caa a22 4500 475742931 CHVBK 20180406123505.0 cr unu---uuuuu 170329e20000401xx s 000 0 eng 10.1007/s002400050146 doi (NATIONALLICENCE)springer-10.1007/s002400050146 Histologic and molecular evidence of obstructive uropathy in rats with hereditary congenital hydronephrosis [Elektronische Daten] [F. Seseke, P. Thelen, B. Hemmerlein, D. Kliese, G. Zöller, R-H. Ringert] Partial obstruction of the upper urinary tract, a frequent challenge for the pediatric urologist, leads to renal damage, if deobstruction is delayed. Several but sometimes unsatisfactory animal models have been developed to study this phenomenon. Obstruction created by surgical manipulation lacks adequate correlation with a developing congenital obstruction. In some animals with congenital hydronephrosis, evidence of renal obstruction is absent. A study of the renal morphology of rats with hereditary unilateral hydronephrosis has exhibited clear evidence of renal obstruction distinguishable from renal dilatation. The renal mRNA expression of renin and transforming-growth factor- β1 (TGF-β1) was measured by a semiquantitative RT-PCR technique. In hydronephrotic kidneys, a marked loss of parenchyma, atrophy and dilation of tubuli and collecting ducts and interstitial fibrosis was observed. The mRNA expression of renin was increased significantly in comparison to controls, whereas the contralateral kidneys showed renin activity below control levels. TGF-β1 expression was markedly increased in hydronephrotic kidneys, whereas contralateral kidneys did not differ significantly from control values. These data suggest the presence of renal obstruction and not only renal dilatation in these rats with congenital hydronephrosis. This colony seems to be a representative animal model to study congenital renal obstruction even in the fetal period without the need of surgical manipulation. Springer-Verlag Berlin Heidelberg, 2000 Key words Congenital hydronephrosis nationallicence Renal obstruction nationallicence Renin-Angiotensin-System nationallicence Transforming-growth factor-β1 nationallicence Interstitial fibrosis nationallicence Seseke F. Department of Urology, Georg-August-University Göttingen, Robert-Koch-Strasse 40, 37075 Göttingen, Germany, DE aut Thelen P. Department of Urology, Georg-August-University Göttingen, Robert-Koch-Strasse 40, 37075 Göttingen, Germany, DE aut Hemmerlein B. Department of Pathology, Georg-August-University Göttingen, Germany, DE aut Kliese D. Department of Urology, Georg-August-University Göttingen, Robert-Koch-Strasse 40, 37075 Göttingen, Germany, DE aut Zöller G. Department of Urology, Georg-August-University Göttingen, Robert-Koch-Strasse 40, 37075 Göttingen, Germany, DE aut Ringert R-H Department of Urology, Georg-August-University Göttingen, Robert-Koch-Strasse 40, 37075 Göttingen, Germany, DE aut https://doi.org/10.1007/s002400050146 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/s002400050146 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Seseke F. Department of Urology, Georg-August-University Göttingen, Robert-Koch-Strasse 40, 37075 Göttingen, Germany, DE aut NATIONALLICENCE 700 1- Thelen P. Department of Urology, Georg-August-University Göttingen, Robert-Koch-Strasse 40, 37075 Göttingen, Germany, DE aut NATIONALLICENCE 700 1- Hemmerlein B. Department of Pathology, Georg-August-University Göttingen, Germany, DE aut NATIONALLICENCE 700 1- Kliese D. Department of Urology, Georg-August-University Göttingen, Robert-Koch-Strasse 40, 37075 Göttingen, Germany, DE aut NATIONALLICENCE 700 1- Zöller G. Department of Urology, Georg-August-University Göttingen, Robert-Koch-Strasse 40, 37075 Göttingen, Germany, DE aut NATIONALLICENCE 700 1- Ringert R-H Department of Urology, Georg-August-University Göttingen, Robert-Koch-Strasse 40, 37075 Göttingen, Germany, DE aut Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer