The basic lesion in renal papillary necrosis (RPN) originates from impairment of the vascular supply, resulting in focal or diffuse ischemic necrosis of the distal segments of the renal pyramids. If the ischemia is temporary and circulation is restored, the involved tissues may recover. However, continuous lack of perfusion leads to irreversible coagulation necrosis, tubular fibrosis, and lobar infarcts result. The renal medulla and papillae are highly vulnerable due to their peculiar blood supply and hypertonic environment. RPN develops in various chronic tubulointerstitial nephropathies. Major underlying causes are often multifactorial and include pyelonephritis, obstructive uropathy, sickle cell disease, tuberculosis, calculi, analgesics, renal vein thrombosis, and diabetes mellitus. Contrast-enhanced CT is favored as it clearly depicts typical features, such as contrast-filled clefts in the medulla, nonenhanced lesions, medullary calcifications, and papillary sloughing, and the epithelialized, blunted papillary tip.