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I read plant et al’s short report ‘Does antenatal pelvic dilation
predict renal scarring’ with interest. They conclude that moderate
renal pelvic dilation of 5-15 mm is not a marker for increased risk of
urine infection or renal scarring, and suggest that it is inappropriate to
perform cystograms on these babies.
I want to bring to their attention 2 recent cases that we dealt with
I want to bring to their attention 2 recent cases that we dealt with
– both with borderline antenatal renal pelvic dilation but subsequently
developing very significant renal problems.
Case 1: Antenatal scans showed borderline dilation of renal pelvis –
6.6 mm on the right and 6.7 mm on the left. She was born at term with
birth weight of 3.24 kg. Postnatal scan showed left renal pelvis measuring
7 mm. The right pelvis was normal. She was commenced on trimethoprim
prophylaxis. Cystogram done at 6 months of age confirmed bilateral grade 3
vesico-ureteric reflux. DMSA scan showed no evidence of focal scarring and
split renal function was normal on both sides.
Case 2: Antenatal scans showed R renal pelvic dilation of 6.5 mm.
Born at 34 weeks’ gestation with birth weight of 2.42 kg. Postnatal scan
on day 4 was normal. He was discharged from neonatal unit on day 17.
Presented with projectile vomiting at 5 weeks age. Abdominal ultrasound
scan performed to rule out pyloric stenosis confirmed L hydronephrosis
with hydroureter. Cystogram showed no evidence of vesicoureteric reflux or
posterior urethral valves. MAG 3 renogram confirmed obstruction to left
ureteric system with L hydronephrosis. R kidney was normal. He was treated
with a course of antibiotics and is awaiting review from paediatric
In the light of our recent experience, it is fair to say that
clinicians may be falsely reassured by borderline dilation of renal pelvis
on antenatal scans and hence there may be a case for undertaking further
investigations to rule out significant renal problems.
1. Plant ND, Hornung RJ, Coulthard MG, Keir MJ et al. Does antenatal
pelvic dilation predict renal scarring? Arch Dis Child Fetal Neonatal Ed
2005; 90: F339-F340.
I read with interest the report by Plant et al. , in which it is suggested that children with antenatal renal pelvic diameter of 5-15 mm do not require postnatal investigations or treatment as their rate of renal scarring with DMSA after the age of 4 years (1/189 children) was 0.5% (95% confidence interval 0 to 2.9) for both sexes combined. It is not clear however if their results represent antenatal...
I read with interest the report by Plant et al. , in which it is suggested that children with antenatal renal pelvic diameter of 5-15 mm do not require postnatal investigations or treatment as their rate of renal scarring with DMSA after the age of 4 years (1/189 children) was 0.5% (95% confidence interval 0 to 2.9) for both sexes combined. It is not clear however if their results represent antenatal renal dilatation diagnosed at 20 or at 28 weeks of gestation; as more than half of such findings subside
between 20 and 28 weeks, the resulting calculation of prevalence of abnormalities could vary by a factor of at least 2 if the cases they reported were diagnosed at 20 weeks of gestation.
Their results contrast with our findings, hereby described. Over a 5-year period, out of 355 children with antenatal pelvic dilatation at 20 weeks of gestation, 137 children were found to have an antenatal renal pelvic diameter of 5-15 mm at 28 week gestation and were investigated
postnatally while on antibiotic prophylaxis. Those with a defined multicystic kidney, pelvic dilatation over 15 mm, suggestive findings of posterior urethral valve, or with multiple congenital anomalies, were not included in the study. None of the 137 children developed a urinary tract
infection throughout the study period. Postnatal investigations within few months of birth, including ultrasonographic evidence of increase in renal
pelvic diameter in 50 infants, confirmed the presence of obstructive uropathy in 4 children, with a prevalence of 2.9% (95% CI 0.7 to 7.4), including one child with posterior urethral valve and 3 with unilateral
pelvi-ureteral junction obstruction. A high prevalence of obstructive uropathies has already been well documented in infants with pelvic dilatation > 8mm at 28 weeks, well below the 15 mm upper limit suggested by Plant.
Renal scarring on DMSA (in the few months of life) was found in 2 children with a prevalence of 1.4% (95% CI 0.1 to 5.3) and vesicoureteric reflux was diagnosed in 5 children with a prevalence of 3.6% (95% CI 1.1 to 8.5). No DMSA scans were carried out after the age of 4 years in our study. Without dwelling on the controversy surrounding the clinical significance (or lack of it) of vesicoureteric reflux, the
relative risk of renal scarring in our series was therefore 2.75 times that in Plant's report (if their infants were scanned at 28 weeks of gestation) but this was not statistically significant (95% CI 0.3 to 10.1; p value 0.2). However, and more importantly, without postnatal imaging of these children with moderate antenatal renal pelvic dilatation, 4 cases of obstructive uropathy (2.9% of these children) would not have been detected early nor benefited from antibiotic prophylaxis and prompt evaluation by a paediatric urologist. They may still have probably been
diagnosed later, with the occurrence of obstructive symptoms or urinary tract infections, but after some possible damage to the affected kidney(s), which would have been, to some extent, preventable if the diagnosis was made earlier. If, like in Plant's report, postnatal imaging had not been carried out in this cohort and the DMSA scans were carried
out at 4 years of age, a higher number of infants with scarred kidneys on DMSA would be expected, in addition to the 2 we reported, due to potential renal damage resulting from diagnostic and therapeutic delays in the 4 infants with obstructive uropathies who would not have been identified in
the newborn period.
While we strongly agree that the majority of children with moderate antenatal pelvic dilatation would not benefit from antibiotic prophylaxis and postnatal imaging, and with the absence of other published evidence to support such a change in practice at this stage, we cannot yet agree with
Plant's recommendations of not offering postnatal evaluation unless the antenatal pelvic dilatation is more than 15 mm, as this would miss approximately 3% who have an underlying obstructive uropathy. While we recognise that invasive imaging studies with exposure to radiation, such as cystogram, DMSA or MAG scintigraphy, may not be required in the majority, we strongly feel that a postnatal ultrasound still remains indicated in all these children, with antibiotic prophylaxis and further imaging reserved to those with persistent or worsening ultrasound findings until a significant uropathy has been ruled out. Such a strategy based on postnatal ultrasound for antenatal pelvis dilatation up to 10 mm (below the limit of 15 mm suggested by Plant) is recommended to exclude an underlying uropathy.
Until better criteria and/or diagnostic tools have been developed, we cannot at this stage endorse Plant's recommendation of avoiding any postnatal investigation in many such infants(at risk) because only a few (with significant problems) may benefit.
1. Plant ND, Horning RJ, Coulthard MG, Keir MJ, Matthews JNS, Robson
SC. Does antenatal pelvic dilatation predict renal scarring? Arch Dis
2. Adra AM, Mejides AA, Dennaoui MS, Beydoun SN. Fetal pyelectasis:
is it always "physiologic"? Am.J.Obstet.Gynecol 1995;173:1263-1266.
3. Harding LJ, Malone PS, Wellesley DG. Antenatal minimal
hydronephrosis: is its follow-up an unnecessary cause of concern?