Literature DB >> 10495796

Obstruction of the fetal urinary tract.

C A Peters1.   

Abstract

Understanding the mechanisms of fetal obstructive uropathy will be essential for the specific management of the wide clinical spectrum of congenital obstructive conditions, including selecting observational therapy for mild cases and attempting to maximize renal function in severe cases. Recognition of the unique aspects of fetal renal obstruction is essential to formulate a useful research program, as the lessons of postnatal acquired obstruction are not directly transferable to congenital obstruction. Experimental studies of renal obstruction have demonstrated alterations in the developmental regulation of growth and differentiation in the fetal kidney. Depending on the gestational timing and severity of obstruction, growth may be impaired or accelerated. Similarly, patterns of altered differentiation may indicate immaturity or accelerated maturation, as well as aberrant differentiation. Concomitant with altered development, there is evidence that normal renal regulatory mechanisms, including the renin-angiotensin system and renal hemodynamics, may be affected by obstruction, possibly as compensatory responses. The mechanisms of these various alterations remain to be defined, but are likely to involve combinations of biomechanical signal transduction, growth factor expression, and responses of specific renal autoregulatory mechanisms. Fetal renal obstruction remains incompletely defined. The body of experimental evidence indicates that investigation of mechanisms regulating growth and differentiation is likely to yield important understanding of fetal renal obstruction to permit more accurate prognosis and management. Viewing fetal renal obstruction as a disorder of kidney development, with disordered growth and differentiation, suggests a definition of obstruction as a condition, that--if uncorrected--will lead to impairment in the ultimate functional potential of the kidney. Intervention should aim to maximize functional potential rather than to simply maintain the status quo.

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Year:  1997        PMID: 10495796     DOI: 10.1681/ASN.V84653

Source DB:  PubMed          Journal:  J Am Soc Nephrol        ISSN: 1046-6673            Impact factor:   10.121


  6 in total

1.  Short-term urinary flow impairment deregulates PAX2 and PCNA expression and cell survival in fetal sheep kidneys.

Authors:  R Attar; F Quinn; P J Winyard; P D Mouriquand; P Foxall; M A Hanson; A S Woolf
Journal:  Am J Pathol       Date:  1998-05       Impact factor: 4.307

Review 2.  Congenital ureteropelvic junction obstruction: human disease and animal models.

Authors:  Julie Klein; Julien Gonzalez; Mathieu Miravete; Cécile Caubet; Rana Chaaya; Stéphane Decramer; Flavio Bandin; Jean-Loup Bascands; Bénédicte Buffin-Meyer; Joost P Schanstra
Journal:  Int J Exp Pathol       Date:  2010-07-30       Impact factor: 1.925

3.  Age-dependent renal expression of acid-base transporters in neonatal ureter obstruction.

Authors:  Guixian Wang; Sukru Oguzkan Topcu; Troels Ring; Jianguo Wen; Jens Christian Djurhuus; Tae-Hwan Kwon; Søren Nielsen; Jørgen Frøkiaer
Journal:  Pediatr Nephrol       Date:  2009-06-03       Impact factor: 3.714

Review 4.  Mechanisms of renal injury and progression of renal disease in congenital obstructive nephropathy.

Authors:  Robert L Chevalier; Barbara A Thornhill; Michael S Forbes; Susan C Kiley
Journal:  Pediatr Nephrol       Date:  2009-10-21       Impact factor: 3.714

5.  Age-related changes in expression in renal AQPs in response to congenital, partial, unilateral ureteral obstruction in rats.

Authors:  Guixian Wang; Weitang Yuan; Tae-Hwan Kwon; Zhenzhen Li; Jianguo Wen; Sukru Oguzkan Topcu; Jens Christian Djurhuus; Søren Nielsen; Jørgen Frøkiær
Journal:  Pediatr Nephrol       Date:  2011-10-25       Impact factor: 3.714

Review 6.  Embryology and Morphological (Mal)Development of UPJ.

Authors:  Ali Avanoglu; Sibel Tiryaki
Journal:  Front Pediatr       Date:  2020-04-07       Impact factor: 3.418

  6 in total

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