Rapid loss of renal parenchyma after acute obstruction

Urinary tract obstruction (UTO) is a frequent cause of renal failure in the pediatric population. We report a patient with type I/I cystinuria, followed prospectively from birth with yearly ultrasonography, who developed acute UTO due to a cystine stone at 10 years of age. In animal models of UTO, a...

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Bibliographic Details
Published in:Pediatric nephrology (Berlin, West) West), 2001-12, Vol.16 (12), p.1076-1079
Main Authors: PARVEX, P, PIPPI-SALLE, J. L, GOODYER, P. R
Format: Article
Language:English
Subjects:
Acute Disease
Biological and medical sciences
Child
Female
Humans
Hydronephrosis - etiology
Kidney - diagnostic imaging
Kidney Calculi - complications
Kidney Calculi - diagnosis
Kidney Calculi - therapy
Medical sciences
Nephrology. Urinary tract diseases
Prospective Studies
Radiography
Radionuclide Imaging
Stents
Ultrasonography
Ureteral Obstruction - diagnostic imaging
Ureteral Obstruction - etiology
Ureteral Obstruction - therapy
Ureteroscopy
Urinary system involvement in other diseases. Miscellaneous
Urinary tract. Prostate gland
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Summary:Urinary tract obstruction (UTO) is a frequent cause of renal failure in the pediatric population. We report a patient with type I/I cystinuria, followed prospectively from birth with yearly ultrasonography, who developed acute UTO due to a cystine stone at 10 years of age. In animal models of UTO, acute obstruction produces rapid loss of renal parenchyma secondary to apoptosis of tubular cells. Since we had prospectively obtained serial ultrasonographic measurements of renal growth, we were able to document sudden decrease in kidney size and function following UTO, suggesting that programmed cell death may similarly have caused the rapid irreversible loss of renal parenchyma in our patient. Despite surgical relief of the obstruction, kidney size decreased for at least 3-4 months. We speculate that anti-apoptotic drugs might be considered as a therapeutic strategy to protect ongoing renal parenchyma loss in UTO.
ISSN:0931-041X
1432-198X
DOI:10.1007/s004670100031