Congenital Renal Arteriovenous Malformation Presenting With Gross Hematuria After a Routine Jog: A Case Report

Erin L Dames; Lay Guat Ng; Kiang Hiong Tay

Disclosures

J Med Case Reports. 2014;8(65) 

In This Article

Case Presentation

A 44-year-old Chinese man presented to the emergency department with the chief complaint of gross hematuria with blood clots, which he had noticed after a routine morning run. He had a known medical background of hypertension. He was a nonsmoker with a moderately active lifestyle, jogging regularly. He had no personal or familial history of bleeding disorders.

The initial physical examination was unremarkable, and the bedside ultrasound examination showed a large amount of clots in the urinary bladder, without any evidence of hydronephrosis. Initial investigations showed no evidence of anemia, infection, coagulopathy or renal impairment. Initial hematologic and biochemical investigations showed a hemoglobin of 16.1g/dL, hematocrit of 47.3%, creatinine level of 83umol/L, urea of 4.2mmol/L, activated partial thromboplastin time of 31.4 seconds and prothrombin time of 10 seconds.

He was catheterized, draining gross hematuria with a substantial amount of clots. A manual bladder clot evacuation was performed, after which he was started on continuous bladder irrigation, intravenous antibiotic coverage and subsequently admitted to the general inpatient ward.

Plain, nephrographic and pyelographic phase computed tomography (CT) imaging of the kidneys was performed, which showed blood clots within the left kidney along with delayed contrast excretion, but failed to demonstrate any cause for the hematuria (Figures 1 and 2). A flexible cystoscopy showed no bladder lesions and no active bleeding from the ureteric orifices. The working diagnosis was then a possible recent passage of a stone with acute pyelovenous leakage and bleeding.

Figure 1.

Axial computed tomography image in the plain, nephrographic and pyelographic phases. A large amount of perinephric fluid is seen on the left side (long arrow in first panel). Delayed enhancement of the left kidney with delayed excretion of contrast is apparent (short arrow in second panel), but no solid mass or urinary calculus is seen. Dependent material is seen in the nondilated collecting system of the left kidney consistent with blood (arrowhead in third panel).

Figure 2.

Sagittal oblique multiplanar reformat image of the computed tomography angiogram shows early filling of the left renal vein (arrowhead) and several hypertrophic peripheral renal artery branches in the lower pole of the left kidney (arrows), this is consistent with a renal arteriovenous malformation.

Our patient complained of left flank pain on day 2 of his admission and continued experiencing multiple intermittent episodes of mild to moderate hematuria over a period of about 6 days. Management consisted of continuous bladder irrigation and with this the patient was relatively well and stable. On day 6, our patient had an episode of gross hematuria with acute clot retention. He became symptomatically anemic with a hemoglobin level as low as 8.9g/dL and a hematocrit level of 29.5%, requiring transfusion of a total of 1L of packed cells.

A CT angiogram was performed, which demonstrated an AVM in the left lower pole, being fed by a lower polar intersegmental renal artery branch (Figure 2). He underwent arterial embolization of this structure later on the same day. Using a right common femoral artery approach, selective renal angiogram and subsequent superselective left lower pole renal artery catheterization were performed (Figure 3). Embolization was performed using absolute alcohol and lipiodol in a 1:1 ratio and 355 to 500 microns polyvinyl alcohol (PVA) particles (Contour®; Boston Scientific, Natick, MA, USA). He subsequently made a full recovery and was discharged well and stable on day 10 of his admission.

Figure 3.

Selective left renal angiogram demonstrates the hypertrophic peripheral renal artery branches in the lower pole (arrowheads in first panel) with a large nidus (arrowhead in second panel), and rapid shunting to the lower pole renal vein (arrow in the third panel). A balloon catheter has been placed in the left renal vein to prevent reflux of the embolic agent (arrow in fourth panel), and superselective catheterization of the left lower pole renal artery has been performed using a microcatheter (arrowhead in fourth panel). Selected image after embolization of the renal arteriovenous malformation with absolute alcohol and polyvinyl alcohol particles show truncation of the hypertrophic left lower pole peripheral renal artery branches with absence of shunting to the lower pole renal vein (fifth panel).

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