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197

19–22 APRIL, 2017, BARCELONA, SPAIN

S18: PRENATAL UROLOGY

Moderators: Anthony Herndon (USA), Claudio di Carli (Argentina)

ESPU Meeting on Friday 21, April 2017, 16:00–16:24

16:00–16:03

S18-1 (PP)

CONGENITAL SOLITARY FUNCTIONING KIDNEY,

HYPERTROPHY OR HYPERPLASIA? – A FETAL

ULTRASOUND STUDY

R. SNOEK

1

, R. DE HEUS

1

, K.L. DE MOOIJ

2

, L.R. PISTORIUS

3

, M.N. BEKKER

1

and T.P.V.M. DE JONG

4

1) University Utrecht Medical Center, Obstetrics, Utrecht, NETHERLANDS - 2) University Utrecht Medical Center,

Pediatric Urology, Utrecht, NETHERLANDS - 3) Tygerberg Hospital and Stellenbosch University, Obstetrics, Cape Town

And Stellenbosch, SOUTH AFRICA - 4) University Utrecht Medical Center and Academic Medical Center, Pediatric

Urology, Utrecht And Amsterdam, NETHERLANDS

PURPOSE

Congenital solitary functioning kidney (CSFK) occurs in unilateral renal agenesis and multicystic

dysplastic kidney. The ‘hyperfiltration hypothesis’ states that the theoretical 50% loss of nephrons

leads to hyperfiltration, with subsequent nephron hypertrophy and risk of renal injury. However,

animal studies report signs of hyperplasia (increase in actual number of functioning nephrons) and

an increase in the number of renal papillae. We aim to assess renal papilla number (RPN) with fetal

ultrasound (US) to assess the role of hyperplasia in CSFK. 

PATIENTS AND METHODS

A case-control study was performed on conventional and three dimensional fetal US images of

fetuses with CSFK and healthy control fetuses. ‘Renal papilla’ was defined as a hyperechogenic

focus near the renal pelvis. All imaging was assessed twice by two independent observers.

RESULTS

Sixty CSFK fetuses and 60 controls were included. Mean RPN is higher (p<0.001) in CSFK

(8.00±1.14) than in controls (6.05±1.23). RPN increases (p>0.001-0.001) with 0.11 and 0.09 papil-

lae per gestational week in cases and controls respectively. This does not differ between groups

(p=0.48). Conventional and three dimensional US are comparable (p=0.39) and moderately reliable

in assessing RPN, with 0.90 (95% CI 0.85-0.94) and 0.68 (95% CI 0.44-0.81) interclass correlation

coefficients in intra- and inter-observer measurements respectively.

CONCLUSIONS

We pose that the higher RPN in CSFK supports our hypothesis of nephron hyperplasia and not

(only) hyperfiltration resulting in hypertrophy, challenging the hyperfiltration hypothesis. RPN might

serve as a predictor for risk of developing renal injury, as a higher nephron number would result

in lower risks of renal injury.