Your activity: 205 p.v.
your limit has been reached. plz Donate us to allow your ip full access, Email: sshnevis@outlook.com

Renal and perinephric abscess

Renal and perinephric abscess
Author:
Alain Meyrier, MD
Section Editor:
Stephen B Calderwood, MD
Deputy Editor:
Allyson Bloom, MD
Literature review current through: Jan 2023. | This topic last updated: Sep 21, 2022.

INTRODUCTION — Renal and perinephric suppurations (or abscesses) commonly share similar clinical manifestations, but their pathophysiology, complications, and treatment are not identical.

The clinical manifestations, diagnosis, and management of renal and perinephric abscesses will be reviewed here. Pyelonephritis in general, emphysematous pyelonephritis, malakoplakia, and xanthogranulomatous pyelonephritis are discussed in detail separately. (See "Acute complicated urinary tract infection (including pyelonephritis) in adults" and "Emphysematous urinary tract infections" and "Xanthogranulomatous pyelonephritis".)

MICROBIOLOGY — Renal and perirenal abscesses can complicate a urologic infection (usually due to gram-negative enteric bacilli or a polymicrobial infection) [1-4] or occur secondary to hematogenous seeding (mostly due to Staphylococcus aureus). As an example, in a retrospective study from China that included 98 patients with renal or perinephric abscesses over a 10-year period, the main causative pathogens were Escherichia coli (51.4 percent), S. aureus (10.0 percent), and Klebsiella pneumoniae (8.6 percent) [5].

PATHOGENESIS — Both renal and perinephric abscesses start with tissue necrosis (lobar necrosis in renal abscess; perirenal fat necrosis in perinephric abscess). Renal abscess forms a walled-off cavity; perinephric abscess consists of a more diffuse liquefaction located between the renal capsule and Gerota’s fascia. Septation of the perinephric abscess is frequent, which makes drainage more difficult than that of renal abscess.

Renal abscess — Focal renal abscesses typically occur in the setting of pyelonephritis, particularly in patients with anatomical abnormalities that predispose to infection. As an example, approximately two-thirds of renal abscesses caused by gram-negative organisms occur in patients with a renal stone or vesicoureteral reflux [6]. In such cases, the kidney may have suffered previous episodes of infection and be chronically pyelonephritic and scarred. However, even in patients with pyelonephritis who have a normal urinary tract, small abscesses (<1 cm, (image 1)) are not uncommon on initial ultrasound; larger ones (>2 cm (image 2)) typically develop in patients with diabetes mellitus or in the setting of delayed diagnosis and treatment.

Local complement activation drives vasoconstriction and inflammatory edema that results in renal tissue necrosis and a pus-filled cavity [7,8]. These ischemic lesions appear as hypodense areas on contrast-enhanced computed tomography (CT) imaging, as the contrast media does not penetrate the infected area.

Radiologists sometimes use the term "lobar nephronia" (analogous to "lobar pneumonia") to describe a single round or wedge-shaped hypodense image (often poorly defined) in a single lobe on CT following contrast injection [7-12]. In contrast to renal abscess, which can be visualized prior to contrast injection, lobar nephronia is poorly visualized in pre-contrast images. Thus, rather than a variant of renal abscess, lobar nephronia refers to a radiologic image of kidney tissue ischemia and represents a continuum of bacterial renal infection. However, an area of lobar nephronia in the setting of pyelonephritis may rapidly (eg, within one to three days) progress to tissue necrosis and formation of a walled-off cavity [7,13-15]. This mostly occurs in diabetics and can be associated with papillary necrosis. Following antibiotic treatment, the initial lesion evolves to a cortical scar.

In the pre-antibiotic era, a renal abscess (also called a renal carbuncle [16]) or multiple miliary renal abscesses were classic complications of staphylococcal bacteremia that typically developed one to eight weeks after the initial infection [6,13,16-20]. This presentation of renal abscess is now rare, since staphylococcal infections are, in most cases, treated early in their course. Renal abscess from a hematogenous source can, however, still be seen in certain settings, such as an intravenous drug abuser with staphylococcal endocarditis [14]. Hematogenous spread can also occur from an infection originating in the contralateral kidney [6,19] or from extrarenal sources. As an example, renal abscesses may occur in patients without overt bacteremia who suffered from a seemingly minor skin lesion, such as staphylococcal pyoderma [16,19].

Renal abscesses arising as a consequence of focal suppuration in the setting of acute pyelonephritis can occur in the cortex, medulla, or both, whereas those due to hematogenous spread are usually located in the cortex of the kidney.

Perinephric abscess — Perinephric abscesses, like renal abscesses, can also occur through local or hematogenous spread.

With local spread, perinephric suppuration can develop from the outward diffusion of a renal infection (generally due to gram-negative organisms) to the perirenal fat, ie, the infection progresses eccentrically toward the lumbo-abdominal wall and also toward adjacent visceral structures. Perirenal fat infection may also complicate a renal abscess that ruptures through the capsule [6] or a cortical staphylococcal renal abscess [16]. Rarely, perinephric suppuration may arise from non-renal contiguous infection originating from the liver, the gallbladder, the pancreas, small bowel Crohn’s disease, a retrocecal appendix, or vertebral osteomyelitis [6].

Conversely, perirenal fat infection can occur from hematogenous seeding, mostly staphylococcal, and in such cases, the kidney is in most instances normal.

Risk factors — Predisposing factors for renal and perinephric abscesses include diabetes mellitus, pregnancy, and urinary tract abnormalities. Anatomical abnormalities that can be complicated by infection include a renal stone, especially large staghorn calculi, vesicoureteral reflux, neurogenic bladder, obstructive tumor, papillary necrosis, benign cyst, and polycystic kidney disease [1-4,6,13,14,16,17,21].

CLINICAL MANIFESTATIONS — Clinical manifestations of renal and perinephric abscess are often similar and protean. Renal abscess occurs more frequently than perinephric abscess.

Symptoms and physical findings — Both renal and perinephric abscesses are characterized by the insidious onset of fever, vague lumbo-abdominal pain, pallor, fatigue, sweats, and general signs and symptoms of deep-seated suppuration such as weight loss. Symptoms typical of a urinary tract infection, such as dysuria and/or urinary frequency, are not reported in many patients with renal or perinephric abscesses.

In a Korean series of 56 patients hospitalized with renal or perinephric abscesses, the most common presenting symptoms were fever and chills (reported in 75 and 63 percent of patients, respectively) [20]. Other symptoms included abdominal pain, anorexia, and dysuria (46, 38, and 9 percent, respectively). The average duration of symptoms prior to admission was 12 days.

The presentation of the abscess may be particularly indolent in older adults and in individuals with autonomic neuropathy (as in the setting of diabetes or chronic alcoholism) [18,20,22,23].

As perinephric abscesses can extend to involve adjacent structures, symptoms related to such involvement (eg, right upper quadrant pain with liver involvement or chest pain with an empyema or subphrenic abscess) may also be present.

On examination, costovertebral angle tenderness to percussion is common. In the Korean series above, it was the most common physical finding, in 75 percent of the patients. Occasionally, a palpable mass can be appreciated. In the setting of perirenal suppuration, the overlying skin may demonstrate an inflammatory reaction [24].

Laboratory findings — Leukocytosis is frequently observed in the setting of renal and perinephric abscess, although it is not a specific finding. In diabetics, acidosis is also a common early finding. Inflammatory markers, such as the erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), are virtually always elevated, reflective of a deep seated infection.

Abnormal findings in the urine depend on the pathogenesis of the abscess and whether the infectious process communicates with the collecting system. In the setting of renal abscesses, urinalysis usually demonstrates abundant pyuria and moderate proteinuria along with bacteriuria. However, not all renal abscesses communicate with the collecting system, particularly in cases of infected cysts, and in such cases, the urinalysis may be unremarkable. Similarly, urine studies are usually normal with a perinephric abscess that develops as a result of hematogenous spread and does not communicate with the collecting system [6].

For patients who have hematogenous seeding of the kidneys or perinephric fat, blood cultures may grow the causative organism. However, some patients who develop renal abscesses from presumed spread from a distant site may have sterile blood cultures.

Radiographic findings — Abnormalities associated with renal and perinephric abscesses can be visualized on various imaging modalities, although computed tomography (CT) is the preferred imaging procedure.

Plain radiography – Radiographs occasionally reveal signs suggestive of renal and perinephric abscesses. Such findings on abdominal plain films include scoliosis with the concavity toward the lesion, an abdominal mass, an enlarged kidney with indistinct outlines, a loss of psoas margin, a radio-opaque calculus (image 1), and/or a poorly defined renal shadow. Chest radiography may demonstrate a pleural effusion, ipsilateral pneumonia, atelectasis and/or an elevated hemidiaphragm.

Ultrasonography – Ultrasound typically demonstrates a thick-walled cavity filled with fluid in the setting of renal abscess (image 3). Pus may be difficult to distinguish from sterile urine or blood, and echoes due to renal tissue debris can be difficult to distinguish from necrosis within a necrotic renal cancer. Ultrasonography is strongly suggestive of suppuration when it shows a horizontal separation between an upper level of low-density fluid (urine) and an underlying level of more dense fluid (pus).

Computed tomography (CT) – CT with contrast enhancement is the best imaging procedure for identification of renal (image 2) and/or perinephric abscesses (image 4) and evaluation for extension of perinephric suppuration to adjacent structures (image 5 and image 1), such as the liver, diaphragm, and mediastinum. Films taken one or two hours following injection of contrast may typically show an enhanced rim around the abscess cavity.

On CT, renal abscesses appear as intrarenal walled-off cavities; following contrast injection, there is often a rim of hyperdensity. CT may also demonstrate thickening of Gerota's fascia, renal enlargement, parenchymatous inflammation, decreased renal attenuation, and lobar necrosis. Focal or perirenal fluid and/or gas may be seen [9,10,25-27]. Perinephric abscesses are usually confined to the perinephric space by Gerota's fascia but may extend to the retroperitoneal structures and/or rupture into the collecting system [6,13,18,20,22-24,28]. An abscess in the perinephric space may also penetrate into the flank muscles or into the psoas muscle; it may extend caudally between the diverging layers of Gerota's fascia and present as an abscess in the groin or paravesical area. Less commonly, there may be extension into the peritoneal cavity. Cephalad extension may lead to formation of a subphrenic abscess [28], penetration of the diaphragm and empyema formation, progression to the mediastinum, lung abscess, or nephrobronchial fistula. Rupture into the colon occurs infrequently [6].

Radiologists sometimes use the term "lobar nephronia" to describe a single round or wedge-shaped hypodense image (often poorly defined) in a single lobe on CT following contrast injection [7-12]. In contrast to renal abscess, which can be visualized prior to contrast injection, lobar nephronia is poorly visualized in pre-contrast images. Lobar nephronia is not a distinct type of abscess but a potential precursor to abscess formation. (See 'Renal abscess' above.)

Nuclear imaging and magnetic resonance imaging (MRI) – Nuclear imaging and MRI have limited utility. However, in an Italian series that included 170 adults with acute pyelonephritis with consistent CT findings, of the 26 who were also evaluated with nuclear imaging, 21 also had positive findings on nuclear imaging, and in one case, nuclear imaging showed an abscess which had not been documented by CT [29]. This might indicate that in some rare cases, nuclear imaging may have an advantage over CT for diagnosing a renal abscess. However, the precise role of MRI in the diagnosis of renal/perirenal infection would require further studies.

DIAGNOSIS AND EVALUATION

Clinical suspicion — The clinical diagnosis of renal or perinephric abscess should be suspected in a patient presenting with consistent signs and symptoms, including prolonged fever and flank pain as well as laboratory evidence of chronic inflammation (eg, elevated ESR and CRP) (see 'Clinical manifestations' above). In addition, the possibility of a renal or perinephric abscess should be suspected in patients being treated for pyelonephritis who do not or are slow to respond to antimicrobial therapy following three days of appropriate antibiotic treatment (see "Acute complicated urinary tract infection (including pyelonephritis) in adults"). Identification of a renal or perinephric abscess on imaging (ideally computed tomography) confirms the diagnosis. The clinical diagnosis of renal or perinephric abscesses is often delayed, sometimes by weeks, until imaging is finally performed, which highlights the importance of a high level of clinical suspicion for these entities.

A microbiological diagnosis may require cultures of urine, blood, or the abscess itself.

Radiography — Radiography should be used for definitive diagnosis of renal or perinephric abscess; the most useful modalities are ultrasonography and computed tomography (CT) [8-10,25-27,30]. While ultrasound can be used to make the diagnosis, CT with contrast medium enhancement is the best imaging procedure for evaluation of renal and/or perinephric abscesses and for diagnosing a possible extension of perinephric suppuration to adjacent structures, such as liver, diaphragm, and mediastinum. Findings consistent with renal or perinephric abscesses are discussed elsewhere. (See 'Radiographic findings' above.)

Microbiological diagnosis — Blood and urine cultures should be collected at the time of presentation in order to identify a causative pathogen. However, in some cases, particularly with perinephric abscesses, the abscess does not communicate with the collecting system, and culture of a sample of the abscess itself may be required for a microbiological diagnosis. (See 'Perinephric abscess' below.)

Other laboratory tests — Routine blood work (eg, chemistry panel and complete blood count) is helpful to assess underlying kidney function or the presence of leukocytosis. Urinalysis should also be performed to assess for the presence of pyuria and proteinuria; however, a normal urinalysis does not refute the diagnosis of renal or perinephric abscess, as they might not necessarily communicate with the collecting system.

Inflammatory markers, such as the ESR and CRP, are not only helpful in supporting the clinical diagnosis but are also useful markers to follow to assess for appropriate clinical response to therapy. (See 'Follow-up' below.)

DIFFERENTIAL DIAGNOSIS — Other entities may present with similar clinical findings as renal or perinephric abscess. These include acute lobar nephronia without renal tissue necrosis, acute pyelonephritis complicated by papillary necrosis, emphysematous pyelonephritis, malakoplakia, and renal cell carcinoma. Most of these can be distinguished from renal or perinephric abscesses on computed tomography (CT) imaging, although in occasional cases, sampling of the tissue or abscess for histology and culture is necessary to make the alternate diagnosis.

Papillary necrosis can also complicate acute pyelonephritis, particularly in patients with diabetes mellitus. On contrast-enhanced CT, the entire papillary tip disappears and the calyceal fornix appears eroded and club-shaped; the sloughed papilla may appear as a round foreign body in the calyx and can migrate to the pelvis. Ureteral obstruction with renal colic and sudden deterioration of kidney function may complicate the migration of a necrotic papilla or of papillary fragments [31,32]. Papilla migration is a rare but severe complication that can result in sepsis; patients often warrant treatment in the intensive care unit with intravenous antibiotics and supportive care. Urologic intervention for ureteral catheterization may be warranted; for some cases of severe infection with a nonfunctioning kidney, rescue nephrectomy is an option.

Emphysematous pyelonephritis is a gas-producing necrotizing infection that involves the renal parenchyma and, in some cases, the perirenal tissues. CT demonstrates gas in the tissues as opposed to a predominantly suppurative process with renal and perinephric abscesses. (See "Emphysematous urinary tract infections", section on 'Emphysematous pyelonephritis and pyelitis'.)

Malakoplakia is a rare granulomatous inflammatory disease associated with E. coli infection [8]. It usually affects the bladder; the kidney is the primary site of involvement in about 15 percent of cases [33-35]. The classic appearance on CT is an enlarged kidney with multiple hypovascular masses [36]. Although generally distinctive from imaging findings of a renal abscess, the diagnosis is definitively made based on histological findings including PAS-positive Michaelis-Gutmann (MG) bodies, which are thought to result from inadequate intracellular killing of phagocytosed bacteria. Therapy should consist of antimicrobial therapy tailored to culture and sensitivity data.

Xanthogranulomatous pyelonephritis is an unusual variant of chronic pyelonephritis in which there is typically massive destruction of the kidney due to granulomatous tissue containing lipid-laden macrophages. Although presenting symptoms may be similar to renal and perinephric abscesses, the imaging findings are quite distinct. (See "Xanthogranulomatous pyelonephritis".)

Occasionally, renal cell carcinoma may be difficult to distinguish radiographically from a renal abscess, in which cases a tissue diagnosis may be necessary. Additionally, abscess formation can complicate renal cell carcinoma if it results in obstruction. This entity is discussed in detail separately. (See "Clinical manifestations, evaluation, and staging of renal cell carcinoma".)

MANAGEMENT — The approach to management of renal and perinephric abscess includes antimicrobial therapy in conjunction with percutaneous drainage (when warranted) [37-39]. In addition, urologic obstruction, if present, should be relieved promptly. In cases in which the abscess cannot be successfully treated with antibiotics and percutaneous drainage or when the underlying kidney is chronically diseased, surgical intervention may be indicated.

Antibiotics

Empiric therapy — We typically initially treat patients with renal or perinephric abscess with intravenous therapy, which we start as soon as blood and urine cultures have been collected. For perinephric abscess, empiric therapy can be delayed until drainage of the abscess can be performed, as long as it can be done promptly and the patient is stable, since a sample of the perinephric abscess may be the only microbiologically informative specimen. (See 'Microbiological diagnosis' above.)

For empiric therapy, we suggest targeting both S. aureus and gram-negative bacilli (see 'Microbiology' above). Because patients with renal abscess frequently have diabetes mellitus, other complications, or health care exposures that increase the likelihood of resistant organisms, we favor using an agent that covers methicillin-resistant S. aureus along with a broad-spectrum gram-negative agent:

Vancomycin 20 to 35 mg/kg intravenous loading dose followed by 15 to 20 mg/kg intravenously every 8 to 12 hours (table 1)

Plus one of the following:

Piperacillin-tazobactam 3.375 g intravenously every 4 hours or 4.5 g intravenously every 6 hours

Cefepime 1 g intravenously every 8 hours or 2 g intravenously every 12 hours

Meropenem 1 g intravenously every 8 hours

Imipenem 500 mg intravenously every 6 hours or 1 g intravenously every 8 hours

We typically use the higher doses listed for patients with more severe illness. Additionally, for some patients with very severe disease, such as critical illness or septic shock, we add another gram-negative agent, such as levofloxacin 750 mg intravenously daily or ciprofloxacin 400 mg intravenously twice daily, to increase the likelihood of active antibiotic coverage in the event of resistance. For patients who have had prior recent urinary tract infections, the empiric regimen should also cover prior urinary isolates.

If blood or urine cultures suggest a gram-positive organism, the vancomycin alone can be continued; if they suggest a gram-negative organism, the vancomycin can be discontinued.

Directed therapy and duration — The initial empiric antibiotic regimen should be tailored to culture and susceptibility results once these are available. In many cases, the patient warrants continuous intravenous therapy, in which case we transition to a narrower-spectrum regimen (eg, ceftriaxone for susceptible gram-negative bacilli or cefazolin for methicillin-susceptible S. aureus) if possible. Patients with a gram-negative infection can be transitioned to an oral regimen once the abscess has been drained (if appropriate) and they are clinically improving. Directed therapy for patients with S. aureus renal abscess in the setting of bacteremia (ie, antibiotic choice, use of parenteral agents, duration) is the same as for S. aureus bacteremia in general and is discussed in detail elsewhere. (See "Clinical approach to Staphylococcus aureus bacteremia in adults", section on 'Management'.)

Antibiotics commonly used for renal or perinephric abscess and their doses are listed in the table (table 2).

We generally continue antibiotic therapy throughout and after drainage for a total duration of at least two to three weeks. The final duration of antibiotic therapy should be determined by the extent of infection, the patient's clinical response to initial management, and normalization of inflammatory markers. As an example, patients with abscesses that are difficult to drain or slow to resolve on follow-up imaging may require longer courses of antibiotic therapy, tailored to resolution of clinical symptoms. (See 'Follow-up' below.)

Patients should be monitored for adverse effects of antibiotics (eg, drug allergy, Clostridioides difficile colitis) during therapy, particularly if they remain on intravenous therapy. This is discussed in detail elsewhere. (See "Outpatient parenteral antimicrobial therapy", section on 'Commonly encountered problems'.)

Drainage — The approach to drainage differs somewhat between renal and perinephric abscesses. Indications for renal abscess drainage depend on the size of the abscess, whereas drainage is generally indicated for perinephric abscesses of all sizes for diagnostic purposes. Percutaneous drainage is generally preferred if possible because of decreased morbidity compared with surgical drainage [39-42].

Urologic intervention may be warranted for abscesses that occur in the context of anatomic abnormalities or are too large for effective treatment with antibiotics and catheter drainage. (See 'Urologic/surgical intervention' below.)

Renal abscess — The size of the renal abscess generally dictates the need for drainage, which is ideally performed percutaneously (CT or ultrasound guided).

For renal abscesses <5 cm in diameter, antimicrobial therapy alone (without drainage) is appropriate initial management [40-42]. These lesions frequently respond well to prolonged antibiotic treatment, and radiographic localization for drainage can be difficult. If clinical symptoms and radiographic findings persist after several days of antimicrobial therapy, percutaneous drainage of abscesses <5 cm should be considered, if technically possible.

Patients with renal abscesses >5 cm should be managed with percutaneous drainage in conjunction with antimicrobial therapy [2,4,13,17,18,37,40,41].

Drainage catheters should remain in place until discharge is minimal (usually up to seven days).

The success of this approach was illustrated in a retrospective review of 52 patients with renal abscesses [41]. Resolution with antimicrobial therapy alone was observed in most patients with renal abscesses <3 cm and 3 to 5 cm (100 and 92 percent, respectively). Those with abscesses >5 cm did equally well with percutaneous or open surgical drainage. Similarly, in a series from Korea of 63 patients initially diagnosed with renal or perirenal abscesses, 51 abscesses measured 5 cm or less (mean size 3.6 cm), and 49 of those were treated with broad-spectrum intravenous antibiotics alone [40]. All 49 patients showed complete clinical regression and resolution of the renal lesions shown by CT between 3 and 14 weeks.

Perinephric abscess — Percutaneous drainage (CT or ultrasound-guided) is generally indicated for perinephric abscesses for diagnostic purposes [38,39]. As above, since perinephric abscesses do not always communicate with the collecting system, a sample of the abscess itself may be the only microbiologically informative specimen. If prompt drainage is feasible, it should ideally be performed prior to initiation of antimicrobial therapy, unless a causative organism has been clearly established, so that the Gram stain and culture results can be used to guide selection of therapy. If drainage cannot be performed promptly, empiric antibiotic therapy should be initiated as outlined elsewhere. (See 'Antibiotics' above.)

If cultures of other specimens are informative and drainage is not necessary for a microbial diagnosis, antibiotic treatment without drainage can be successful for small abscesses (eg, <3 cm), as suggested by several observational studies [19,37,42]. Drainage is generally necessary for resolution of larger perinephric abscesses or when medical therapy alone is not sufficient. Typically, a higher proportion of perinephric and mixed abscesses warrants drainage compared with renal abscesses [18].

In some cases, septation of the necrotic and liquefied perirenal fat may complicate adequate drainage [6] and make surgical intervention the best approach.

Urologic/surgical intervention — Consultation with a urologic specialist should be pursued when there is a urologic obstruction that needs relief, when an abscess occurs in the context of an anatomic abnormality (such as large, obstructing renal stones or vesicoureteral reflux), or when the abscess is too large for effective treatment with antibiotics and catheter drainage [1,13,17,21]. For abscesses that are not amenable to percutaneous drainage, surgical drainage and/or rescue nephrectomy may be required if medical treatment has failed.

Nephrectomy may also be warranted for a renal abscess that has developed in a small, scarred chronically pyelonephritic and poorly functioning kidney destroyed by previous episodes of infection [6].

Perinephric abscesses may also develop in the setting of a chronically infected and atrophic kidney, as in the case of a staghorn calculus, and nephrectomy may be warranted in such cases. However, when perinephric abscesses develop in the setting of perirenal fat infection from hematogenous (mainly staphylococcal) seeding, the kidney is generally normal and treatment will be limited to that of the perirenal fat necrosis and liquefaction.

Follow-up — Clinical response should be assessed throughout the course of therapy. Useful clinical parameters to follow include temperature, flank pain, white blood cell count, ESR, and CRP, which are all expected to improve with successful treatment.

Repeat imaging is warranted in the setting of persistent clinical symptoms and laboratory abnormalities or if drainage is not proceeding as expected. Many clinicians also reimage with ultrasound to assess for clinical improvement prior to hospital discharge.

PROGNOSIS — Renal and perinephric abscesses can be severe illnesses, depending on the extent of the infection and the underlying host factors. In a series from Korea of 63 patients with renal or perinephric abscesses, the average hospital stay was 15.3 days (range, 5 to 31 days) [40]. Significant predictors of a longer hospital stay were age, diabetes mellitus, and abscess size. Old age, lethargy, and renal insufficiency have also been associated with poor prognosis [13,18,20,22-24].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Urinary tract infections in adults".)

SUMMARY AND RECOMMENDATIONS

Microbiology and pathogenesis – Renal and perinephric abscess can occur as complications of pyelonephritis (usually due to gram-negative enteric bacilli) or in the setting of bacteremia with hematogenous seeding (usually due to Staphylococcus aureus). Both processes start with tissue necrosis. Renal abscess is a walled-off cavity, whereas perinephric abscess consists of a more diffuse liquefaction located between the renal capsule and Gerota’s fascia. (See 'Microbiology' above.)

Clinical manifestations – Clinical manifestations of renal and perinephric abscess are similar and often initially do not evoke a specific diagnosis: fever, flank pain, and laboratory evidence of chronic inflammation. Although dysuria, pyuria, and proteinuria may be present, urinary symptoms and urinalysis abnormalities are not uniformly reported. The presentation may be especially subtle and insidious in older adults and in individuals with autonomic neuropathy (usually in the setting of diabetes or chronic alcoholism). (See 'Clinical manifestations' above.)

Imaging findings – Abnormalities associated with renal and perinephric abscesses can be visualized on various imaging modalities, including plain radiographs, ultrasound, and computed tomography (CT). On CT, renal abscesses appear as intrarenal walled-off cavities (image 2). Perinephric abscesses are usually confined to the perinephric space by Gerota's fascia but may extend to the retroperitoneal structures and/or rupture into the collecting system (image 4 and image 5 and image 1). (See 'Radiographic findings' above.)

Evaluation and diagnosis – A high level of suspicion is required for the diagnosis of renal or perinephric abscess which should be considered in a patient presenting with such symptoms and signs or in patients with pyelonephritis who are slow to respond to therapy. Identification of a renal or perinephric abscess on ultrasound or computed tomography (CT) confirms the diagnosis. CT with contrast enhancement is the best imaging procedure for identification of renal and/or perinephric abscesses and evaluation for extension of perinephric suppuration to adjacent structures. (See 'Diagnosis and evaluation' above.)

Blood and urine cultures should be collected at presentation in order to identify a causative pathogen. In some cases, particularly with perinephric abscesses, a sample of the abscess itself may be required for microbiologic diagnosis, in which case drainage is indicated. (See 'Microbiological diagnosis' above.)

Antibiotic therapy – For empiric therapy, we suggest a parenteral regimen that provides broad-spectrum coverage against methicillin-resistant S. aureus and gram-negative bacilli (Grade 2C). Examples include vancomycin plus one of the following: piperacillin-tazobactam, cefepime, meropenem, or imipenem.

Once culture and susceptibility results return, the regimen can be tailored to a narrower agent, and following abscess drainage (if indicated) and clinical improvement, it can be transitioned in most cases to an active oral agent (table 2). Duration depends on the clinical course and abscess resolution, and is generally at least two to three weeks. (See 'Antibiotics' above.)

Percutaneous drainage – Indications for renal abscess drainage for therapeutic purposes depend on the size of the abscess, whereas drainage is often indicated for perinephric abscesses for diagnostic purposes. Percutaneous drainage is generally preferred if possible because of decreased morbidity compared with surgical drainage. (See 'Drainage' above.)

For renal abscesses ≥5 cm in diameter, we suggest immediate percutaneous drainage (Grade 2C).

For perinephric abscesses ≥3 cm in diameter, we suggest immediate percutaneous drainage (Grade 2C). Smaller abscesses may also warrant percutaneous drainage for microbial diagnostic purposes.

Otherwise, for smaller abscesses, we defer drainage and manage with antibiotics alone. If clinical symptoms and radiographic findings persist despite several days of appropriate antibiotic therapy, we proceed with percutaneous drainage. (See 'Drainage' above.)

Surgical intervention for selected cases – Surgical consultation is warranted when an abscess occurs in the context of an anatomic abnormality (such as large, obstructing renal stones or vesicoureteral reflux) or when the abscess is too large for effective treatment with antibiotics and catheter drainage. (See 'Urologic/surgical intervention' above.)

  1. Yen DH, Hu SC, Tsai J, et al. Renal abscess: early diagnosis and treatment. Am J Emerg Med 1999; 17:192.
  2. Fair WR, Higgins MH. Renal abscess. J Urol 1970; 104:179.
  3. Siroky MB, Moylan R, Austen G Jr, Olsson CA. Metastatic infection secondary to genitourinary tract sepsis. Am J Med 1976; 61:351.
  4. Saiki J, Vaziri ND, Barton C. Perinephric and intranephric abscesses: a review of the literature. West J Med 1982; 136:95.
  5. Liu XQ, Wang CC, Liu YB, Liu K. Renal and perinephric abscesses in West China Hospital: 10-year retrospective-descriptive study. World J Nephrol 2016; 5:108.
  6. Hill GS. Renal infection. In: Uropathology, 1st Ed, Hill GS (Ed), Churchill Livingstone, New York 1989; 33.
  7. Meyrier A, Condamin MC, Fernet M, et al. Frequency of development of early cortical scarring in acute primary pyelonephritis. Kidney Int 1989; 35:696.
  8. Roberts JA. Etiology and pathophysiology of pyelonephritis. Am J Kidney Dis 1991; 17:1.
  9. Demertzis J, Menias CO. State of the art: imaging of renal infections. Emerg Radiol 2007; 14:13.
  10. Huang JJ, Sung JM, Chen KW, et al. Acute bacterial nephritis: a clinicoradiologic correlation based on computed tomography. Am J Med 1992; 93:289.
  11. Talner LB, Davidson AJ, Lebowitz RL, et al. Acute pyelonephritis: can we agree on terminology? Radiology 1994; 192:297.
  12. Rosenfield AT, Glickman MG, Taylor KJ, et al. Acute focal bacterial nephritis (acute lobar nephronia). Radiology 1979; 132:553.
  13. Dembry LM, Andriole VT. Renal and perirenal abscesses. Infect Dis Clin North Am 1997; 11:663.
  14. Hoverman IV, Gentry LO, Jones DW, Guerriero WG. Intrarenal abscess. Report of 14 cases. Arch Intern Med 1980; 140:914.
  15. Lee BK, Crossley K, Gerding DN. The association between Staphylococcus aureus bacteremia and bacteriuria. Am J Med 1978; 65:303.
  16. Graves RC, Parkins LE. Carbuncle of the kidney. J Urol (Baltimore) 1970; 104:179.
  17. Anderson KA, McAninch JW. Renal abscesses: classification and review of 40 cases. Urology 1980; 16:333.
  18. Coelho RF, Schneider-Monteiro ED, Mesquita JL, et al. Renal and perinephric abscesses: analysis of 65 consecutive cases. World J Surg 2007; 31:431.
  19. Shu T, Green JM, Orihuela E. Renal and perirenal abscesses in patients with otherwise anatomically normal urinary tracts. J Urol 2004; 172:148.
  20. Lee BE, Seol HY, Kim TK, et al. Recent clinical overview of renal and perirenal abscesses in 56 consecutive cases. Korean J Intern Med 2008; 23:140.
  21. Fowler JE Jr, Perkins T. Presentation, diagnosis and treatment of renal abscesses: 1972-1988. J Urol 1994; 151:847.
  22. Hutchison FN, Kaysen GA. Perinephric abscess: the missed diagnosis. Med Clin North Am 1988; 72:993.
  23. Sheinfeld J, Erturk E, Spataro RF, Cockett AT. Perinephric abscess: current concepts. J Urol 1987; 137:191.
  24. Tsukagoshi D, Dinkovski B, Dasan S, Jethwa J. Perinephric abscess secondary to a staghorn calculus presenting as a subcutaneous abscess. CJEM 2006; 8:285.
  25. Bova JG, Potter JL, Arevalos E, et al. Renal and perirenal infection: the role of computerized tomography. J Urol 1985; 133:375.
  26. Kaplan DM, Rosenfield AT, Smith RC. Advances in the imaging of renal infection. Helical CT and modern coordinated imaging. Infect Dis Clin North Am 1997; 11:681.
  27. Gerzof SG, Gale ME. Computed tomography and ultrasonography for diagnosis and treatment of renal and retroperitoneal abscesses. Urol Clin North Am 1982; 9:185.
  28. Reese JH, Anderson RU, Friedland G. Splenic abscess arising by direct extension from a perinephric abscess. Urol Radiol 1990; 12:91.
  29. Rollino C, Beltrame G, Ferro M, et al. Acute pyelonephritis in adults: a case series of 223 patients. Nephrol Dial Transplant 2012; 27:3488.
  30. Kuligowska E, Newman B, White SJ, Caldarone A. Interventional ultrasound in detection and treatment of renal inflammatory disease. Radiology 1983; 147:521.
  31. HARVALD B. RENAL PAPILLARY NECROSIS. A CLINICAL SURVEY OF SIXTY-SIX CASES. Am J Med 1963; 35:481.
  32. Fadel MG, Carey M, Bolgeri M. Infected and obstructed kidney secondary to sloughed necrotic renal papilla. BMJ Case Rep 2018; 2018.
  33. Kobayashi A, Utsunomiya Y, Kono M, et al. Malakoplakia of the kidney. Am J Kidney Dis 2008; 51:326.
  34. Stanton MJ, Maxted W. Malacoplakia: a study of the literature and current concepts of pathogenesis, diagnosis and treatment. J Urol 1981; 125:139.
  35. van Crevel R, Curfs J, van der Ven AJ, et al. Functional and morphological monocyte abnormalities in a patient with malakoplakia. Am J Med 1998; 105:74.
  36. Craig WD, Wagner BJ, Travis MD. Pyelonephritis: radiologic-pathologic review. Radiographics 2008; 28:255.
  37. Meng MV, Mario LA, McAninch JW. Current treatment and outcomes of perinephric abscesses. J Urol 2002; 168:1337.
  38. Lang EK. Renal, perirenal, and pararenal abscesses: percutaneous drainage. Radiology 1990; 174:109.
  39. Deyoe LA, Cronan JJ, Lambiase RE, Dorfman GS. Percutaneous drainage of renal and perirenal abscesses: results in 30 patients. AJR Am J Roentgenol 1990; 155:81.
  40. Lee SH, Jung HJ, Mah SY, Chung BH. Renal abscesses measuring 5 cm or less: outcome of medical treatment without therapeutic drainage. Yonsei Med J 2010; 51:569.
  41. Siegel JF, Smith A, Moldwin R. Minimally invasive treatment of renal abscess. J Urol 1996; 155:52.
  42. Dalla Palma L, Pozzi-Mucelli F, Ene V. Medical treatment of renal and perirenal abscesses: CT evaluation. Clin Radiol 1999; 54:792.
Topic 8057 Version 21.0

References