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Am J Physiol Renal Physiol 286: F1087-F1099, 2004. First published January 13, 2004; doi:10.1152/ajprenal.00201.2003
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Early release of neonatal ureteral obstruction preserves renal function

Yimin Shi,1,2 Michael Pedersen,1 Chunling Li,1,2 Jian Guo Wen,1 Klaus Thomsen,5 Hans Stødkilde-Jørgensen,1 Troels Munch Jørgensen,1 Mark A. Knepper,6 Søren Nielsen,2,4 Jens Christian Djurhuus,1 and Jørgen Frøkiær1,2,3

1Institute of Experimental Clinical Research, Aarhus University, and 3Department of Clinical Physiology, Aarhus University Hospital, DK-8200 Aarhus N; 2The Water and Salt Research Center and 4Institute of Anatomy, Aarhus University, DK-8000 Aarhus C; 5Institute for Basic Psychiatric Research, Department of Biological Psychiatry, Aarhus University Hospital, DK-8240 Risskov, Denmark; and 6Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892

Submitted 27 May 2003 ; accepted in final form 9 January 2004

The incidence of congenital hydronephrosis is ~1% and is often associated with renal insufficiency. It is unknown whether early release is essential to prevent deterioration of renal function. Rats were subjected to partial unilateral ureteral obstruction (PUUO) on postnatal day 2. The obstruction was left in place or released after 1 or 4 wk. Renal blood flow (RBF) and kidney size were measured sequentially over 24 wk using MRI. In rats in which the obstruction was left in place, RBF of the obstructed kidney was progressively reduced to 0.92 ± 0.17 vs. 1.79 ± 0.12 ml·min–1·100 g body wt–1 (P < 0.05) after 24 wk. Similarly, glomerular filtration rate of the obstructed kidney was severely reduced at 24 wk: 172 ± 36 vs. 306 ± 42 µl·min–1·100 g body wt–1 (P < 0.05). These changes were preceded by development of severe hydronephrosis and obstructive nephropathy with a reduction in total protein content: 45 ± 3 vs. 58 ± 4 mg/kidney. Moreover, nonreleased PUUO caused a marked natriuresis (0.32 ± 0.07 vs. 0.11 ± 0.02 µmol·min–1·100 g body wt–1, P < 0.05) and impaired solute free water reabsorption (0.47 ± 0.16 vs. 2.71 ± 0.67 µl·min–1·100 g body wt–1, P < 0.05), consistent with a significant downregulation of Na-K-ATPase to 62 ± 7%, aquaporin-1 to 53 ± 3%, and aquaporin-3 to 53 ± 7% of sham levels. Release after 1 wk completely prevented development of hydronephrosis, reduction in RBF and glomerular filtration rate, and downregulation of renal transport proteins, whereas release after 4 wk had no effect. These results suggest that early release of neonatal obstruction provides dramatically better protection of renal function than release of obstruction after the maturation process is completed.

rat; obstructive nephropathy; kidney function; magnetic resonance imaging; aquaporin; sodium transporter


Address for reprint requests and other correspondence: J. Frøkiær, The Water and Salt Research Center, Institute of Experimental Clinical Research, Aarhus Univ. Hospital-Skejby, DK-8200 Aarhus, Denmark (E-mail: jf{at}iekf.au.dk).




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