renal physiology2013
Chronic unilateral ureteral obstruction in the neonatal mouse delays maturation of both kidneys and leads to late formation of atubular glomeruli.
Article in American journal of physiology. Renal physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 29 citations in OpenAlex.
- Preterm Birth Increases Susceptibility to Hyperglycemia-Induced Kidney Injury With Sex-Specific Differences in Structural and Molecular Responses.Endocrinology, diabetes & metabolism · 2026Article
- Case Report: Giant congenital hydronephrosis presenting as massive retroperitoneal cystic lesion with literature review.Frontiers in surgery · 2026Article
- Chronic kidney disease in children: an update.Clinical kidney journal · 2023Review
- Cells of the renin lineage promote kidney regeneration post-release of ureteral obstruction in neonatal mice.Acta physiologica (Oxford, England) · 2023Article
- Genistein improves renal disease in a mouse model of nephropathic cystinosis: a comparison study with cysteamine.Human molecular genetics · 2023Article
- Magnetic resonance imaging accurately tracks kidney pathology and heterogeneity in the transition from acute kidney injury to chronic kidney disease.Kidney international · 2021Article
- Mast Cell Chymase and Kidney Disease.International journal of molecular sciences · 2020Review
- Neonatal obstructive nephropathy induces necroptosis and necroinflammation.Scientific reports · 2019Article
- Changes in cell fate determine the regenerative and functional capacity of the developing kidney before and after release of obstruction.Clinical science (London, England : 1979) · 2018Article
- The molecular biology of pelvi-ureteric junction obstruction.Pediatric nephrology (Berlin, Germany) · 2018Review
- Mast Cells and MCPT4 Chymase Promote Renal Impairment after Partial Ureteral Obstruction.Frontiers in immunology · 2017Article
- Loss of Zeb2 in mesenchyme-derived nephrons causes primary glomerulocystic disease.Kidney international · 2016Article
- Prognostic factors and biomarkers of congenital obstructive nephropathy.Pediatric nephrology (Berlin, Germany) · 2016Review
- Prevention of apoptosis averts glomerular tubular disconnection and podocyte loss in proteinuric kidney disease.Kidney international · 2016Article
- The proximal tubule is the primary target of injury and progression of kidney disease: role of the glomerulotubular junction.American journal of physiology. Renal physiology · 2016Review
- A population of mitochondrion-rich cells in the pars recta of mouse kidney.Cell and tissue research · 2016Article
- The Fate of Nephrons in Congenital Obstructive Nephropathy: Adult Recovery is Limited by Nephron Number Despite Early Release of Obstruction.The Journal of urology · 2015Article
- Congenital urinary tract obstruction: the long view.Advances in chronic kidney disease · 2015Review
- Tubular obstruction leads to progressive proximal tubular injury and atubular glomeruli in polycystic kidney disease.The American journal of pathology · 2014Article
- Dipeptidyl peptidase IV inhibitor protects against renal interstitial fibrosis in a mouse model of ureteral obstruction.Laboratory investigation; a journal of technical methods and pathology · 2014Article
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6 authors at 1 institution in 1 country.
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Abstract
Unilateral ureteral obstruction (UUO) in the adult mouse is the most widely used model of progressive renal disease: the proximal tubule is the nephron segment most severely affected and atubular glomeruli are formed after only 7 days of UUO. To determine the proximal nephron response to UUO in the maturing kidney, neonatal mice were examined 7 to 28 days following complete UUO under general anesthesia. Proximal tubular mass and maturation were determined by staining with Lotus tetragolonobus lectin. Superoxide was localized by nitroblue tetrazolium and collagen by Sirius red. Cell proliferation, cell death, PAX-2, megalin, α-smooth muscle actin (α-SMA), renin, and fibronectin were identified by immunohistochemistry. During the first 14 days of ipsilateral UUO, despite oxidative stress (4-hydroxynonenal staining), glomerulotubular continuity was maintained and mitochondrial superoxide production persisted. However, from 14 to 28 days, papillary growth was impaired and proximal tubules collapsed with increased apoptosis, autophagy, mitochondrial loss, and formation of atubular glomeruli. Fibronectin, α-SMA, and collagen increased in the obstructed kidney. Oxidative stress was present also in the contralateral kidney: renin was decreased, glomerulotubular maturation and papillary growth were delayed, followed by increased cortical and medullary growth. We conclude that neonatal UUO initially delays renal maturation and results in oxidative stress in both kidneys. In contrast to the adult, proximal tubular injury in the neonatal obstructed kidney is delayed at 14 days, followed only later by the formation of atubular glomeruli. Antioxidant therapies directed at proximal tubular mitochondria during early renal maturation may slow progression of congenital obstructive nephropathy.
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