Unilateral ureteral obstruction: beyond obstruction

Unilateral ureteral obstruction is a popular experimental model of renal injury. However, the study of the kidney response to urinary tract obstruction is only one of several advantages of this model. Unilateral ureteral obstruction causes subacute renal injury characterized by tubular cell injury,...

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Bibliographic Details
Published in:International urology and nephrology 2014-04, Vol.46 (4), p.765-776
Main Authors: Ucero, Alvaro C., Benito-Martin, Alberto, Izquierdo, Maria C., Sanchez-Niño, Maria D., Sanz, Ana B., Ramos, Adrian M., Berzal, Sergio, Ruiz-Ortega, Marta, Egido, Jesus, Ortiz, Alberto
Format: Article
Language:English
Subjects:
Acute Kidney Injury - drug therapy
Acute Kidney Injury - etiology
Acute Kidney Injury - metabolism
Acute Kidney Injury - pathology
Animals
Apoptosis
Disease Models, Animal
Fibrosis - etiology
Fibrosis - metabolism
Fibrosis - pathology
Humans
Kidney - pathology
Medicine
Medicine & Public Health
Mice
Molecular Targeted Therapy
Nephritis, Interstitial - etiology
Nephritis, Interstitial - metabolism
Nephrology
Nephrology - Review
Rats
Renal Insufficiency, Chronic - etiology
Ureteral Obstruction - complications
Urology
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Summary:Unilateral ureteral obstruction is a popular experimental model of renal injury. However, the study of the kidney response to urinary tract obstruction is only one of several advantages of this model. Unilateral ureteral obstruction causes subacute renal injury characterized by tubular cell injury, interstitial inflammation and fibrosis. For this reason, it serves as a model both of irreversible acute kidney injury and of events taking place during human chronic kidney disease. Being a unilateral disease, it is not useful to study changes in global kidney function, but has the advantage of a low mortality and the availability of an internal control (the non-obstructed kidney). Experimental unilateral ureteral obstruction has illustrated the molecular mechanisms of apoptosis, inflammation and fibrosis, all three key processes in kidney injury of any cause, thus providing information beyond obstruction. Recently this model has supported key concepts on the role in kidney fibrosis of epithelial–mesenchymal transition, tubular epithelial cell G2/M arrest, the anti-aging hormone Klotho and renal innervation. We now review the experimental model and its contribution to identifying novel therapeutic targets in kidney injury and fibrosis, independently of the noxa.
ISSN:0301-1623
1573-2584
DOI:10.1007/s11255-013-0520-1