Relationship Between Uncommon Computed Tomography Findings and Clinical Aspects in Patients With Acute Pyelonephritis

Acute pyelonephritis (APN) is the most common upper urinary tract infection, and approximately 20% to 35% of females experience an episode of APN in their lifetime [1]. The annual incidence of APN is reportedly as high as 35.7 per 10,000 individuals in South Korea, and the incidence of hospitalization for APN is reportedly 9.96 per 10,000 Korean women [2]. APN usually occurs secondary to an ascending infection of gram-negative bacteria in females, and the diagnosis is made clinically [3]. Computed tomography (CT) has not been primarily applied in patients with APN; it is preferred in patients with diabetes, equivocal diagnoses, no response to antimicrobial treatment, or immunosuppression. CT can provide important information on the range of inflammation and other accompanying complications to help to establish a precise diagnosis [4, 5, 6]. The most common radiologic CT finding of APN is a striated or wedge-shaped area of hypoperfusion or mass-like lesion after contrast injection [7, 8]. Other uncommon radiologic findings such as perirenal fat infiltration, ureteral wall edema, renal abscess formation, pelvic ascites, portal edema, and renal scarring are also observed on CT scans [9, 10].

Although the use of CT in the diagnosis of APN has rapidly increased recently, the relationship between APN and CT findings has rarely been reported. We investigated the relationship between uncommon CT findings and clinical parameters in patients with APN.

The mean peak fever was 38.7℃±0.8℃, and the mean fever duration was 7.3±3.1 days. The mean blood leukocyte count was 11,733±4,665 /µL, the mean CRP level was 12.8±7.5 mg/dL, and the mean grade of pyuria was grade 4.6±1.2 (Table 1). The most common CT finding was perirenal fat infiltration (69 cases, 55%), followed in turn by pelvic ascites (50 cases, 40%), ureteral wall edema (39 cases, 31%), and renal abscess formation (20 cases, 16%; Table 2).

TABLE 1
Patients' characteristics

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TABLE 2
Incidence of six computed tomography (CT) findings in acute pyelonephritis

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When we compared the six CT findings with the clinical parameters, the fever duration was longer and the CRP level and grade of pyuria were higher in cases with perirenal fat infiltration (p=0.010, p=0.033, and p=0.049, respectively). The CRP level was significantly higher in patients with renal abscess formation and ureteral wall edema (p=0.005 and p=0.015, respectively). Pelvic ascites, periportal edema, and renal scarring had no relationship with clinical parameters (Table 3). Although bacteriuria was found in 74 patients (59.2%), bacteriuria positivity was not related to any of the CT findings (Table 3).

TABLE 3
Correlations between computed tomography findings and clinical and laboratory parameters

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APN is usually diagnosed on the basis of typical clinical symptoms (fever, chills, nausea, and flank pain), physical examination findings (costovertebral angle tenderness), and laboratory findings including leukocytosis, pyuria, and a positive urine culture [3]. The clinical risk factors of APN are female gender, diabetes mellitus, immunosuppression, postmenopausal state, previous recurrent urinary tract infection, and vesicoureteral reflux [11]. Although intravenous pyelography (IVP) and renal ultrasound were the main radiologic diagnostic tools used in the past, CT has recently become popular in the diagnosis of APN and its related complications. Although IVP can show the anatomical structure of the renal pelvis and calyces as well as the urinary drainage from the kidney to the bladder, it is not suitable for evaluation of renal parenchymal diseases such as APN [12]. Ultrasonography is also frequently performed in patients with APN; however, positive findings have been shown in only 20% to 24% of patients in prospective studies [13, 14]. CT is the new gold standard in the evaluation of APN. It can show pathologic states in both intrarenal and extrarenal areas as precise images and can provide comprehensive anatomical and physiological information.

After administration of contrast material, APN most commonly manifests as one or more striated or wedge-shaped areas of hypoperfusion or streaky zones of lesser enhancement that extend from the papilla to the renal cortex. This pattern of differential enhancement reflects the underlying pathophysiology of tubular obstruction caused by inflammatory debris within the lumen, interstitial edema, and vasospasm [9, 12]. This area of hypoperfusion is formed by obstruction of blood vessels resulting from spasm, edema of the interstitium, and the presence of intraluminal inflammatory metabolites [9]. Radiologic CT findings other than wedge-shaped hypoperfusion include renal abscess formation or renal scarring found in intrarenal areas and perirenal fat infiltration, ureteral wall edema, pelvic ascites, and periportal edema found in extrarenal areas. Although other CT findings can be observed in intrarenal areas, including thickening of Gerota's fascia, obliteration of the renal sinus, pelvicalyceal wall thickening and enhancement, poor contrast excretion, urinary tract stones, and pelvicalyceal air, we excluded these findings because of difficulties in obtaining a precise diagnosis and their low incidence [15].

In the present study, perirenal fat infiltration was the most common CT finding in patients with APN, and the fever duration, CRP level, and grade of pyuria were more severe in these cases. Perirenal fat infiltration is observed when the inflammation of the renal parenchyma is severe and the inflammatory infiltration spreads beyond the renal capsule to the perirenal fat. The CRP level was significantly higher in patients with renal abscesses and ureteral wall edema in our study. Acute-phase inflammatory responses accompany increases in the levels of various proteins, such as CRP, fibrinogen, haptoglobin, lactoferrin, and various cytokines including interleukin-1 and tumor necrosis factor [16]. CRP is widely used in the diagnosis of various acute inflammatory diseases because it is increased as early as 6 hours after inflammation and doubles every 8 to 9 hours [17]. Renal abscess formation, perinephric abscess formation, and pyonephrosis are considered to indicate a more severe disease status than uncomplicated APN. Although gram-negative bacteria are the main cause of renal abscess formation, urine culture results are usually negative. CT is the diagnostic procedure of choice for renal abscesses, in which cases a focal rounded area of decreased enhancement is usually found [18].

Neither bacterial ureteritis nor pyeloureteritis have been reported in the literature because of their rarity as separate disease entities and because of difficulties in their precise diagnosis. The clinical significance and pathophysiology of ureteral wall or pelvicalyceal wall thickening in APN are also unknown for these reasons. Both renal abscess formation and ureteral wall thickening were risk factors for an increased CRP level in our study, and we regarded ureteral wall or pelvicalyceal wall thickening as an indicator of severe inflammation of the pelvicalyceal system or ureter and of ascending infection. Tsugaya et al. [10] reported that cortical scars were detected in six of seven patients in whom the inflammatory lesions occupied 30% or more of the renal parenchyma. Because we performed CT scans at admission, our renal CT scan findings seemed to be evidence of previous recurrent or severe renal inflammation. Although the CT finding of renal scarring was not related with the severity of inflammation and clinical parameters in our study, a follow-up CT scan or dimercaptosuccinic acid renal scan may be needed in patients with severe inflammation, even in adults.

Periportal edema and ascites are nonspecific radiologic findings representing accumulation of fluid within third spaces [19]. The periportal region is the area around the portal vein and its branches, within which the hepatic artery, bile duct branches, autonomic nerves, and lymphatics are found [20]. The other radiologic findings associated with hepatic periportal tracking include a thickened gallbladder wall, pleural effusion, and a dilated inferior vena cava [21]. A multifactorial etiology for periportal edema in acute infectious disease has been suggested, including altered sodium reabsorption as a result of the infectious process involving the renal interstitium and increased vascular permeability secondary to systemic sepsis or hypoalbuminemia [21].

Our study had several limitations. First, we did not include the most frequent CT finding in APN, namely, a focal or multifocal wedge-shaped area of hypoperfusion, because all patients had this finding and it was difficult to quantify. Exclusion of patients with only CT findings of a wedge-shaped area of hypoperfusion may be the reason for the relatively small number of cases in our study. Second, we used a retrospective design, and many other intrarenal and extrarenal findings were not included because of their low incidence, which was also likely due to the relatively small number of cases.

The uncommon CT findings that were related with aggravated clinical and laboratory parameters of APN were perirenal fat infiltration, ureteral wall edema, and renal abscess formation. The inflammatory reaction and tissue destruction may be more aggressive in patients with these CT findings. These results may helpful in terms of predicting the clinical course and creating a treatment plan for patients with APN.