DOI: 10.1148/rg.266065039
RadioGraphics 2006;26:1827-1836
© RSNA, 2006
Renal Papillary Necrosis: Review and Comparison of Findings at Multi–Detector Row CT and Intravenous Urography1
Dae Chul Jung, MD,
Seung Hyup Kim, MD,
Sung Il Jung, MD,
Sung Il Hwang, MD and
Sun Ho Kim, MD
1 From the Department of Radiology, Seoul National University College of Medicine, 28 Yongon-Dong, Chongno-Gu, 110–744, Seoul, Republic of Korea (D.C.J., S.H.K.); Department of Radiology, Cheil General Hospital and Women’s Healthcare Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea (S.I.J.); Department of Radiology, Hallym University College of Medicine, Anyang, Republic of Korea (S.I.H.); and Department of Radiology, Dongguk University College of Medicine, Goyang, Republic of Korea (S. Ho Kim). Recipient of a Certificate of Merit for an education exhibit at the 2005 RSNA Annual Meeting. Received March 23, 2006; revision requested May 12 and received July 10; accepted July 11. All authors have no financial relationships to disclose.
Address correspondence to S.H.K. (e-mail: kimsh{at}radcom.snu.ac.kr).
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Abstract
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Renal papillary necrosis is not a pathologic entity but rather a descriptive term for a condition—necrosis of the renal papillae—that has various possible causes. The renal medulla and papillae are vulnerable to ischemic necrosis because of the peculiar arrangement of their blood supply and the hypertonic environment. The etiology of renal papillary necrosis includes diabetes, analgesic abuse or overuse, sickle cell disease, pyelonephritis, renal vein thrombosis, tuberculosis, and obstructive uropathy. Renal papillary necrosis has been diagnosed with the use of intravenous urography and ultrasonography, but contrast material–enhanced computed tomography (CT) may better depict a full range of typical features, including contrast material–filled clefts in the renal medulla, nonenhanced lesions surrounded by rings of excreted contrast material, and hyperattenuated medullary calcifications. In the presence of papillary sloughing, CT may depict hydronephrosis and filling defects in the renal pelvis or ureter, which also may contain calcifications. During healing, the epithelialized papillary tip appears blunted. Shrinkage of the kidney, a common sequela, also may be detected at CT. Multi–detector row CT depicts these and other features more clearly and directly than single–detector row CT, given the advantages of thinner sections and multiplanar reformation, and it may help identify the condition at an earlier stage, when effective treatment can reverse the ischemic process. Familiarity with the CT features of the condition therefore is useful for its successful diagnosis and management.
© RSNA, 2006
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Introduction
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Renal papillary necrosis is not a unique pathologic entity but, rather, a condition that may arise from various diseases that induce chronic tubulointerstitial nephropathy, which predominantly affects the inner medulla. The lesions that characterize this condition originate from impairment of the vascular supply and from subsequent focal or diffuse ischemic necrosis of the distal segments of the renal pyramids (1).
Although pathologic findings of renal papillary necrosis were first described in 1877, the clinical diagnosis of the condition remains problematic. Traditionally, renal papillary necrosis has been diagnosed primarily with the use of intravenous (IV) urography. Computed tomography (CT) is not commonly used to detect renal papillary necrosis, and there are relatively few published reports about the CT features of the condition. Renal papillary necrosis is visible when contrast material (eg, at IV urography) in the urinary collecting system fills a necrotic cavity located centrally or peripherally in the papillae. Contrast material–enhanced CT during the excretory phase can depict necrosis as clearly as does IV urography and thus allow accurate diagnosis of the condition. Multi–detector row CT can demonstrate these findings even more clearly and directly than single–detector row CT, because of the advantages of thinner sections and multiplanar reformations (2–7).
In this article, the authors survey the imaging features of various disease entities that are frequently associated with renal papillary necrosis and compare the findings at multi–detector row CT with those at IV urography. Evidence is provided for the superiority of multi–detector row CT over other imaging modalities for the early detection of reversible ischemic changes that lead to renal papillary necrosis.
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Anatomic Features
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The renal collecting system has its origins in the renal cortex, at the microscopic level of the glomerulus, where the first urinary filtrate enters the glomerular capsule. The urinary effluent finally enters collecting tubules, which coalesce to form collecting ducts as they again extend inward through the renal medulla to empty at the apex of the medullary pyramid, the renal papilla. The number of renal papillae may vary from as few as four to as many as 18, although seven to nine are present in the typical kidney. Each papilla is cupped by a corresponding minor calix, which receives urinary output from collecting ducts. The minor calices are the first structures of the gross renal collecting system (8).
The renal medulla and papilla are particularly vulnerable to ischemic necrosis because of the peculiar arrangement of their blood supply and the hypertonic environment (Fig 1). Even when healthy, they exist in a state of relative hypoxia because of the slow rate of blood flow in the vasa recta. Thus, conditions that further reduce blood flow may produce frank ischemic necrosis.
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Figure 1. Intrarenal arterial anatomy. The main renal artery is divided into four or more segmental arteries that are further subdivided into lobar and interlobar arteries. At the base of each renal pyramid, the interlobar arteries branch into arcuate arteries, which parallel the renal contour along the corticomedullary junction. The arcuate arteries give rise to multiple radial arterial branches called interlobular arteries, which in turn have multiple side branches from the afferent arterioles to the glomeruli. Blood leaves the glomerular capillary network via efferent arterioles, which either form a secondary capillary network around the urinary tubules in the cortex or descend into the renal medulla as long, straight vascular loops called vasa recta. The vasa recta form wide and plentiful vascular bundles at the base of the medullary pyramid, but the bundles taper as they continue distally toward the apex and papilla; as a result, the papillary tip receives only a marginal blood supply, a predisposing factor for ischemia and the subsequent development of renal papillary necrosis.
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Pathophysiologic and Radiologic Findings
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Common Causes
Renal papillary necrosis has a wide range of causes, including diabetes, analgesic abuse or overuse, sickle cell disease, pyelonephritis, renal vein thrombosis, tuberculosis, and obstructive uropathy. The most common of these diseases among adults is diabetes, which often is associated with urinary tract infection and impaired renal function but which may be present also in patients without any apparent diabetic nephropathy. Analgesic nephropathy is caused by the excessive intake of analgesics and is most common in middle-aged women. The high concentration of these drugs in the renal medulla and papilla probably contributes to the occurrence of papillary necrosis in association with analgesic overuse. Medullary ischemia caused by sickling is the main cause of renal papillary necrosis in patients with sickle cell disease, in whom sickling is intensified by a hypertonic and relatively hypoxic renal medulla. Pyelonephritis also may result in papillary necrosis, and infection is present in most cases. However, the importance of pyelonephritis as a cause of renal papillary necrosis is difficult to determine, because infection also may develop as a result of obstruction or diabetes. Other very rare causes of renal papillary necrosis include acute tubular necrosis, chronic alcoholism, and severe infantile diarrhea. Acute tubular necrosis is uniquely associated with renal papillary necrosis but represents a dysfunction of nephrons and not collecting ducts (papillae). Actual tubular necrosis (eg, in glycol poisoning) affects the tubular cells of the nephron unit and is rarely reversible, as is seen with acute tubular necrosis (eg, amino-glycoside antibiotics). However, in many cases, the cause is multifactorial. Transplanted kidneys, particularly cadaveric allografts, appear to be susceptible to renal papillary necrosis (9–19).
Early Ischemic Change in the Medullary Pyramid
Renal papillary necrosis is the consequence of an ischemic process in the renal papillae. Infection that causes inflammation of the interstitium also may lead to compression of the medullary vasculature and thus predispose the vessels to ischemic change. Perfusion compromise as a consequence of vasculitis in diabetes mellitus, tuberculosis, or the curtailment of flow observed in hemoglobinopathy, analgesic nephropathy, or acute urinary obstruction, also sets the stage for ischemic changes in the medullary pyramid (20).
If the ischemic process in the medullary region is caused by a temporary spasm and normal circulation is restored within a reasonable period, or if predisposing conditions are corrected within a reasonable period, the involved tissues may recover. However, if ischemia continues and perfusion is not restored, irreversible coagulation necrosis, tubular fibrosis, and lobar infarcts result (21).
Urographic findings during this period of early ischemic change are usually normal. Ischemic changes of the medulla are identified more often and localized more accurately with multi–detector row CT than with IV urography or ultrasonography (US). At multi–detector row CT, the ischemic changes that lead to renal papillary necrosis can be observed during the early corticomedullary phase but are best depicted on nephrographic phase scans as small, poorly marginated areas of diminished enhancement at the tip of the medullary pyramid (Figs 2, 3).
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Figure 2a. Early ischemic change in the medullary pyramid in a 50-year-old man with diabetes. (a) Contrast-enhanced parenchymal phase CT image shows multiple poorly marginated, hypoattenuated lesions (arrowheads) in the papillary regions and the excretion of contrast material into the renal pelvis (arrow). (b) Follow-up CT image obtained 1 year later shows that the lesions disappeared after predisposing conditions were corrected and the tissues involved in ischemia recovered.
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Figure 2b. Early ischemic change in the medullary pyramid in a 50-year-old man with diabetes. (a) Contrast-enhanced parenchymal phase CT image shows multiple poorly marginated, hypoattenuated lesions (arrowheads) in the papillary regions and the excretion of contrast material into the renal pelvis (arrow). (b) Follow-up CT image obtained 1 year later shows that the lesions disappeared after predisposing conditions were corrected and the tissues involved in ischemia recovered.
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Figure 3a. Early ischemic change in the medullary pyramid in a 77-year-old woman with a ureteral stone. (a) Contrast-enhanced parenchymal phase CT image shows a hypoattenuated lesion (arrowhead) in the papillary region. (b) Follow-up CT image obtained 1 year later shows marked contraction of the left kidney, an irreversible result of continued ischemia.
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Figure 3b. Early ischemic change in the medullary pyramid in a 77-year-old woman with a ureteral stone. (a) Contrast-enhanced parenchymal phase CT image shows a hypoattenuated lesion (arrowhead) in the papillary region. (b) Follow-up CT image obtained 1 year later shows marked contraction of the left kidney, an irreversible result of continued ischemia.
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The vascular bundles of the vasa recta are more abundant at the base of the medulla but taper as they approach the papillary tip, a fact that results in more pronounced coagulation necrosis due to ischemia in the papillae than at the base of the pyramid. Because of the propensity of endarteritis to propagate, areas involved in papillitis tend to enlarge. The resultant lesion, referred to as necrotizing papillitis, frequently is associated with infection (Figs 4, 5). In pathologic terms, necrotizing papillitis is a coagulative necrosis of the renal papillae that is associated with an inflammatory reaction. In the presence of infection, there may be an extension of inflammation and necrosis to the cortex, and pyelonephritic cortical scars may result (22,23).
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Figure 4. Early-stage renal papillary necrosis with necrotizing papillitis. Contrast-enhanced parenchymal phase CT image in a 47-year-old diabetic woman with flank pain, fever, and pyuria shows markedly swollen kidneys with hypoattenuated lesions (arrowheads) in papillary regions.
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Figure 5a. (a) Contrast-enhanced CT image in a 71-year-old diabetic woman with clinical findings of acute pyelonephritis shows markedly swollen kidneys with hypoattenuated lesions (white arrowheads) in papillary regions and, at the right kidney periphery, a wedge-shaped lesion (black arrowheads). (b) Photograph of a gross section from the right kidney shows abscesses in the cortex (arrowheads) and hemorrhagic infarcts in papillary regions (arrows), findings indicative of pyonephrosis and necrotizing papillitis, respectively.
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Figure 5b. (a) Contrast-enhanced CT image in a 71-year-old diabetic woman with clinical findings of acute pyelonephritis shows markedly swollen kidneys with hypoattenuated lesions (white arrowheads) in papillary regions and, at the right kidney periphery, a wedge-shaped lesion (black arrowheads). (b) Photograph of a gross section from the right kidney shows abscesses in the cortex (arrowheads) and hemorrhagic infarcts in papillary regions (arrows), findings indicative of pyonephrosis and necrotizing papillitis, respectively.
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Clefts from the Caliceal Fornices to the Medullary Pyramid
Renal papillae may undergo complete or partial necrosis. In the advanced stage of necrosis, clefts originate from the fornices and extend into and dissect the medullary pyramids and papillae, ultimately causing the papillae to slough. Caliceal deformities in renal papillary necrosis occur in three forms: medullary, papillary, and in situ (Fig 6).
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Figure 6. Schematic shows a normal calix (a), papillary (b) and medullary (c) forms of renal papillary necrosis, and caliceal blunting after papillary sloughing and epithelialization (d).
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In the medullary form, central necrosis takes place at the tip of the pyramid. Detachment of necrotic papillae starts in the central part of the calix, and a round or oval cavity opens. In the papillary form, necrosis of a larger portion of the papilla occurs. The detachment of necrotic papillae usually begins in the region of the caliceal fornices, and the resulting defect is triangular in shape. The descriptive term lobster claw refers to the radiographic pattern of papillary (forniceal) excavation. The necrotic papillary tip may remain within the excavated calix, producing a signet ring sign when the calix is filled with contrast material. The devitalized papilla also may act as a nidus for calcification, which creates a stone at the center of the signet ring (24,25).
Various stages of this process may be seen in a single urographic examination. Clefts that originate from the fornices and that undermine and ultimately sever the papillary tip are classic manifestations of renal papillary necrosis. These features are most visible at CT in the excretory phase, when hyperattenuated urine with contrast material fills the clefts and delineates the destructive process. Contrast material in the collecting system fills a necrotic cavity that may be located centrally within or at the periphery of the papillae (Figs 7, 8). Excretory phase CT thus allows the diagnosis of renal papillary necrosis, although its sensitivity for detection of the condition has not been determined (21,22).
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Figure 7a. Papillary form of renal papillary necrosis in a 58-year-old woman who had taken nonsteroidal analgesics for several years. (a) IV urogram shows multiple clefts that extend from the fornices to the pyramid tips (arrows). (b, c) Contrast-enhanced excretory phase CT images show a cleft filled with urine and contrast material that extends from the fornices (arrow in b) to a pyramid tip (arrow in c).
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Figure 7b. Papillary form of renal papillary necrosis in a 58-year-old woman who had taken nonsteroidal analgesics for several years. (a) IV urogram shows multiple clefts that extend from the fornices to the pyramid tips (arrows). (b, c) Contrast-enhanced excretory phase CT images show a cleft filled with urine and contrast material that extends from the fornices (arrow in b) to a pyramid tip (arrow in c).
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Figure 7c. Papillary form of renal papillary necrosis in a 58-year-old woman who had taken nonsteroidal analgesics for several years. (a) IV urogram shows multiple clefts that extend from the fornices to the pyramid tips (arrows). (b, c) Contrast-enhanced excretory phase CT images show a cleft filled with urine and contrast material that extends from the fornices (arrow in b) to a pyramid tip (arrow in c).
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Figure 8a. Focal papillary necrosis of the medullary form in a 69-year-old woman. (a) IV urogram shows a teardrop-shaped papillary cavity in the upper polar calix of the left kidney (arrowhead). (b, c) Reformatted coronal (b) and axial (c) contrast-enhanced CT images from the excretory phase show a small cavity (arrow) in the central portion of the papilla, extending from the fornix.
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Figure 8b. Focal papillary necrosis of the medullary form in a 69-year-old woman. (a) IV urogram shows a teardrop-shaped papillary cavity in the upper polar calix of the left kidney (arrowhead). (b, c) Reformatted coronal (b) and axial (c) contrast-enhanced CT images from the excretory phase show a small cavity (arrow) in the central portion of the papilla, extending from the fornix.
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Figure 8c. Focal papillary necrosis of the medullary form in a 69-year-old woman. (a) IV urogram shows a teardrop-shaped papillary cavity in the upper polar calix of the left kidney (arrowhead). (b, c) Reformatted coronal (b) and axial (c) contrast-enhanced CT images from the excretory phase show a small cavity (arrow) in the central portion of the papilla, extending from the fornix.
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Sloughing of Papillae
If the papilla detaches completely, a typical ring-like shadow is produced by the necrotic papilla in a contrast material–filled cavity. The necrotic papilla may remain within the cavity, be absorbed or passed in urine, or calcify. After a necrotic papilla sloughs, a cavity that communicates with the collecting system is depicted at multi–detector row CT (Fig 9). A sloughed papilla may be observed as a triangular filling defect within a calix, a feature that is occasionally accompanied by ring-shaped peripheral calcifications. Sloughed papillae may cause acute ureteral obstruction. Moreover, in the in situ form of papillary necrosis, in which the necrotic papilla remains attached, shrinks, and may become calcified, papillary calcifications may be passed as small stones. The calcification of necrotic papillae is common in patients with analgesic nephropathy (23–26) and usually evidences a change in urinary pH from acidity (in the presence of Escherichia coli) to alkalinity (due to Proteus species, which decompose urea) (Fig 10).
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Figure 9. Triangular cavity that communicates with the collecting system in a 68-year-old woman with a recurrent urinary tract infection due to a large pelvic stone. Reformatted coronal contrast-enhanced CT image shows a triangular excavation in the upper polar calix (arrowheads) of the left kidney and advanced scarring of the right kidney.
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Figure 10a. Diffuse papillary calcifications in a 62-year-old man with renal papillary necrosis due to long-term use of analgesics. Posteroanterior radiograph (a) and axial unenhanced CT image (b) show multiple calcifications (arrows) in the medullae of both kidneys.
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Figure 10b. Diffuse papillary calcifications in a 62-year-old man with renal papillary necrosis due to long-term use of analgesics. Posteroanterior radiograph (a) and axial unenhanced CT image (b) show multiple calcifications (arrows) in the medullae of both kidneys.
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Healing Phase
During the healing phase, the papilla may epithelialize, and its tip may take on a blunted appearance. In addition, shrinkage of the kidney may occur with reduction of parenchymal thickness. This common sequela of renal papillary necrosis has been attributed to the secondary atrophy of nephrons caused by necrosis of the loops of Henle, which pass deeply into the medulla. Moreover, the loss of renal cortex and associated hypertrophy of the Bertin columns result in a typical irregular wavy renal outline (5,15) (Figs 11–13).
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Figure 11a. Diffuse bilateral renal papillary necrosis in a 50-year-old woman with tuberculosis. (a) IV urogram shows blunt-tipped calices (arrows) in both kidneys. (b, c) Contrast-enhanced CT images from the excretory phase in the right (b) and left (c) kidneys show blunt-tipped calices (arrow), features that correspond to the IV urographic findings.
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Figure 11b. Diffuse bilateral renal papillary necrosis in a 50-year-old woman with tuberculosis. (a) IV urogram shows blunt-tipped calices (arrows) in both kidneys. (b, c) Contrast-enhanced CT images from the excretory phase in the right (b) and left (c) kidneys show blunt-tipped calices (arrow), features that correspond to the IV urographic findings.
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Figure 11c. Diffuse bilateral renal papillary necrosis in a 50-year-old woman with tuberculosis. (a) IV urogram shows blunt-tipped calices (arrows) in both kidneys. (b, c) Contrast-enhanced CT images from the excretory phase in the right (b) and left (c) kidneys show blunt-tipped calices (arrow), features that correspond to the IV urographic findings.
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Figure 12a. Loss of renal cortex in a 44-year-old woman with a recurrent urinary tract infection. (a) IV urogram shows blunt-tipped calices (arrows) in the left kidney. (b) Contrast-enhanced CT image from the excretory phase shows caliceal blunting and severe cortical thinning in the kidney (arrow).
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Figure 12b. Loss of renal cortex in a 44-year-old woman with a recurrent urinary tract infection. (a) IV urogram shows blunt-tipped calices (arrows) in the left kidney. (b) Contrast-enhanced CT image from the excretory phase shows caliceal blunting and severe cortical thinning in the kidney (arrow).
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Figure 13. Loss of renal cortex in a 22-year-old woman with chronic renal failure due to long-standing vesicoureteral reflux. Contrast-enhanced CT image from the parenchymal phase shows a triangular area of hypoattenuation in an atrophic left kidney (arrow).
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Differential Diagnosis
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During the early ischemic stage of renal papillary necrosis, corticomedullary or parenchymal phase multi–detector row CT shows a poorly marginated area of decreased enhancement at the tip of the medullary pyramid. Pyelonephritis also may be visible as a circumscribed area of reduced enhancement at CT during the corticomedullary and parenchymal phases, but the lesions in pyelonephritis are typified by lobar or segmental involvement instead of being limited to the medullary pyramid. Moreover, during the late parenchymal phase, the margins of the lesions show the intense venous hyperemia that characterizes inflammatory disease. Attenuation coefficients and locations may help differentiate ischemic lesions from cysts, abscesses, and hematomas. Rarely, cysts occur in the medulla as a result of medullary cystic disease. Abscesses often are located in the cortex or at the corticomedullary junction, and, depending on their age, frequently have an enhancing wall (20).
In cases of advanced disease with sloughing of necrotic papillae and during the healing phase, cavities are seen that are continuous with calices in renal medullary areas. In these cases, other causes of cystic lesions in the areas of renal medullae or sinuses should be considered in the differential diagnosis. Other possible causes include hydronephrosis, congenital megacalices, parapelvic cysts, and caliceal diverticula. In particular, the location of the arcuate artery relative to cystic lesions may be helpful for differentiation (1). Cavities produced by renal papillary necrosis can be differentiated from those in hydronephrosis by an irregular cavity contour and by extension of the cavity to arcuate arteries. Moreover, in hydronephrosis all calices are blunt tipped, whereas in papillary necrosis one or more calices may extend beyond the levels of others (Fig 14). Like the cavities in renal papillary necrosis, pelvocaliceal diverticula may manifest as contrast material–filled fluid collections adjacent to calices. However, these two entities can usually be distinguished on the basis of location: Pelvocaliceal diverticula are not found in papillae but, rather, adjacent to the caliceal fornices or, less commonly, to an infundibulum or the renal pelvis (5,27–30).
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Figure 14a. Focal papillary necrosis in a 61-year-old man with a neuropathic bladder. (a) Longitudinal color Doppler US image shows blunting of the upper polar calices (arrows), which are bordered by arcuate vessels (arrowheads). (b) IV urogram shows focal blunting of the upper polar calices (arrows).
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Figure 14b. Focal papillary necrosis in a 61-year-old man with a neuropathic bladder. (a) Longitudinal color Doppler US image shows blunting of the upper polar calices (arrows), which are bordered by arcuate vessels (arrowheads). (b) IV urogram shows focal blunting of the upper polar calices (arrows).
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Conclusions
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Renal papillary necrosis results from ischemia in the renal papillae in a variety of diseases. Multi–detector row CT, unlike excretory urography, can help identify renal papillary necrosis at an early stage, when effective treatment of the underlying cause may reverse the ischemic process. Multi–detector row CT, more clearly and directly than single–detector row CT, depicts classic signs of renal papillary necrosis such as excavation of calices, regression of papillae, sloughed papillae floating in the collecting system or ureter, caliceal blunting at the papillary tip, and evidence of progression and involvement of the cortex with pyelonephritic scarring. Familiarity with these multi–detector row CT features may aid in diagnosis and facilitate prompt and appropriate management.
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Footnotes
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Abbreviations: IV = intravenous
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Abstract
Introduction
