I get asked frequently by pediatricians how to evaluate newborns postnatally with antenatally detected hydronephrosis. I am writing this post to hopefully answer that question.
We now refer to hydronephrosis as urinary tract dilation (UTD). I will use the term UTD from now on. Would highly recommend reading the consensus statement regarding the UTD classification. Briefly: P stands for postnatal and A for Antenatal. Antenatal UTD is divided in mild (UTD A1) and moderate to severe (UTD A2-3). Postnatal UTD is classified as follows:
- UTD P1: anterior-posterior diameter (APD) in between 10-15 mm, dilation only in the center of the kidney. Normal bladder, ureters, and renal parenchyma.
- UTD P2: AAPD >15 mm, peripheral dilation, or the ureter is visible. Bladder and renal parenchyma normal.
- UTD P3: thick bladder or abnormal renal parenchyma.
Around 1% of pregnancies get diagnosed with antenatal UTD. Three diagnoses comprise the majority of UTD cases:
- Physiologic dilation (50-85%)
- Ureteropelvic junction obstruction (15-25%)
- Vesicoureteral reflux (15-25%)
Physiologic dilation is non-pathologic UTD due to “too much urine output in relation to the size of the baby”. As babies grow and their urine output in relation to body size decreases, this type of UTD goes away. Physiologic dilation is not associated with urinary tract infections or damage to the kidney.
Ureteropelvic junction obstruction (UPJO) is caused by a blockage in between the kidney and the ureter. This blockage is usually functional due to poor peristalsis in that area. Most mild cases get better and even half of the severe cases also improve in the first few years of life. UPJOs are very different in the newborn compared to the older child where the UPJO is usually symptomatic, more often associated with a real obstruction (crossing vessels), and less likely to go away on their own.
Vesicoureteral reflux as a cause of UTD is inconsistent: a patient with VUR is just as likely to have UTD as to not have it. Patients with very severe vesicoureteral reflux tend to have abnormal renal parenchyma and UTD.
Less than 5% of cases of UTD are due to ectopic ureters, posterior urethral valves, ureteroceles, neurogenic bladder, etc.
Which patients should be evaluated by pediatric urology right at birth?
- Boys suspected of having posterior urethral valves (thick bladder, bilateral UTD, oligohydramnios).
- Anyone with a thick bladder or ureterocele.
- Anyone with bilateral UTD P3
Which patients should be evaluated by pediatric urology at 1-2 weeks of life?
- UTD P2 and P3 except the ones described above
Which patients can be followed by their PCP?
- UTD P1
Postnatal follow-up and evaluation of mild cases of UTD
The rest of this post will cover the follow up of UTD P1 dilation.
The central question when deciding on the evaluation and follow up for patients with UTI P1 is how many ultrasounds, cystograms, and nuclear medicine scans the doctor and family are willing to do to prevent a urinary tract infection or avoid one kidney from losing function. Are you willing to perform 100 cystograms to prevent one symptomatic febrile urinary infection? Are you ok putting 1000 children through serial ultrasounds to prevent one kidney from losing function?
The truth is that most cases of UTD P1 dilation are false alarms (physiologic dilation) and thus any test done on these children will be unnecessary. When reviewing the literature, it is important to know about the Society of Fetal Urology (SFU) classification that ranges from SFU grade 1 to 4. In general terms UTD P1 encompasses SFU grades 1-2, UTD P2 corresponds to SFU grade 3 and UTD P3 to SFU grade 4.
A Meta-analysis of data extracted from seven papers showed stabilization of UTD in 98% of patients with SFU grades 1–2. Lower SFU grades resolved with a higher frequency than higher SFU grades. Grade SFU 1 hydronephrosis resolved in all cases. Grade 2 resolved in 70%. All patients with APD < or equal to 12 mm resolved. I like to use this 12 mm cutoff to tell families that continued ultrasound follow up is extremely unlikely to be beneficial for their child with UTD P1 and less than 12 mm APD.
Another study I like to quote to families is the one by Matsui et al with almost 300 patients with SFU 1 and 2 — none of which were operated. Of the 394 kidneys followed non-operatively 4 (1%) improved spontaneously on serial postnatal ultrasonography then worsened later in life. Mean age at worsening of hydronephrosis was 40 months (range 22 to 60). All patients presented with clinical symptoms (abdominal pain in 4, gross hematuria in 1, vomiting in 1) and underwent pyeloplasty. None of these patients had renal function loss. Again, I tell the families that even if their child was the unlucky 1% whose UTD worsened after it had gotten better, we would typically find about it before the kidney loses function.
Another retrospective review reported outcomes in 56 SFU grade 1 and 51 SFU grade 2 kidneys after prenatal detection. During mean follow-up of 15 months (1.5-142, median 12), spontaneous resolution occurred in 34 (61%) and 33 (65%), with none progressing to a higher grade or having surgery.
What to do specifically and conclusions
For UTD A1 I would obtain a renal ultrasound in the first 1-2 weeks of life. If the UTD is still UTD P1, then I would repeat the renal US at 2-6 months of age to confirm stability — and because I don’t really trust the renal ultrasounds done soon after birth. If the repeat renal ultrasound shows APD less than 12 mm I would stop doing follow up renal ultrasounds telling the families that the chances of deterioration/function loss are extremely rare.
For patients with follow up renal US showing APD 12-15 mm (still UTD P1) I would repeat the renal ultrasound in 6 months.