The lesions usually are caused by significantly diminished renal arterial perfusion secondary to vascular spasm, microvascular injury, or intravascular coagulation. RCN usually is extensive, although focal and localized forms occur. In most cases, the medulla, juxtamedullary cortex, and a thin rim of subcapsular cortex are spared.
Cases usually are bilateral.
Although the pathogenesis remains unclear, the presumed initiating factor is intense vasospasm of the small vessels. If this vasospasm is brief and vascular flow is reestablished, acute tubular necrosis results. More prolonged vasospasm can cause necrosis and thrombosis of the distal arterioles and glomeruli, and RCN ensues. RCN in placental abruption may be due to a combination of a hypercoagulable state, endothelial injury, and intravascular thrombosis. Early initiation of dialysis significantly diminishes this rate.