Perinephric Abscess

Updated: Sep 21, 2023
  • Author: Edward David Kim, MD, FACS; Chief Editor: Bradley Fields Schwartz, DO, FACS  more...
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Practice Essentials

A perinephric abscess is a collection of suppurative material in the renal parenchyma or perinephric space, with a presentation that is insidious (patients may not present until more than 2 weeks after onset). This abscess formation occurs secondary to urinary tract obstruction and/or hematogenous spread from infection sites. [1] A perinephric abscess can pose a great diagnostic challenge, even to an astute clinician. This is very important because a delay in diagnosis increases the risk of morbidity and mortality. 

Diagnosis of a perinephric abscess should be considered in any patient with fever and abdominal or flank pain. The increased use of CT scanning has allowed for earlier and accurate diagnoses of this condition, and newer antibiotics have been helpful in the appropriate treatment during the last 3 decades.

All perinephric abscesses should be promptly treated; failure to treat can result in severe morbidity or even death. Treatment is usually with percutaneous drainage and adjunctive antibiotics. Open surgical debridement with placement of large drains may be necessary if percutaneous drainage is ineffective; nephrectomy may be indicated in some cases (eg, if the kidney is nonfunctional or severely infected). Certain conditions, such as renal cortical abscess or enteric fistulas, may require immediate surgical intervention (see Treatment). [2]


Relevant Anatomy

Knowledge of the retroperitoneal structures is vital in understanding the development of perinephric abscesses.

Anterior and posterior layers of renal fascia divide the retroperitoneum into the following 3 extraperitoneal spaces:

  • The anterior paranephric space extends from the posterior peritoneum to the anterior renal fascia (Gerota).
  • The perinephric space lies between 2 layers of the renal fascia.
  • The posterior paranephric space extends from the posterior renal fascia to the fascia that lies anterior to the psoas and quadratus lumborum muscles.

The renal (Gerota) fascia surrounds the kidney and adrenal gland. Perinephric fat is present between the renal capsule and this fascia. The perinephric space also contains blood vessels and lymphatics, which facilitate the spread of infection. The 2 layers join above the adrenal glands and are attached to the diaphragmatic fascia. They join laterally, posterior to the colon, to form the lateroconal fascia. The anterior fascia of Zuckerkandl extends anterolaterally and then blends with the parietal peritoneum. Posteriorly, the Gerota fascia joins the quadratus lumborum fascia medially, while the anterior fascia joins the root of the mesentery and lies behind the pancreas and the duodenum.

Zuckerkandl described the posterior renal fascia in 1883, but did not recognize the presence of the anterior renal fascia. In 1895, Gerota documented the presence of the anterior renal fascia and assigned Zuckerkandl's name to the posterior renal fascia. Thus, the terms Zuckerkandl fascia and posterior renal fascia are synonymous, as are Gerota fascia and anterior renal fascia. [3]

The perinephric space becomes cone-shaped as it narrows inferiorly and medially and then joins with the iliac fascia. The inferomedial angle of the space is the weakest point, accounting for the extension of fluid collection across the midline and into the pelvis.



Perinephric abscesses are located between the capsule of the kidney and the Gerota fascia. The abscesses remain confined in this location because of the Gerota fascia. Perinephric abscesses usually occur because of disruption of a corticomedullary intranephric renal abscess, recurrent pyelonephritis, xanthogranulomatous pyelonephritis, or an obstructing renal pelvic stone causing pyonephrosis. [4] Approximately 30% of cases are attributed to hematogenous dissemination of organisms from sites of infection such as wound infection, furuncles, or pulmonary infections. Abscesses can also be caused by ascending urinary tract infection.

The most common mechanism for gram-negative bacterial abscess to develop is the rupture of a corticomedullary abscess, while the most common mechanism for the development of a staphylococcal infection is the rupture of a renal cortical abscess. This finding frequently is observed in association with a previous renal operation such as a partial nephrectomy or nephrolithiasis or, most commonly, as a complication of diabetes mellitus (60-90%).

Perforation of a ureter or a calyceal fornix may rarely result in perinephric abscess formation.

Occasionally, a perinephric abscess results from the spread of infection from extraperitoneal sites, such as in retroperitoneal appendicitis, diverticulitis, pancreatitis, and pelvic inflammatory conditions. In some instances, perinephric abscess is caused by bowel perforation, Crohn disease, or osteomyelitis from the spine.

Patients with polycystic renal disease who undergo hemodialysis may be particularly susceptible to developing perinephric abscess (62% of cases).

Predisposing factors for perinephric abscess include neurogenic bladder, vesicoureteral reflux, bladder outlet obstruction, renal papillary necrosis, obstructing calculus, genitourinary tuberculosis, trauma (eg, renal biopsy, [5] urinary instrumentation, urologic surgery), immunosuppression, and intravenous drug abuse.

When a perinephric infection ruptures through the Gerota fascia into the pararenal space, it leads to the formation of a paranephric abscess. Paranephric abscesses may also be caused by infectious disorders of the intestine, pancreas, liver, gall bladder, prostate, and pleural cavity, and they may be caused by osteomyelitis of adjacent ribs or vertebrae. Sometimes, with a superimposed infection, a perirenal hematoma can progress to a perinephric abscess.



Perinephric abscess may boccur as a complication of urinary tract infections. Escherichia coli, Proteus species, and Staphylococcus aureus are the usual pathogens. Perinephric abscesses due to S aureus are usually secondary to hematogenous seeding of infection. [6] The use of antibiotics for skin and wound infections has decreased the incidence of staphylococcal infection from 45% to 6% over the last 6 decades. However, this rate has increased from 8% to 30% for E coli infections and from 4% to 44% for Proteus mirabilis infection. Other gram-negative bacteria that can cause this infection include Klebsiella, Enterobacter, Pseudomonas, Serratia, and Citrobacterspecies.

Although C koseri has been isolated with increased frequency from the urine of hospitalized patients, fewer than 6 reported cases of renal or perinephric abscess have been attributed to this opportunistic infection. [7] Risk factors for this pathogen include diabetes, the presence of an indwelling Foley catheter, and a history of genitourinary instrumentation or obstruction. [8]

Occasionally, perinephric abscess may be caused by enterococci. Streptococcus infection (Group B, S pneumoniae)has been reported. [5, 9] Anaerobes such as Clostridium, Bacteroides, and Actinomyces can be present in as many as 25% of cases.

Perinephric abscess secondary to Candida infection usually occurs in patients with diabetes. Predisposing factors include surgery (including kidney transplantation [10] ) and prolonged antibiotic therapy.

Splenectomy may increase the risk of perinephric abscess. A population-based retrospective cohort study from Taiwan found that the adjusted hazard ratio (HR) of renal and perinephric abscesses was 2.24 for the splenectomy group compared with the non-splenectomy group. The adjusted HR was markedly increased, to 7.69, for splenectomized persons with diabetes mellitus. [11]  



The incidence of perinephric abscess ranges from 1-10 cases for every 10,000 hospital admissions. Men and women are affected with equal frequency. Patients with diabetes mellitus account for one third of all perinephric abscess cases. [12]



Perinephric abscess is a life-threatening entity, with a mortality rate of up to 56%. Even with modern surgical therapy, the mortality rate is 8-22% and significant morbidity occurs in 35% of patients. The high morbidity and mortality rates are partly due to long delays in diagnosis and the comorbid conditions in these patients. Diagnosis may be delayed because the findings on history and physical examination are typically nonspecific. 

Factors associated with higher mortality rate include the following:

  • More severe illness and sepsis
  • Urinary tract obstruction
  • Lethargy
  • Higher temperature (> 104°F)
  • The presence of additional underlying diseases and related conditions, such as diabetic ketoacidosis
  • Obscure presentation
  • White blood cell count greater than 25,000 cells/μL
  • High blood urea nitrogen (BUN) level 
  • Positive blood cultures
  • Diagnostic delay
  • Previous urinary tract infections

Early diagnosis, immediate drainage, and antibiotic therapy can markedly reduce mortality rates. Criteria for successful treatment include the presence of negative cultures and the resolution of any underlying obstruction.