Renal vein thrombosis (RVT) is the most frequently occurring vascular condition in the new-born kidney. The predisposing factors include dehydration, sepsis, birth asphyxia, maternal diabetes, polycythaemia and the presence of an indwelling umbilical venous catheter. (RVT) may present clinically with a flank mass, haematuria, hypertension or renal failure. Many imaging modalities have been employed, but ultrasound is the technique most commonly used in the evaluation of neonates with suspected RVT. Thrombosis commences in the small renal veins and subsequently propagates via larger interlobar veins to the main renal vein and inferior vena cava (IVC). The ultrasound appearances depend upon the stage at which the examination is performed and extent of the thrombus. Initially, the interlobular and interlobar thrombus appears as highly echogenic streaks. These streaks commence in a peripheral, focal segment of the involved kidney and only persist for a few days. In the first week the affected kidney swells and becomes echogenic with prominent echopoor medullary pyramids. Later, the swelling increases and the kidney becomes heterogenous with loss of corticomedullary differentiation. Grey scale ultrasound readily demonstrates thrombus within the renal vein and IVC. Adrenal haemorrhage is a recognized association and may be identified ultrasonically. Colour Doppler scanning provides additional information. In the early stages of RVT, colour Doppler may demonstrate absent intrarenal and renal venous flow. Ultimately, the kidney may recover, show focal scarring or become atrophic. Thus, ultrasound provides an accessible and reliable tool in the assessment of suspected neonatal RVT.

A prospective ultrasound study of the urinary tracts of 85 neonates (64 term, 21 preterm) was performed to assess the incidence of transient renal medullary hyperechogenicity (RMH) in the first week of life. None of the neonates examined had evidence of renal dysfunction. Echogenic material was observed in the renal papillae/calyces, ureter, or bladder of 33 of the 64 term babies, but in the bladder of only one pre-term infant. The distribution of the echogenicity differs from that seen in medullary hyperechogenicity due to crystal deposition, suggesting that calyceal involvement is a common feature. Follow-up ultrasound scans at 10-14 days were possible in eight of the term neonates and demonstrated complete resolution of the RMH. The aetiology of transient neonatal RMH is unclear, although it may be related to protein cast deposition in the renal tubules. RMH may rarely be associated with transient renal dysfunction, but in healthy neonates should be recognized as a normal variant.

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