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Special Feature
March 2001

Radiological Case of the Month

Arch Pediatr Adolesc Med. 2001;155(3):416. doi:10.1001/archpedi.155.3.415
Denouement and Discussion: Inferior Vena Cava and Renal Vein Thrombosis in a Neonate

Figure 1. Computed tomographic scan of the abdomen demonstrating a markedly enlarged right kidney (thick arrow), calcification of the inferior vena cava (arrowhead), and a small, calcified left kidney (thin arrow).

Figure 2. Computed tomographic scan of the abdomen demonstrating calcifications in the left renal vein extending into the inferior vena cava (arrowhead).

All abdominal masses detected in the neonatal period require further investigation with ultrasonography.1 Most of these masses originate in the genitourinary tract,1,2 and ultrasonography should be performed to localize and differentiate between cystic and solid structures. The differential diagnosis of cystic abdominal masses includes hydronephrosis; multicystic-dysplastic kidney disease; intestinal duplication; hydrometrocolpos; and choledochal, ovarian, renal, and pancreatic cysts. The differential diagnosis of solid abdominal masses includes neuroblastoma, teratoma, and Wilms tumor. A solid flank mass of a neonate in the presence of hematuria, hypertension, renal failure, and thrombocytopenia suggests a diagnosis of renal vein thrombosis.

Two types of renal vein thrombosis are recognized. In the first, the thrombus begins intrarenally at the level of the arcuate and interlobular veins, successively extending into the larger renal veins and to the inferior vena cava.3 It is thought that this type is more frequent during infancy.4,5 However, Demirci et al6 presented a case of bilateral renal vein thrombosis in which the inferior vena cava was completely filled with thrombus, suggesting that the thrombus arose initially in the inferior vena cava with subsequent retrograde extension into the renal veins.

Clinically, renal vein thrombosis is characterized by the presence of a palpable flank mass associated with acute renal failure. Hematuria, proteinuria, and oliguria are usually present. Predisposing factors are dehydration, asphyxia, polycythemia, sepsis, shock, coagulopathies, and maternal diabetes.7 Ultrasound examination will show perivascular streaking with increased echogenicity of the renal parenchyma.8 Computed tomography will demonstrate persistent parenchymal opacification and enlargement of the affected kidney, dilation of the renal vein, and renal vein and/or inferior vena caval thrombus.9

Surgical management with removal of the affected kidney has historically been the treatment of choice,10 but it has been recognized more recently that with supportive therapy alone, the short-term prognosis of renal vein thrombosis occurring during infancy is good. However, the involved kidney progressively becomes atrophic resulting in a small, scarred kidney.11,12 Treatment with systemic anticoagulation agents may result in a better long-term prognosis.13,14 In our patient, treatment with low-molecular-weight heparin resulted in a return of normal renal function by age 4 months.

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Article Information

Accepted for publication February 12, 1999.

This report was sponsored by the Chief Bureau of Medicine and Surgery, Navy Department, Washington, DC, Clinical Investigation Program, report 84-16-1968-665, as required by NSHSBETHINST 6000.41A.

The views expressed in this article are those of the authors and do not reflect the official policy or position of the Department of the Navy, Department of Defense, or the US Government.

Reprints: Clinical Research Department, Medical Editing Division, Naval Medical Center San Diego, 34800 Bob Wilson Dr, Suite 5, San Diego, CA 92134-1005 (e-mail: wmacal@snd10.med.navy.mil).

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Pohl  MZimmerhackl  LBHeinen  F  et al.  Bilateral renal vein thrombosis and venous sinus thrombosis in a neonate with factor V mutation (FV Leiden). J Pediatr. 1998;132159- 161Article
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