Renal Corticomedullary Abscess Clinical Presentation
- Author: Aaron Benson, MD; Chief Editor: Edward David Kim, MD, FACS more...
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.
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.
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. Several risk factors 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.
Approximately 30% of patients with corticomedullary abscess have nephrolithiasis. 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.
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.
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.
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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