Vesicoureteral reflux in male and female neonates as detected by voiding ultrasonography.
BACKGROUND: Vesicoureteral reflux (VUR) is assumed to be congenital, and its early diagnosis is desired in order to prevent acquired renal damage. However, the incidence of VUR in neonates remains to be revealed. METHODS: Two thousand newborn babies (1048 boys and 952 girls) underwent voiding ultrasonography (an ultrasound examination of urinary tract during provoked voiding). Those who showed transient renal pelvic dilation during voiding, who had small kidneys, or who subsequently developed urinary infection underwent voiding cystourethrography. RESULTS: Transient renal pelvic dilation was observed in 16 babies (0.8%), including one boy with small kidneys. Among the rest of the babies, one boy had a small kidney, and nine babies subsequently developed urinary infection. Voiding cystourethrography revealed VUR in 24 ureters of 16 children (11 boys and 5 girls). Dimercaptosuccinate renoscintigraphy confirmed small kidneys, with generally reduced tracer uptake in a total of three boys, all having VUR. Voiding ultrasonography detected transient renal pelvic dilation in 17 (71%) of the 24 kidneys with VUR and, strikingly, 16 of the 17 (94%) kidneys with high-grade VUR (grade III or more). CONCLUSION: This study effectively detected VUR in 0.8% of the neonates (mostly of high grades and predominantly in males) and voiding ultrasonography showed a decided usefulness for the detection of VUR. The male preponderance of VUR in neonates was considered to be due to the occurrence of congenitally small kidneys, with reflux found exclusively in males and easier ultrasound detection of VUR in male neonates because the majority of diagnoses are reported to be high grades of VUR. (+info)
The renal lesions that develop in neonatal mice during angiotensin inhibition mimic obstructive nephropathy.
BACKGROUND: Inhibition of angiotensin action, pharmacologically or genetically, during the neonatal period leads to renal anomalies involving hypoplastic papilla and dilated calyx. Recently, we documented that angiotensinogen (Agt -/-) or angiotensin type 1 receptor nullizygotes (Agtr1 -/-) do not develop renal pelvis nor ureteral peristaltic movement, both of which are essential for isolating the kidney from the high downstream ureteral pressure. We therefore examined whether these renal anomalies could be characterized as "obstructive" nephropathy. METHODS: Agtr1 -/- neonatal mice were compared with wild-type neonates, the latter subjected to surgical complete unilateral ureteral ligation (UUO), by analyzing morphometrical, immunohistochemical, and molecular indices. Agtr1 -/- mice were also subjected to a complete UUO and were compared with wild-type UUO mice by quantitative analysis. To assess the function of the urinary tract, baseline pelvic and ureteral pressures were measured. RESULTS: The structural anomalies were qualitatively indistinguishable between the Agtr1 -/- without surgical obstruction versus the wild type with complete UUO. Thus, in both kidneys, the calyx was enlarged, whereas the papilla was atrophic; tubulointerstitial cells underwent proliferation and also apoptosis. Both were also characterized by interstitial macrophage infiltration and fibrosis, and within the local lesion, transforming growth factor-beta 1, platelet-derived growth factor-A and insulin-like growth factor-1 were up-regulated, whereas epidermal growth factor was down-regulated. Moreover, quantitative differences that exist between mutant kidneys without surgical obstruction and wild-type kidneys with surgical UUO were abolished when both underwent the same complete surgical UUO. The hydraulic baseline pressure was always lower in the pelvis than that in the ureter in the wild type, whereas this pressure gradient was reversed in the mutant. CONCLUSION: The abnormal kidney structure that develops in neonates during angiotensin inhibition is attributed largely to "functional obstruction" of the urinary tract caused by the defective development of peristaltic machinery. (+info)
PGE2 increases substance P release from renal pelvic sensory nerves via activation of N-type calcium channels.
Activation of renal pelvic sensory nerves by increased pelvic pressure results in a renal pelvic release of substance P that is dependent on intact prostaglandin synthesis. An isolated renal pelvic wall preparation was used to examine whether PGE2 increases the release of substance P from renal pelvic sensory nerves and by what mechanisms. The validity of the model was tested by examining whether 50 mM KCl increased substance P release from the pelvic wall. Fifty millimolar KCl produced an increase in substance P release, from 9.6 +/- 1.6 to 26.8 +/- 4.0 pg/min, P < 0.01, that was blocked by the L-type calcium blocker verapamil (10 microM). PGE2 (0.14 microM) increased the release of substance P from the pelvic wall from 8.9 +/- 0.9 to 20.6 +/- 3.3 pg/min, P < 0.01. PGE2 failed to increase substance P release in a calcium-free medium. The PGE2-induced substance P release was blocked by the N-type calcium blocker omega-conotoxin (0.1 microM) but was unaffected by verapamil. In conclusion, PGE2 increases the release of substance P from renal pelvic sensory nerves by a calcium-dependent mechanism that requires influx of calcium via N-type calcium channels. (+info)
Prospective study of outcome in antenatally diagnosed renal pelvis dilatation.
AIMS: To ascertain the outcome associated with antenatal renal pelvis dilatation; to recommend guidelines for postnatal investigation and determine an upper limit of normal for the anterioposterior dimensions of the fetal renal pelvis. METHODS: Infants whose antenatal ultrasound scan showed a fetal renal pelvis of 5 mm or greater were investigated using postnatal renal tract ultrasound and a micturating cystogram. Isotope studies were also performed, where appropriate. RESULTS: Vesicoureteric reflux (VUR), the most common diagnosis, was evident in 23/104 (22%). In 14 infants with VUR the postnatal ultrasound scan was normal. There was no evidence of renal scarring or dysplasia in any of the refluxing kidneys. Other diagnoses were pelviureteric junction obstruction, renal dysplasia, and idiopathic dilatation. Antenatal counselling and parental information facilitated postnatal assessment. CONCLUSIONS: Infants with antenatal renal pelvis measurements of 5 mm or greater should be investigated postnatally, as a significant percentage will have VUR. A normal postnatal ultrasound scan does not preclude the presence of VUR. (+info)
Resistive indices in the evaluation of infants with obstructive and nonobstructive pyelocaliectasis.
Diagnosing obstructive uropathy by renal resistive indices calculated from duplex Doppler sonographic waveforms has been supported as well as challenged in the radiology literature relating to adults. Despite reports of normally higher resistive indices in children as compared to adults, two studies have documented high sensitivity and specificity of renal Doppler sonography in the diagnosis of obstructive uropathy in children, using the same discriminatory criterion of a resistive index of 0.7 or greater as used in adults. We evaluated 43 infants with significant or bilateral pyelocaliectasis secondary to both obstructive and unobstructive uropathy and found no significant difference in the mean resistive indices or the mean difference in resistive indices of two kidneys in one patient. We conclude that Doppler sonography in infants has no value in differentiating obstructive from nonobstructive pyelocaliectasis. (+info)
Quantitative SPECT of 99mTc-DMSA uptake in kidneys of infants with unilateral ureteropelvic junction obstruction: assessment of structural and functional abnormalities.
We evaluated individual renal function using quantitative SPECT of dimercaptosuccinic acid (DMSA) uptake by the kidneys (QDMSA) in infants with unilateral ureteropelvic junction (UPJ) obstruction and compared our findings with infants without obstruction. METHODS: QDMSA was performed on 13 infants (mean age of 2.8 +/- 2.8 mo) with unilateral UPJ obstruction and on 15 age-matched controls without obstruction. RESULTS: Control kidneys (n = 30) had a volume of 43.5 +/- 8.8 mL, a percentage injected dose (%ID)/mL 0.62 +/- 0.12 and uptake of 26.1% +/- 3.9%. Kidneys with UPJ obstruction (n = 13) had a volume of 61.2 +/- 19.3 mL, a %ID/mL of 0.42 +/- 0.11 and uptake of 25.4% +/- 8.2%. Contralateral kidneys (n = 13) had a volume of 44.0 +/- 11.9 mL, a %ID/mL of 0.57 +/- 0.16 and uptake of 24.2% +/- 4.6%. The uptake in obstructed kidneys was similar to that observed in contralateral and control kidneys (t = -0.77, P = 0.45; t = -0.37, P = 0.71; respectively). UPJ kidneys had a statistically significant increased volume and decreased %ID/mL, compared with contralateral kidneys (t = 3.35, P < 0.006 and t = 3.75, P < 0.003, respectively) and control kidneys (t = -4.2, P < 0.001 and t = 4.7, P < 0.001, respectively). There was no significant difference between contralateral kidneys and control kidneys regarding volume (t = -0.16, P = 0.87), %ID/mL (t = 0.98, P = 0.33) and uptake (t = -1.41, P = 0.16). Of 13 infants, 11 (85%) showed large kidneys with thinning of the renal cortex. In 1 infant, there was no difference between the obstructed and contralateral kidneys regarding volume, %ID/mL and uptake, and 1 infant showed significant decreased uptake in the UPJ kidney compared with the contralateral kidney. CONCLUSION: Although the overall renal function of the obstructed kidneys remained unchanged, there was a statistically significant decrease in the %ID/mL of renal tissue in UPJ kidneys, which may represent renal dysfunction. Increased functional volume with a thin cortex may represent a compensatory mechanism of the obstructed kidney. Such changes may contribute to the understanding of pathophysiologic mechanisms and may be an early sign of obstruction in infants with hydronephrosis. Further longitudinal studies with an extended number of infants and serial measurements of kidney volumes and %ID/mL are warranted to assess the significance of QDMSA in the management of infants with asymptomatic unilateral renal pelvic dilatation. (+info)
Cyclooxygenase-2 involved in stimulation of renal mechanosensitive neurons.
Stretching of the renal pelvic wall activates renal mechanosensitive neurons, resulting in an increase in afferent renal nerve activity (ARNA). Prostaglandin (PG)E(2) plays a crucial role in the activation of renal mechanosensitive neurons through facilitation of the release of substance P from the sensory neurons in the renal pelvic wall. Because wall stretch may induce cyclooxygenase-2 activity, we examined whether cyclooxygenase-2 was expressed in the renal pelvic wall and whether activation of cyclooxygenase-2 contributed to the ARNA response produced through increased renal pelvic pressure. In situ hybridization showed a strong cyclooxygenase-2 mRNA signal in the papilla and subepithelial layer of the renal pelvic wall from time control kidneys and from kidneys exposed to 15 minutes of increased renal pelvic pressure in anesthetized surgically operated rats. In anesthetized rats, an increase in renal pelvic pressure increased ARNA by 40+/-2% and increased renal pelvic release of PGE(2) from 289+/-46 to 1379+/-182 pg/min (P<0.01). Renal pelvic perfusion with the cyclooxygenase-2 inhibitor etodolac reduced the increases in ARNA and PGE(2) by 66+/-7% and 55+/-13%, respectively (P<0.01). Likewise, the cyclooxygenase-2 inhibitor 5, 5-dimethyl-3-(3-fluorophenyl)-4-(4-methylsulfonyl)phenyl-2(5H)-furanone reduced the increases in ARNA and PGE(2) by 43+/-5% and 47+/-8%, respectively. We conclude that cyclooxygenase-2 is expressed in the renal pelvic wall and that the activation of cyclooxygenase-2 contributes to the stimulation of renal mechanosensitive neurons in the pelvic wall. (+info)
Effects of selective inhibitors of cyclo-oxygenase-1 (COX-1) and cyclo-oxygenase-2 (COX-2) on the spontaneous myogenic contractions in the upper urinary tract of the guinea-pig and rat.
The role of cyclo-oxygenase-1 (COX-1) and cyclo-oxygenase-2 (COX-2) in the upper urinary tract of the guinea-pig and rat was examined using simultaneous tension recordings of the proximal and distal regions of the renal pelvis and the ureter. The guinea-pig upper urinary tract contracted at a frequency (7.52+/-0.3 min(-1) at 35 degrees C) significantly lower than the frequency in the proximal renal pelvis (21.6+/-1.3 min(-1)) and in the distal renal pelvis and ureter (20.2+/-1.4 min(-1)) of the rat (at 30 degrees C). Indomethacin (>/=1 microM for 60 min), decreased the motility index (amplitudexfrequency) (MI) in all three regions of the guinea-pig upper urinary tract, an effect which mainly arose from a decrease in the frequency of contractions. In the rat, indomethacin (1 - 30 microM for 60 min) significantly decreased the MI calculated in the proximal renal pelvis (>/=30 microM indomethacin), and in the distal renal pelvis (>/=10 microM indomethacin), arising from a significant decrease in the amplitude of contractions. The COX-1 inhibitor, valeryl salicylate (VSA) (5 - 100 microM for 60 min), had no effect on either the amplitude or frequency of contractions in the guinea-pig upper urinary tract. In contrast, VSA increased the force of contractions in the proximal and distal renal pelvis of the rat, whilst having little effect on the frequency of contractions. The COX-2 inhibitor, NS-398 (10 - 100 nM for 60 min) reduced the MI in the guinea-pig upper urinary tract in a concentration-dependent manner. The MIs calculated for the proximal renal pelvis, distal renal pelvis and ureter, were decreased by 72, 64 and 72% respectively, in 100 nM NS-398. NS-398 (10 - 100 nM) had no effect on any of the three parameters measured in either the proximal or distal renal pelvis of the rat. These data suggest that endogenously-released prostaglandins (PGs) maintain the myogenic contractility of the upper urinary tract in both the guinea-pig and rat. Moreover COX-2 is the primary enzyme involved in synthesizing PGs in the guinea-pig upper urinary tract, while COX-1 appears to be the predominantly active enzyme in the rat. (+info)