As focal ischemia is an early event in APN, it seems logical to expect high sensitivity for Doppler sonography in its detection. The classic color Doppler ultrasound of the kidney outlines the speed and direction of moving blood through the larger intrarenal blood vessels but does not visualize smaller cortical vessels resulting in poor sensitivity in detection of APN. In contradistinction, power Doppler sonography displays the strength of the Doppler signal from all moving blood cells regardless of speed or direction and is therefore more sensitive than color Doppler for detection of blood flow in the small vessels (Fig. 12.3). Stogianni et al. described effective use of power Doppler in the diagnosis of APN utilizing linear 5–10 MHz transducers in children less than 3 months old and convex 5 MHz transducers in children older than 3 months [33]. Axial and longitudinal images were obtained to develop intricate vascular maps of the kidneys. APN was defined by the decreased or absent blood flow in specific zones of the renal parenchyma as well as renal swelling and loss of corticomedullary differentiation [33] (Fig. 12.4).

Recently Brader et al. retrospectively studied a combination of grayscale and power Doppler renal sonography in children with clinical APN and compared the findings with DMSA scans [34]. Expanding criteria for APN to include changes in flow characteristics on power Doppler in addition to changes on grayscale sonography, they found combined sensitivity of 92.1 %, specificity of 97.8 %, and positive predictive value of 88–92 %. When compared with DMSA scan, they found sensitivity and specificity of 94 and 100 %, respectively. However, in an experimentally induced APN in piglets, sensitivity of power Doppler for the detection of histopathologically confirmed lesions was significantly lower than DMSA SPECT, CT, and MRI [35].

Renal cortical scintigraphy with 99m Tc dimercaptosuccinic acid (DMSA) is considered the imaging modality of choice for detecting renal parenchymal involvement in children with UTI and as a marker to assess the extent and progression of renal damage [36]. Approximately 60 % of administered radiolabeled DMSA is picked up by the proximal tubular cells, and the remaining is filtered and excreted at a low concentration. Therefore, the delayed images show excellent visualization of the renal cortex without any significant tracer activity in the pelvicalyceal systems.

Approximately 2 h after intravenous administration DMSA (≤0.05 mCi/kg body weight; minimum 0.03 mCi, maximum 3 mCi), images of the kidneys are obtained. Basically two imaging techniques can be used: planar imaging with magnification or single-photon emission computerized tomography (SPECT).

For planar imaging with pinhole magnification, a high-resolution, parallel-hole collimator is used to obtain posterior image of both kidneys together for calculation of differential renal function. In addition posterior and posterior-oblique images of each kidney are acquired using a pinhole collimator with 3–4 mm aperture insert (Fig. 12.5).

For SPECT imaging, usually a dual detector rotating gamma camera equipped with high-resolution, low-energy collimators is used to acquire 120 images of the kidneys (3° apart). Data acquisition takes approximately 20 min. The images are then reconstructed in coronal, transverse, and axial planes (Fig. 12.6).

Uptake of DMSA in normal kidneys reflects the morphology of renal cortex. High-resolution images show the details of the cortex and cortical columns with good differentiation from the collecting systems and medulla. Irregularities in the contour of the kidneys due to fetal lobulation may be present between the medullary pyramids (over cortical columns) and can be differentiated from the cortical scars which occur over the pyramids (between cortical columns) (Fig. 12.7).

The typical manifestation of APN on DMSA scan is decreased cortical uptake, usually focal or multifocal, without volume loss or contraction of the renal cortex. In severe cases diffusely decreased uptake of DMSA may be observed (Fig. 12.8).

A mature cortical scar is usually associated with contraction and loss of volume of the involved cortex manifested as wedge-shaped defect, cortical thinning, or flattening of the renal contour (Fig. 12.9).

Early clinical reports showed that renal cortical scintigraphy using 99m Tc DMSA was significantly more sensitive than intravenous urogram (IVU) and renal sonography in the detection of APN [37–39]. To evaluate the true sensitivity and specificity of renal cortical scintigraphy for the detection and localization of APN, studies were conducted in a piglet model of surgically inducing unilateral vesicoureteral reflux of infected urine and using strict histopathologic criteria as the standard of reference [40, 41]. Planar DMSA scans using pinhole magnification were highly reliable for detecting and localizing experimental APN with a sensitivity of 87–89 % and specificity of 100 % in both studies. When individual pyelonephritic lesions were analyzed, DMSA scan findings correlated with histopathological changes with an agreement rate of 89–94 %. Those lesions not detected were microscopic foci of inflammation not evident on gross examination and not associated with significant parenchymal damage.

Not only is DMSA scintigraphy highly sensitive and specific for the diagnosis of APN, but it also provides important information regarding renal function and the extent of renal parenchymal inflammation. Documentation of renal parenchymal damage associated with APN is fundamental to understanding the relative roles of infection and vesicoureteral reflux in the etiology of pyelonephritis and renal scarring.

In some clinical studies, SPECT imaging is reported to be more sensitive than pinhole imaging for detecting APN [42–44]. However, in experimentally induced pyelonephritis in piglets, using histopathologic criteria as the standard of reference, the sensitivity and specificity for detecting affected renal zones were 86 % and 95 % for pinhole imaging and 91 % and 82 % for SPECT. The overall accuracy was 88 % for both techniques in assessing kidney involvement [45] (Fig. 12.10). Thus, SPECT imaging appears to be slightly more sensitive than standard pinhole imaging but may result in more false-positive findings. Furthermore, it may be easier to differentiate acute inflammatory changes from chronic renal scarring with pinhole imaging.

Renal fungal infections are most often recognized in high-risk groups of neonates and infants. Reported mortality rates in children with candidemia range from 19 to 31 % and with invasive aspergillosis from 68 to 77 % [49]. Premature, low-birth-weight infants are at highest risk for disseminated candidiasis secondary to immature immune systems, increased invasive procedures, use of H2 blockers, and multiple courses of antibiotics [50].

Renal candidiasis is a combination of candiduria and ultrasound evidence of renal parenchymal infiltration or fungal bezoars in the collecting system. Fungal bezoars are a rare complication that may cause urinary obstruction [51]. In neonates with candiduria, the reported incidence of renal candidiasis varies between 35 and 58 %, whereas patients with candidemia have a 61–70 % prevalence of candiduria and 5–33 % incidence of renal candidiasis [51]. Term infants and older children with congenital abnormalities of the urinary tract are also at higher risk for candiduria [52].

The presentation of candiduria may be asymptomatic or as an acute urinary infection with symptoms of dysuria, cloudy urine, fever, or failure to thrive. Currently there is no standard definition used for diagnosis of candida UTI; however, most of the reported literature uses 10⁴ colony-forming units/mL via catheterized specimen. Obstructive renal candidiasis may present with sepsis, acute renal failure, or palpable flank mass. The clinical presentation of systemic candidemia is similar to bacterial sepsis with lethargy, feeding intolerance, apnea, and/or respiratory distress [51]. Neonatal candidemia often involves multiple organ systems. Due to the invasive nature of this disease work-up should be performed to rule out systemic fungal infection if candida UTI is found. This includes blood, urine, and cerebral spinal fluid cultures, eye examination, echocardiogram, and imaging of the liver, spleen, and kidneys [53].

Genitourinary tuberculosis (GUTB) is the second most common site of extrapulmonary tuberculosis. While 90 % of GUTB cases occur in non-westernized populations where TB is still endemic [59], a resurgence is anticipated in western countries due to the spread of HIV and acquired immunodeficiency syndrome (AIDS) [60]. The classic presentation of renal TB is kidney damage from obstruction or massive caseous destruction [62]. TB infection occurs through inhalation of aerosolized Mycobacterium tuberculosis bacilli. The kidneys are infected through hematogenous spread of the bacilli. The bacilli pass down the renal tubules involving the renal calyces and can eventually enter the renal pelvis and attach to the urothelium. Stricture formation commonly results in hydroureter or hydronephrosis, and up to 10 % of patients with renal TB have bladder contractures [59]. In addition, GUTB may spread to the prostate and epididymis.

Renal abscess is a rare form of pediatric infection. The three basic pathophysiologic mechanisms of renal abscess formation are hematogenous spread, ascending infection, and contamination by proximity to an infected area [68]. In the past, the majority of renal abscesses were not thought to be caused by ascending infection. Historically, Staphylococcus aureus was the most common reported offending agent presumably as a result of hematogenous seeding from a peripheral cutaneous site of origin [69, 70]. More cases of gram-negative infections in the presence of vesicoureteral reflux or other anatomic abnormalities of the urinary tract are now being seen [71].

Abscesses can originate in the corticomedullary portion of the kidney, the renal cortex, or within layers of Gerota’s fascia [68]. Symptoms of renal abscess are often nonspecific which may lead to a delay in treatment. It can mimic symptoms of appendicitis or, when a palpable mass is present, may be mistaken for neoplasm, i.e., Wilms’ tumor or neuroblastoma. The most common presentation of a renal abscess includes high fever, lethargy, and flank pain associated with laboratory findings of leukocytosis and elevated ESR. Dysuria and/or foul-smelling urine is not regularly seen with initial presentation, and the patient may have sterile urine cultures, particularly in cases of hematogenous seeding. A variety of imaging techniques have been used to diagnose renal abscesses, including IVP, angiography, gallium-67 scintigraphy, sonography, and CT [72–76].

Xanthogranulomatous pyelonephritis (XGP) was first reported in 1916 by Schlagenhaufer [78]. The etiology of XGP remains unknown but is often associated with urinary tract obstruction, infection, and/or renal stones. XGP is an atypical form of severe chronic renal parenchymal infection characterized by unilateral destruction of parenchyma and accumulation of lipid-laden macrophages either surrounding abscess cavities or as discrete yellow nodules. While it predominately affects middle-aged women, it may occur in all ages. It is rare in children with only 265 reported cases since 1960 [79]. The age of presentation has ranged from infancy to 16 years with the most common age of presentation less than 8 years old and rare presentations in infancy [78]. XGP is focal in only about 10 % of cases and is most commonly caused by Proteus mirabilis or Escherichia coli infection with 50–75 % of patients having positive urine cultures [78, 80].

Most patients present with nonspecific symptoms of chronic infection, including weight loss, recurrent fever, failure to thrive, pallor, and lethargy, although those with the focal form often appear healthy [81, 82]. Urinary symptoms are uncommon, and less than half of the patients present with hypertension [83]. A palpable abdominal mass is present in approximately one-third of cases.

Both diffuse and focal forms of the disease have been reported, with the focal form being more common in children [81, 84]. Calcification or stones may be present in 70–79 % of patients with staghorn calculi being common, although this is less often seen in the focal XGP [78]. In children less than 8 years of age, the disease is usually focal, unilateral with left predominance, and without calculus [78]. The pathologic and radiologic differences between focal and diffuse XGP have been described [86]. No radiologic feature is diagnostic of XGP.