Acute segmental renal artery embolism: a distinctive urographic and arteriographic complex.

Abstract

Arterial embolism, the commonest cause of renal infarction, produces a characteristic clinical picture. Renal artery occlusion, whether segmental or total, is accompanied by markedly impaired or completely absent ipsilateral renal function. Acute segmental renal artery embolism, however, may produce a distinctive urographic pattern. We are presenting three cases of acute renal artery embolism, in all of which intravenous urography demonstrated calyceal opacification in only the upper pole of the affected kidney. Renal arteriography, performed immediately thereafter, accurately delineated the emboli and explained the urographic findings. Clinical Material The clinical data are summarized in Table I. Discussion Renal artery embolism most frequently occurs in patients with pre-existing cardiac or vascular disease. The clinical picture has been well documented and is fairly characteristic (6, 7): there is an abrupt onset of severe upper abdominal or flank pain with nausea and vomiting, albuminuria, and often hematuria. The intravenous urogram usually demonstrates marked impairment or complete absence of renal function; a normal retrograde pyelogram in such cases is essentially pathognomonic of renal infarction. Segmental renal artery embolism may, however, be manifested by localized calyceal filling on the intravenous urogram (Figs. 1A, 4, 6). Although this occurrence has been noted in previous reports, insufficient emphasis has been placed on this finding as a distinctive diagnostic feature. In the series of 5 cases presented by Janower and Weber (4), Case IV demonstrated faint opacification of an upper pole calyx associated with segmental renal artery occlusion. In the 13 cases reported by Heitzman and Perchik, Case VI showed nonvisualization of a single calyx, the remaining 12 nonvisualization of the affected kidney (2). The main renal artery divides into two major branches, the ventral and the dorsal. The ventral branch, the larger of the two, is essentially the continuation of the main vessel anatomically. Emboli, therefore, would seem prone to lodge more frequently within the ventral vessel and its branches. The dorsal artery, which is of smaller caliber, usually arises as a distinct branch before the renal artery enters the hilus and often provides the major vascular supply to the upper pole of the kidney (1). Since the renal arteries are end arteries, without interrelating anastomoses, occlusion of the larger ventral branch might thus permit demonstrable urographic function in only the upper pole region, the area supplied by the patent dorsal branch, as in our cases. Segmental renal artery occlusion may, however, result in total absence of opacification, presumably secondary to reflex spasm. Nonopacification of the kidney on intravenous urography, therefore, does not justify the diagnosis of total rather than segmental renal artery occlusion. The usual consequence of renal artery embolus is renal infarction.