Renal infarction is rare although it is likely underreported [1-3]. In a study of 14,411 autopsies, the incidence of renal infarction was 1.4 percent . Because patients present with abdominal or flank pain that mimic other conditions, such as nephrolithiasis and pyelonephritis, the diagnosis is frequently missed or delayed.
The two major causes of renal infarction are thromboemboli, which usually originate from a thrombus in the heart or aorta, and in-situ thrombosis of a renal artery, which is less common .
The manifestations and management of thromboembolic renal infarction are the focus of this review. The general manifestations of atheroembolic disease and thromboembolism from aortic plaque are discussed separately. (See "Embolism from atherosclerotic plaque: Atheroembolism (cholesterol crystal embolism)" and "Embolism from aortic plaque: Thromboembolism".)
ETIOLOGY AND PATHOGENESIS
The major causes of renal infarction include atrial fibrillation and renal artery injury [2,6,7]. In the largest published case series, among 94 patients with renal infarction diagnosed between 1989 and 2011, the following distribution of causes were identified :
- 23 patients (25 percent) had cardiac causes including atrial fibrillation (17 patients), thrombi from atheroma of the suprarenal aorta (4 patients), endocarditis (2 patients).
- 29 patients (31 percent) had underlying renal artery injury, including spontaneous renal artery dissection (19 patients), fibromuscular dysplasia (8 patients), Ehlers-Danlos syndrome with thrombotic aneurysm (2 patients).
- 15 patients (16 percent) had a hypercoagulable state including hereditary thrombophilia (6 patients), hyperhomocysteinemia (4 patients), antiphospholipid syndrome (4 patients) and nephrotic syndrome (1 patient).