Renal Corticomedullary Abscess 

Renal corticomedullary abscess is a term used to describe a spectrum of diseases that encompass various intrarenal infectious processes, such as acute focal bacterial nephritis (eg, lobar nephronia, focal pyelonephritis), acute multifocal bacterial nephritis, emphysematous pyelonephritis, and xanthogranulomatous pyelonephritis (XGP). Renal corticomedullary abscess is caused by ascending spread of bacteria; in contrast, renal cortical abscess (ie, renal carbuncle) is caused by hematogenous spread of bacteria.

Although kidney and perirenal space infections are uncommon, they can exact significant morbidity and carry a risk of mortality.

Renal cortical abscess results from hematogenous spread of bacteria from a primary extrarenal focus of infection. The source is not apparent in up to one third of cases at the time of diagnosis. Staphylococcus aureus is the etiologic agent in 90% of cortical abscess cases. In contrast, renal corticomedullary abscess develops as an ascending infection by organisms already isolated from the urine. Severe renal parenchymal involvement in combination with corticomedullary abscess is more likely to extend to the renal capsule and perforate, thus forming a perinephric abscess. Renal corticomedullary infections include the below acute and chronic infectious processes of the kidney.

Acute focal bacterial nephritis

Acute focal bacterial nephritis (eg, lobar nephronia, focal pyelonephritis) is a well-localized renal infection without frank abscess formation. This form of bacterial interstitial nephritis usually causes interstitial inflammation within a focal area of the kidney. Histologic characteristics include marked infiltration with polymorphonuclear leukocytes at the apex of the medulla with distortion of the glomeruli and renal tubules. In many patients, acute focal bacterial nephritis represents an early phase that eventually progresses to the more severe acute multifocal bacterial nephritis. In these more severe cases, a heavy polymorphonuclear infiltrate is present throughout the kidney with areas of liquefaction and abscess formation.

In children with acute focal bacterial nephritis, which is commonly caused by infection with Escherichia coli^[1] or Klebsiella pneumoniae, a 3-week course of appropriate antibiotic therapy is recommended. This treatment duration precludes failure or relapse and, thereby, subsequent complications such as renal abscess.

Emphysematous pyelonephritis

Emphysematous pyelonephritis is an uncommon but severe necrotizing form of acute multifocal bacterial nephritis. Abdominal radiography (ie, kidneys, ureter, bladder [KUB]) exhibits characteristic intraparenchymal gas. The gas, which is located within the renal parenchyma rather than the collecting system, suggests infection with gas-forming anaerobic or facultative anaerobic pathogens. The gas is produced by bacterial fermentation of glucose in the necrotic infected tissue. Although E coli is the most common organism associated with this disease, any lactose-fermenting organism may be involved. Diabetes mellitus is the most common risk factor associated with emphysematous pyelonephritis. Emphysematous pyelonephritis carries an overall mortality rate of approximately 45%.

Xanthogranulomatous pyelonephritis

XGP is a chronic infection of a renal unit and is often associated with a renal calculus. As a result of long-standing infection, the kidney enlarges and fixes itself to the retroperitoneum by perirenal fibrosis and extension of the granulomatous inflammation. Native tissue planes, such as the plane between Gerota fascia, adjacent retroperitoneal structures, and the peritoneum, are disrupted. Histologically, granulomatous tissue contains lipid-laden macrophages (ie, foam cells) and replaces the renal parenchyma.

Most persons (75%) with XGP usually have accompanying renal calculi, and approximately 50% of those are staghorn calculi. Proteus mirabilis is the most common bacteria associated with XGP, but E coli is also common. A pathologic classification system based on the amount of renal and perirenal involvement stratifies XGP into the following 3 stages:

• Stage I XGP (nephritic) - Characteristic xanthogranulomatous infection in the kidney
• Stage II XGP (perinephric involvement) - Involvement of renal parenchyma and Gerota fascia
• Stage III XGP (paranephric) - Widespread extension into the retroperitoneum

XGP is known as the great imitator because of its clinical, radiologic, and pathologic similarities to renal tumors. XGP is occasionally associated with renal cell carcinoma,^[2] transitional cell carcinoma, and squamous cell carcinoma.

Relevant anatomy

The kidneys lie along the borders of the psoas muscle and are placed obliquely. The right kidney is lower than the left kidney because of the overlying liver. The kidneys demonstrate mobility with inspiration and expiration. Lack of mobility suggests abnormal fixation, which often occurs with either acute inflammatory processes (eg, acute pyelonephritis) or chronic fibrosing processes such as XGP.

The kidney is composed of an outer cortex, central medulla, internal calices, and pelvis. The cortex is homogenous in appearance. The medulla consists of numerous pyramids formed by converging collecting renal tubules, which drain into minor calices. The minor calices unite to form 2 or 3 major calices, which join to form the renal pelvis. Renal calices (most often at the upper and lower poles) affected by the intrarenal reflux of infected urine may result in corticomedullary abscess formation.

The ureter courses from the renal pelvis to the posterolateral aspect of the bladder. Areas of relative narrowing occur at the ureteropelvic junction (UPJ), where the ureter crosses over the iliac vessels, and at the ureterovesical junction (UVJ). These are sites where a ureteral calculus is likely to become obstructed. Of these 3 locations, ureteral obstruction is most likely to occur at the UVJ, followed by the UPJ and the crossing of the iliac vessels.

The nephron is the functioning unit of the kidney. It is composed of the glomerulus, proximal convoluted tubule, descending and ascending limbs of the loop of Henle, distal convoluted tubule, and collecting duct.

The renal arteries carry approximately 20% of the entire cardiac output, and, of this, approximately 90% is filtered by the glomeruli in the renal cortex.

The blood supply to the kidney arises from a single renal artery and leads to multiple branching end arteries. These are without collateral circulation. Therefore, occlusion of any of these vessels produces infarction of the affected renal segment. Occlusion of the main renal artery leads to infarction of the entire kidney.

Usually, one renal artery arising from the aorta enters the renal hilum. At the renal hilum, the renal artery divides into anterior and posterior segmental branches. The posterior branch supplies a large portion of the posterior segment of the kidney. The anterior branch further divides to supply the upper and lower poles and the entire anterior surface of the kidney. Segmental arteries divide into interlobar arteries that ascend between the renal pyramids. At the corticomedullary junction, interlobar arteries branch into arcuate arteries that course along the base of the pyramids, parallel to the surface of the kidney. Arcuate arteries give rise to the interlobular arteries that run into the renal cortex and divide into the afferent glomerular arterioles of the glomerulus. Filtration occurs within the glomerulus. Efferent glomerular arterioles leave the glomerulus to descend as vasa recta to supply the renal medulla.

Intrarenal abscesses develop within the renal capsule. Untreated and fulminant infections can rupture through the capsule and can involve the perinephric space and retroperitoneum. Because the kidneys are positioned retroperitoneally, 3 areas are of considerable importance when discussing infections in this area:

• Anterior perirenal space - Contains portions of the pancreas, bowel, and colon
• Perinephric space - Contains Gerota fascia and the adrenals
• Intrarenal space - Contains renal parenchymal tissue

Spread of infection can adversely affect these vital structures. Once infection spreads to the perinephric spaces, percutaneous or open surgical drainage is required. Identifying and treating an intrarenal abscess before capsular invasion occurs can prevent perinephric and retroperitoneal spread of infection to avoid further complications.

Frequency

United States

The incidence of renal corticomedullary abscess ranges from 1-10 cases per 10,000 hospital admissions. Pyelonephritis that leads to corticomedullary abscess is rare.

Mortality/Morbidity

Renal corticomedullary abscess carries a mortality rate of 1.5-15%.

Sex

Although approximately 75% of renal cortical abscesses occur in males, renal corticomedullary abscess is equally common in males and females. However, renal corticomedullary abscess is rare in the absence of risk factor (see Causes); thus, the likelihood of infection may be influenced by predisposing factors.