Severe Acute Kidney Injury With Significant Uremia in an Infant Found to Have Inferior Vena Cava, Bilateral Renal Vein, and Bilateral Renal Artery Thromboses

Abstract

Background: Common neonatal etiologies of acute kidney injury (AKI) include renal vein and inferior vena cava thromboses, maternal use of nonsteroidal antiinflammatory drugs, and congenital renal disease. The incidence of renal vein thrombosis is estimated to be 0.5 per 1,000 neonatal intensive care unit admissions, with approximately half of cases extending to the inferior vena cava and with unilateral disease being significantly more common than bilateral. Data on abdominal venous thromboembolism in pediatric patients are limited, and the clinical presentation of renal vein thrombosis can vary, although most patients have at least one of the three cardinal signs: hematuria, thrombocytopenia, or abdominal mass.

Case report: We present the case of a 5-month-old female transferred to our pediatric intensive care unit from an outside hospital with AKI and significant uremia (creatinine 6.01 mg/dL, blood urea nitrogen >200 mg/dL) secondary to inferior vena cava, bilateral renal vein, and bilateral renal artery thromboses. The patient was started on a heparin drip and subsequently underwent mechanical thrombectomy of her inferior vena cava and right renal vein in addition to site-directed tissue plasminogen activator to her renal veins, renal arteries, and inferior vena cava. Following the procedure, she developed severe coagulopathy and became hemodynamically labile. The coagulopathy was corrected, but further anticoagulation to prevent further thrombus propagation was not sustainable in the face of ongoing bleeding and hemodynamic instability, so the decision to withdraw mechanical support was made.

Conclusion: Because of the varied presentations of renal vein thrombosis and because prompt intervention significantly improves survival and renal outcomes, a high index of suspicion is warranted when risk factors and any of the three cardinal features of renal vein thrombosis are present.

Keywords: Acute kidney injury; anuria; intensive care–neonatal; intensive care–pediatric; thrombosis–venous; uremia.

Figure 1.. Patient’s timeline with renal function data.

Figure 2.. Angiography of the (A) inferior vena cava (IVC) (downward arrow) and right renal vein (RV) (leftward arrow) prior to angioplasty. Note the stenosis of the right RV and thrombi visible along the IVC. Angiography of the (B) RV (leftward arrow) shows significant thrombotic occlusion (downward arrow).

Figure 3.. Angiography of the inferior vena cava (IVC) (downward arrow) and right renal vein (RV) (leftward arrow) following angioplasty. Note the slightly improved flow through the right RV (rightward arrow in view A, downward arrow in view B).

Figure 4.. Angiography of the left renal vein (RV) (rightward arrow) shows collateral circulation to the portal system (downward arrows).

Figure 5.. Angiography of the innominate vein (IV) (downward arrow) shows possible stenosis of the left subclavian vein (upward arrow) and collateral circulation to the internal jugular vein (rightward arrow).

Figure 6.. Arteriogram of the abdominal aorta shows that bilateral renal arteries are not patent.

Figure 7.. Arteriogram of the (A) right renal artery (RA) (leftward arrow) and the (B) left RA (rightward arrow) following tissue plasminogen activator administration. Note minimal flow through the right RA.