Radiographic Manifestations of Massive Arteriovenous Fistula in Renal Carcinoma

Abstract

THAT kidney carcinoma is frequently quite vascular and may be composed of numerous small arteriovenous fistulas or shunts is well known. The degree of arteriovenous shunting in these malignant tumors may be so pronounced, however, that the lesion may be confused arteriographically and hemodynamically with an arteriovenous fistula (or malformation) from some other cause. The demonstration of this phenomenon by the presentation of the radiographic findings in two cases of renal carcinoma with massive arteriovenous shunting is the purpose of this report. Renal arteriovenous fistulae may be congenital or acquired. The acquired are most often caused by rupture of an arterial aneurysm, trauma (including nephrectomy and percutaneous renal biopsy), or renal carcinoma (1). They have been reported with increasing frequency over the past few years. At present, approximately 60 cases due to varying causes have been described in the literature, the great majority of them in the past ten years (2). Hemodynamically, arteriovenous fistulae of the renal vessels behave somewhat differently from fistulae of similar size vessels in other parts of the body. An arteriovenous fistula results in an increased cardiac output with an increased systolic blood pressure and decreased diastolic pressure due to decreased peripheral resistance which may eventually lead to cardiac decompensation. This picture may be modified, however, in a renal arteriovenous fistula because of the frequent occurrence of renal ischemia. Diastolic hypertension as well will then result in many of these cases. This, of course, would not be true of postnephrectomy fistula of the renal vessels. It is well known that small arteriovenous fistulae and shunts exist in a large percentage of malignant tumors of the kidney parenchyma. The general pathological description of renal adenocarcinoma (hypernephroma) is usually “very vascular (with) venous invasion frequently observed in the histologic sections” (3). This explains the arteriographic finding of hypertrophy of the renal artery leading to these vascular tumors and the early visualization of the renal vein. In studying the arteriograms of 80 cases of renal carcinoma, Boijsen and Folin (4) observed this phenomenon mainly in those tumors which were “richly vascularized and . . . showed wide arteriovenous shunts.” Early filling of the renal vein was considered to be between two and five seconds with the normal filling time eight seconds. This degree of peripheral arteriovenous shunting is common in hypernephroma and is not usually associated with hemodynamic effects such as elevated blood pressure or cardiac output changes. However, when the carcinoma erodes larger vessels near the hilus of the kidney, then a massive arteriovenous fistula occurs. This can have systemic cardiovascular effects and can mimic the arteriovenous fistulae resulting from other causes.