Renal Corticomedullary Abscess

Updated: Jan 21, 2022
  • Author: Wesley R Baas, MD; Chief Editor: Edward David Kim, MD, FACS  more...
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Practice Essentials

Renal corticomedullary abscess is a term used to describe a spectrum of diseases that encompass various intrarenal infectious processes, such as the following:

Traditionally, it is thought that renal corticomedullary abscess is caused by ascending spread of bacteria through the upper urinary tract, whereas renal cortical abscess (ie, renal carbuncle) is caused by hematogenous spread of bacteria.

The most common predisposing risk factors for renal abscesses in adults are diabetes mellitus, nephrolithiasis, and ureteral obstruction. In the pediatric population, urological abnormality (vesicoureteral reflux [VUR], ureteropelvic junction obstruction, and calyceal diverticulum) and urolithiasis are the most important predisposing risk factors. [1]

Although kidney and perirenal space infections are uncommon, they can exact significant morbidity and carry a risk of mortality, especially if diagnosis is delayed. However, the diagnosis is not easy to make without imaging studies. The clinical presentation of renal abscess may be nonspecific, and can include fever, nausea/vomiting, flank pain, and abdominal pain. Laboratory findings include elevated erythrocyte sedimentation rate, leukocytosis, and positive blood/urine cultures.

Computed tomography (CT) scans with IV contrast show specific findings in cases of renal abscess and it remains the best choice for diagnosis. In addition, CT has the advantage of providing a distinction between renal and perirenal abscesses. [1] See Workup.

In most patients with suspected corticomedullary abscess, a prompt attempt at treatment with intravenous antibiotics directed against culture-specific bacteria in addition to intravenous fluid resuscitation may be used. See Treatment and Medication.

For patient education information, see Urinary Tract Infections and Antibiotics, as well as the Infections Center.



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 usually develops as an ascending infection by organisms in 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 acute and chronic infectious processes of the kidney described below.

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 [2, 3] or Klebsiella pneumoniae, a 3-week course of appropriate antibiotic therapy is recommended. [4, 5] 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%. [6]

Xanthogranulomatous pyelonephritis

Xanthogranulomatous pyelonephritis (XGP) is a chronic destructive granulomatous inflammation that is characterized by urinary tract obstruction, urinary calculi, and invasion of the renal parenchyma. [7]   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.

XGP can be found in 2 forms: the diffuse form comprises 85% of cases and the focal (localized, segmental) comprises the remaining 15%. [8]  

Most persons (75%) with XGP have accompanying renal calculi, and approximately 34% of those are staghorn calculi. [8] 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 [9] :

  • 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 has clinical, radiologic, and pathologic similarities to renal tumors. XGP is occasionally associated with renal cell carcinoma, [10]  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 homogeneous 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. Because of their orientation, the upper and lower poles of the calices are most commonly affected by the intrarenal reflux of urine. Infection there 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 lodge. 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 each kidney arises from a single renal artery, which 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 adrenal glands
  • 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.



Renal corticomedullary abscess is caused by infection with enteric gram-negative bacilli, often coupled with urinary tract abnormalities. E coli is responsible for 75% of these infections. Approximately 15-20% of cases are caused by Klebsiella, Proteus, Enterobacter, and Serratia species. The few remaining cases of renal corticomedullary abscess are caused by gram-positive bacteria, including Streptococcus faecalis and, less commonly, S aureus.

Renal corticomedullary abscesses are usually associated with an underlying urinary tract abnormality (eg, vesicoureteral reflux [VUR], urinary tract obstruction). Renal corticomedullary abscesses most commonly occur in individuals with diabetes mellitus with or without urinary tract obstruction. [11]  Several risk factors, described below, may contribute to upper urinary tract infections and possible subsequent renal corticomedullary abscess.

Recurrent urinary tract infections

Enteric gram-negative bacteria are the usual infecting organisms among all age groups. Approximately 66% of patients with renal corticomedullary abscess have a history of recurrent urinary tract infections. Bacterial pathogens causing cystitis ascend to the upper tract and infect the renal medulla. Subsequent liquefaction of the renal parenchyma and eventual involvement of the renal cortex is the postulated pathogenesis for the development of corticomedullary abscess.

Renal calculi

Approximately 30% of patients with corticomedullary abscess have nephrolithiasis. [12]  These patients often have associated urinary tract infections that may result in bacterial seeding of the renal calculi. Longer-standing infections with urea-splitting bacteria (eg, Proteus, Pseudomonas, and Klebsiella species) may lead to the formation of struvite stones (magnesium-ammonium-phosphate). In the presence of an infection nidus such as a renal calculus, the urinary environment may facilitate an ascending infection.

Genitourinary instrumentation

Urologic procedures such as ureteroscopy or endopyelotomy may cause ureteral trauma resulting in ureteral stricture and obstruction. Approximately two thirds of patients with corticomedullary abscess have a history of prior urinary instrumentation.

Vesicoureteral reflux

Normal human anatomy dictates that the ureterovesical junction (UVJ) should allow urine to enter the bladder but prevent urine from refluxing back into the kidney. This protects the kidney from contamination by infected urine. When the UVJ is incompetent, the risk of ascending urinary tract infections increases. The major cause of vesicoureteral reflux (VUR) is weak detrusor backing in combination with a short intramural tunnel of ureter causing decreased resistance pressure to reflux. Primary causes of VUR include congenital trigonal weakness or complete ureteral duplication with refluxing lower-pole moiety. Secondary causes of reflux include poorly compliant neurogenic bladder or infravesical obstruction resulting in a high-pressure bladder. Refluxing infected urine increases the risk of reflux nephropathy, hypertension, pyelonephritis, and corticomedullary abscess.

Diabetes mellitus

More than 50% of patients with corticomedullary abscess have diabetes mellitus. Factors that predispose to intrarenal abscess among patients with diabetes mellitus include diabetic neuropathy, diabetic cystopathy, and impaired leukocyte function.


Splenectomy is associated with renal and perinephric abscesses, particularly comorbid with diabetes mellitus.  A population-based retrospective cohort study of 16,426 patients who underwent splenectomy found the overall incidence rate of renal and perinephric abscesses was 2.14-fold greater in the splenectomy group compared to a sex-matched, age-matched, and comorbidity-matched, randomly selected nonsplenectomy group. In further analysis, the adjusted hazard ratio (HR) markedly increased from 2.24 to 7.69 for those comorbid with splenectomy and diabetes mellitus (95% confidence index 3.31–17.9). [13]



The incidence of renal corticomedullary abscess ranges from 1-10 cases per 10,000 hospital admissions. Pyelonephritis that leads to corticomedullary abscess is rare. 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 factors; thus, the likelihood of infection may be influenced by predisposing factors.



Renal corticomedullary abscess carries a mortality rate of 1.5-15%. Prognosis improves with early recognition of symptoms and early aggressive therapy. Factors associated with poor prognosis include the following:

  • Advanced age
  • Urosepsis
  • Anatomic abnormalities
  • Advanced disease
  • Impaired renal function at presentation

Acute focal bacterial nephritis usually responds to antimicrobial therapy alone. Follow-up radiographic studies typically show complete resolution of the intrarenal lesion. Conversely, patients with acute multifocal bacterial nephritis take longer to improve with antibiotics alone. Occasionally, patients require some form of a drainage procedure. In most situations, patients with large abscesses or xanthogranulomatous disease who require open surgical procedure fully recover, albeit with a higher degree of morbidity.

When treated with antibiotics alone, emphysematous pyelonephritis (EPN) has a mortality rate as high as 80%. [6]