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URINARY TRACT OBSTRUCTION IN CHILDREN

R.A.S HEMAT, MB;BCh, FRCSI, DUL.

Much of the controversy that surrounds the diagnosis and management of hydronephrosis and obstruction stems from a historical lack of understanding of the pathobiology involved, much of which has only recently come to light.
Chronic obstruction is less well understood, due to in part to variable patient response to partial obstruction, and the nonspecificity of the universal finding of hydronephrosis.

Causes of hydronephrosis and hydroureteronephrosis:
1- Vesicoureteral reflux.
2- Urinary tract infection.
3- Previous obstruction.
4- Congenital malformations.
5- Noncompliant bladder.
6- Intrinsic luminal obstruction.
7- Intraluminal obstruction.
8- Extrinsic obstruction.

It is important to eliminate other causes of nonobstructed delayed washout (bladder fullness, patient positioning) when evaluating diuretic scintirenography. Diuretic Doppler ultrasound is better than DU in baseline condition. Diuretic renography is expensive, using ionising radiation and having 10-15% rate of false-positive and intermediate results.
Congenital urinary obstruction is a condition of impaired urinary drainage. GFR may be the last of several excretory functions to deteriorate with obstruction. Functional impairment may be graded and slowly progressive, presented postnatally as filtration, acid-base balance, salt and electrolyte balance, water homeostasis, regulation of blood pressure, and production of erythropoietin and vitamin D.

The foetal kidney is distinct from postnatal kidney in many ways:
1- The principal excretory and homeostatic functions are relatively minimal in the foetus.
2- Foetal renal blood flow is about a tenth of that postnatally, oxygen tension is much lower in the foetus, and the hormonal milieu and responsiveness of the foetal kidney are dissimilar postnatally.
3- Basic responses to obstruction may be significantly different.
Immunological aspect of obstructive uropathy including:
1- Cellular apoptosis modulated by EGF.
2- Interstitial fibrosis initiated by TGF-beta.
3- Activation of kallikrein-kinin system, associated with alteration in glomerular perfusion and Na handling in the obstructed kidney.

Following the release of obstruction, a transient increase in renal blood flow (reperfusion hyperaemia) soon declines again to a level well below the preobstruction level..etc


November, 2001

Note: The information in this article has been excerpted from the following books: urotext-ebook simplifying urology, Principles of modern urology, by Dr. R.A.S HEMAT. Permission is granted to copy and redistribute this document electronically as long as it is unmodified. This article may not be sold in any medium, including electronic, CD-ROM, or database, or published in print, without the explicit, written permission of Dr. R. A. S. Hemat.

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Dr. R.A.S HEMAT declares no conflicts of interest or financial interests in any product or service mentioned in this article, including grants, employment, stock holdings, gifts, or honoraria.

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