Renal infarction is rare [1-7]. In a study of 14,411 autopsies published in 1940, the incidence of renal infarction was 1.4 percent . In a later series of almost 250,000 patients seen at an emergency department over four years, only 17 (0.007 percent) were diagnosed with acute renal infarction .
The frequency of renal infarction is probably higher than reported in the above studies since clinical diagnosis of renal infarction is frequently missed or delayed because the patients present with abdominal or flank pain that mimic other, more common conditions, such as nephrolithiasis and pyelonephritis. (See 'Clinical presentation' below.)
The two major causes of renal infarction are thromboemboli, which usually originate from a thrombus in the heart or aorta, and in-situ thrombosis, which may cause complete occlusion of the main renal artery or a segmental branch artery [1,7]. The renal manifestations are different with atheroemboli, which, because they are typically nondistensible, irregularly shaped, and smaller in size, tend to produce incomplete arterial occlusion of more distal vessels, with secondary ischemic atrophy rather than renal infarction. (See "Clinical presentation, evaluation, and treatment of renal atheroemboli", section on 'Kidney injury'.)
Thromboembolic renal infarction is reviewed here. The major sources of embolism from the heart, thromboembolism from aortic plaque, and the manifestations of atheroembolic disease are discussed separately. (See "Echocardiography in detection of cardiac and aortic sources of systemic embolism" and "Embolism from aortic plaque: Thromboembolism" and "Embolism from atherosclerotic plaque: Atheroembolism (cholesterol crystal embolism)".)
ETIOLOGY AND PATHOGENESIS
The major causes of renal infarction include atrial fibrillation and renal artery injury [1,3,5]. The following findings were noted in the largest published series of 94 patients with renal infarction that was diagnosed between 1989 and 2011 :