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Renal Corticomedullary Abscess Clinical Presentation

  • Author: Aaron Benson, MD; Chief Editor: Edward David Kim, MD, FACS  more...
 
Updated: Dec 06, 2015
 

History

Common symptoms in patients with renal corticomedullary abscess include fever, chills, nausea/vomiting, and flank or abdominal pain. Some individuals with renal corticomedullary abscess develop dysuria and other urinary tract symptoms. Nonspecific constitutional symptoms (eg, malaise, fatigue, weight loss) may occur in patients with a chronic process, especially those with xanthogranulomatous pyelonephritis (XGP).

Obtaining a thorough medical history is important in evaluating patients with a possible renal corticomedullary abscess. Patients with this infection frequently have long-standing (approximately 14 d) symptoms such as fever, back pain, and/or abdominal discomfort. Unfortunately, these symptoms may be vague and do not always reflect the severity of the infection. In addition, various host factors influence the development and severity of renal infection (see Causes). Most patients with renal corticomedullary abscess have a history of recurrent urinary tract infections, renal calculi, and/or prior genitourinary tract instrumentation. Urinary tract obstruction is an important predisposing factor.

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Physical

Signs that accompany renal corticomedullary abscess vary greatly and are nonspecific. However, the physical examination findings usually indicate significant infection, including ill appearance, fever, and hemodynamic instability. In patients with accompanying sepsis, hemodynamic and overall instability may be more pronounced, with tachycardia, hypotension, and tachypnea. In addition, many persons with renal corticomedullary abscess have palpable masses. Seventy percent of patients with XGP have a flank mass. Costovertebral angle tenderness is almost uniformly present with each type of corticomedullary infection.

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Causes

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.[6] Several risk factors may contribute to upper urinary tract infections and possible subsequent renal corticomedullary abscess.

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Risk Factors

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.[7] 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 UVJ should allow urine to enter the bladder but prevent urine from refluxing back into the kidney. Thus, the kidney is protected from contamination by infected urine. When the UVJ is incompetent, the risk of ascending urinary tract infections increases. The major cause of VUR is weak detrusor backing in combination with a short intramural tunnel. 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.

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Contributor Information and Disclosures
Author

Aaron Benson, MD Staff Physician, Department of Urology, Southern Illinois University School of Medicine

Aaron Benson, MD is a member of the following medical societies: American Medical Association, American Urological Association, Illinois State Medical Society

Disclosure: Nothing to disclose.

Coauthor(s)

Keith Steinbecker, MD Consulting Staff, Department of Urology, St John's Mercy Medical Center

Keith Steinbecker, MD is a member of the following medical societies: American Urological Association

Disclosure: Nothing to disclose.

Julius Lynn Teague, MD, FACS, FAAP Medical Director, Pediatric Urology, Greenville Hospital System Children's Hospital

Julius Lynn Teague, MD, FACS, FAAP is a member of the following medical societies: American Academy of Pediatrics, American College of Surgeons, American Urological Association, Christian Medical and Dental Associations

Disclosure: Nothing to disclose.

Thomas H Tarter, MD, PhD Associate Professor, Department of Surgery, Division of Urology, Director of Urologic Oncology, Simmons Cooper Cancer Institute, Southern Illinois University School of Medicine

Thomas H Tarter, MD, PhD is a member of the following medical societies: American Medical Association, American Urological Association, Society of Urologic Oncology, American College of Surgeons Oncology Group

Disclosure: Received ownership interest from Illinois Cryotherapy Enterprise for other.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Shlomo Raz, MD Professor, Department of Surgery, Division of Urology, University of California, Los Angeles, David Geffen School of Medicine

Shlomo Raz, MD is a member of the following medical societies: American College of Surgeons, American Medical Association, American Urological Association, California Medical Association

Disclosure: Nothing to disclose.

Chief Editor

Edward David Kim, MD, FACS Professor of Surgery, Division of Urology, University of Tennessee Graduate School of Medicine; Consulting Staff, University of Tennessee Medical Center

Edward David Kim, MD, FACS is a member of the following medical societies: American College of Surgeons, Tennessee Medical Association, Sexual Medicine Society of North America, American Society for Reproductive Medicine, American Society of Andrology, American Urological Association

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Repros.

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Contrasted CT scan that demonstrates a corticomedullary abscess in a 27-year-old patient with diabetes mellitus who has a history of multiple urinary tract infections. Note the heterogeneous hypodense lesion in the right kidney. Extracapsular extension is not present.
 
 
 
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