The term “absent nephrogram” refers to a lack of any functioning kidney in the renal fossa. This, therefore, includes an absent kidney as well as an abnormal kidney, which is present but does not enhance (Fig. 2). Mechanisms for this pattern include congenital or surgical absence of the kidney, renal ectopia, complete arterial occlusion (embolic or thrombotic), complete renal vein thrombosis, complete longstanding collecting system obstruction with parenchymal atrophy, or absent nephrons (congenital or acquired). Before making a diagnosis of absent kidney, it is important to look carefully for an ectopic kidney (especially a pelvic kidney or a crossed fused ectopic kidney).

With the unilateral delayed pattern, the diseased kidney is delayed in either the angiographic or nephrographic phase while the normal kidney is in the nephrographic or pyelographic phase, respectively (Fig. 3). Mechanisms for this pattern include increased transit time of contrast agent in the diseased kidney or unilateral abnormal nephron function. Increased transit time may result from slow blood in, slow blood out, or slow urine out. Unilateral poor nephron function is usually a result of acute pyelonephritis.

With the unilateral hyperdense pattern, the nephrogram of the diseased kidney becomes denser than that of the contralateral normal kidney and has delayed excretion (pyelographic phase) (Fig. 4). Contrast agent in the delayed or diseased kidney has delayed transit. Because of the continued tubular absorption of the sodium and water, the concentration of the iodine within the nephrons is increased. With the exception of pyelonephritis, the entities in this pattern are identical to the differential diagnoses of the unilateral delayed pyelogram or nephrogram pattern. Acute pyelonephritis does not have a hyperdense nephrogram unless there is concomitant obstruction.

With the bilateral persistent or delayed pattern, both kidneys remain in the angiographic or nephrographic phase longer than 3 minutes after contrast agent injection, which is the usual time of the pyelographic phase (Fig. 5). The bilateral pyelograms are also delayed. Contrast agent remains in the cortex or cortex and collecting tubules. The mechanism of this pattern is slow progression of contrast material through both kidneys. If this pattern is present days after contrast agent administration, it is usually because of functional tubular obstruction (e.g., acute tubular necrosis). When there is an absence of both pyelograms on a 3-, 5-, or 10-minute image, systemic hypotension is the probable cause.

With the rim pattern, the diseased kidney only has enhancement peripherally within the subcapsular zone and centrally in the cortex immediately adjacent to the medulla [4, 5] (Fig. 6). The pathophysiology of this pattern is the result of occlusion of the normal vascular blood supply. After occlusion of the main renal artery or vein, the capsular, peripelvic, and periureteric vessels enlarge. These collateral vessels supply the nephrons in the subcapsular and juxtamedullary regions [6]. The remaining renal parenchyma is not perfused and does not enhance. The rim nephrogram is not seen immediately after global infarction. Rather, it usually takes several days or weeks to become apparent. Eventually, all nonper-fused parenchyma will undergo atrophy, with a resultant small smooth kidney.

With the reverse rim pattern, the only enhancement is seen centrally within the renal medulla [4] (Fig. 7). There is no cortical enhancement. This pattern is almost always identified in the setting of acute cortical necrosis, a rare form of acute renal failure. Cortical necrosis may result from any cause of prolonged systemic hypotension, especially obstetrical complications, transfusion reactions, and transplant rejections [4]. The exact pathophysiology of vascular redistribution is a poorly understood process. It may be due to vasospasm of the cortical vessels due to circulating toxins. With prolonged systemic hypotension, there may be intrarenal vascular shunting redirecting blood from the cortex to the medulla. The necrotic cortex will appear as a hypodense rim surrounding the perfused medullary system [7, 8]. With time, the necrotic cortex atrophies and calcifies resulting in cortical nephrocalcinosis.

With the striated pattern, the normally homogenous nephrogram is replaced by alternating bands of enhanced and unenhanced renal parenchyma (Fig. 8). The bands are arranged radially, similar to the orientation of the collecting ducts. The striations extend through the entire renal parenchyma from the capsule to the papilla.

There are several theories of the patho-physiology of the various densities. The low-attenuating bands may represent collecting tubules that do not contain contrast material or edema between nephrons. The bands that enhance may be of normal density or hyper-dense relative to normal parenchyma. The hyperdense bands result from tubular obstruction (e.g., intratubular obstruction from pus in pyelonephritis) with resultant hyperconcentration. Alternatively, the dense bands may be secondary to contrast agent extravasation from collecting tubules and small vessels or variable perfusion due to vasospasm [5].

With the spotted pattern, the normally homogenous nephrogram is replaced by segmental and subsegmental areas of nonenhancement [4] (Fig. 9). The zones of nonenhancement are more amorphous than the linear bands seen in the striated nephrogram (Fig. 8). The pathophysiologic basis for the zones of nonenhancement is segmental (lobar) and subsegmental infarctions as a result of small-vessel occlusion.