T2-Weighted Sequence

T2-weighted images (T2-WI) are fluid sensitive sequences in which fluid is high signal including free fluid, fluid in structures of the body such as the urinary bladder, spinal canal and gallbladder. Fluid in edema also increases signal in tissues. In addition, neoplasms are typically T2 bright, with some exceptions. Thus, T2-WI are generally anatomic sequences useful as an initial overall view of the overall condition of the patient [8].

T1-Weighted Sequence

Fat, blood and proteinaceous products appear bright on T1-weighted images (T1-WI). Fluid has low-signal on T1-WI. In addition, gadolinium, the intravenous contrast agent used, is also high signal on T1-WI. Thus, all contrast-enhanced images are T1-WI. Typically pre-contrast images are acquired in addition to post-contrast images so that subtraction images can then be obtained to determine which tissues are truly enhancing [8].

Fat Suppressed Sequences

Fat demonstrates high signal intensity on T1-WI and turbo T2-WI. A common option is the suppression of fat from these sequences in order for more problem-solving technique. Fat is suppressed on T2-WI to highlight features of fluid or malignancy. On T1-WI, fat is suppressed on contrast enhanced sequences in order to minimize signals that may confound enhancing structures, which are also T1 hyperintense.

Diffusion-Weighted Sequence

Free flowing water molecules typically move in random patterns called Brownian motion. Water molecules can become trapped in some clinical situations such as in highly cellular neoplasms or abscesses. Diffusion-weighted images (DWI) are acquired at specific “b-values.” Increasing b-values increases the weight of diffusion on imaging, thus DWI with high b-values only show signal of those trapped water molecules while freely diffusing water molecules lose signal. Apparent Diffusion Coefficient (ADC) maps are acquired by calculating the change of signal with multiple b-value sequences. Thus, those regions that maintain signal from low to high b-value will have low change and have low signal on ADC maps. Regions with restricted diffusion will have high signal on high b-value DWI sequences and low value on ADC maps [8].

Contrast-Enhanced Sequences

Similar to CT, intravenous contrast can be administered to increase conspicuity of renal masses, infectious process, or inflammation. Because there is no radiation exposure, images of multiple different time points may be acquired after contrast administration to assess dynamic contrast enhancement. Due to angiogenesis and increased vascularity of tumors, neoplasms tend to enhance earlier. Thus, dynamic contrast enhancement can differentiate lesions from other enhancing structures. Contrast is excreted through the kidneys and delayed urogram can be acquired to evaluated the collecting system, ureters, and bladder [10].

MRI utilizes gadolinium based intravenous contrast. The newer, macrocyclic contrast agents have not been proven to cause nephrogenic sclerosing fibrosis, even in the setting of renal insufficiency and thus can be administered in patients with renal failure. This is advantageous compared to CT intravenous contrast, which increases risk of CIN if administered in patients with renal insufficiency. In addition, gadolinium based contrast agents have not been shown to cause contrast induced nephropathy [11–15]. However, older linear gadolinium based agents have a rare risk of causing nephrogenic systemic fibrosis in patients with renal insufficiency. If such agents are used, renal function should be assessed prior to contrast administration, Gadolinium based contrast administration is however contraindicated in pregnant patients.

Limitation

For the best images, patients must be able to be still during the duration of the examination, which may last up to one hour long. They must also be comfortable within an enclosed space for long periods of time. Care must be taken to ensure any devices and implants of patients are MRI compatible.

Bosniak Classification

The Bosniak classification was initially developed for the CT with intravenous contrast. Contrast enhancement is a major criterion in assessing malignant potential of masses. Application of the classification can be used on MRI studies with intravenous contrast however should not be applied to studies without contrast (including US).

Bosniak I lesions are simple cysts with close to 0% malignant potential. They have thin peripheral walls, no septations, calcifications, or enhancing nodules. The internal density measures fluid density on CT (0–20 HU) and are simple fluid intensity on MRI. These cysts are considered benign and require no follow up (Fig. 13.1) [10].

Bosniak II cysts are slightly increased in complexity with thin, non-enhancing septations or minimal thin calcifications, measuring less than 1 mm in thickness. Hemorrhagic cysts measuring less than 3 cm in diameter are also considered Bosniak II cysts [23, 24]. These lesions are also close to 0% in malignant potential and do not require follow up (Fig. 13.2) [23, 25].

Bosniak IIF (“F” for “follow-up”) cysts are of intermediate complexity and have increased malignant potential, previously reported to be ~5% although more recent studies have demonstrated malignancy rates of 25% in resected Bosniak IIF lesions (~5%) [10, 26]. They have increased number of septations, which may have perceived, though not measurable enhancement (Fig. 13.3). Nodular and thickened calcifications may also be present. Hemorrhagic cysts measuring greater than 3 cm are included in this category [26]. The increased complexity of these cysts necessitates follow-up imaging to ensure stability, typically after 6 months with ultrasound, CT, or MRI [26–28]. Cysts in this category are generally followed with serial imaging, initially every 6 months, and then annually, for 5 years in order to demonstrate stability.

Bosniak III cysts are complex cysts, which demonstrate worrisome findings such as irregular walls, increased number and thickness of septations which may have measurable enhancement. There may be thickened nodular calcifications. Bosniak III cysts have 30–100% malignancy rate [10]. Differential considerations for lesions in this category also include mixed epithelial stromal tumors, renal abscesses, benign multilocular cysts, or benign hemorrhagic cysts (Fig. 13.4). However, due to the inability to confidently distinguish between these entities, resection is generally recommended [24].

Bosniak IV cysts are nearly 100% malignant. They demonstrate solid nodular enhancement and possibly necrotic components (Fig. 13.5). These masses are generally resected if patient condition allows [10, 24, 26].

Benign Renal Cysts

Mixed Epithelial Stromal Tumor

Mixed epithelial stromal tumor (MEST) is a rare cystic tumor characterized by complex cystic and sometimes solid mass. Histologically, the mass resembles ovarian stroma with epithelial components composing the cystic walls. MEST’s are more common in females (11:1 female to male ratio) presenting at an average age of 56 years (range of 17–84 years) [29, 30]. On imaging, they are multiloculated cysts. One feature of MEST that differentiates it from malignant renal cystic masses is that it invaginates into the renal pelvis and the septations have delayed enhancement. MESTs can have internal hemorrhage seen as hyperintensity on T1-WI (Fig. 13.6). MESTs cannot be clearly distinguished from malignant cystic neoplasms and thus are most often surgically resected [29].

Multicystic Nephroma

Another benign multiloculated cyst is the cystic nephroma. The lesion is bimodal in age of presentation, which manifest in boys less than 4 years old and women between 40 and 60 years old [31]. Cystic nephromas have similar histological appearances to MEST and have been suspected to be on a similar spectrum of stromal tumor. They present as encapsulated multiloculated cystic masses, at times with hemorrhagic or proteinaceous contents. Multicystic nephromas can also invaginate into the renal pelvis and have delayed enhancement of septations, which likely reflects the fibrous content of the lesion [31, 32]. There is no imaging criteria which can definitively distinguish a cystic nephroma from a cystic malignancy, and for this reason, most are resected.

Renal Cystic Disease

Autosomal Dominant Polycystic Kidney Disease

Autosomal dominant polycystic kidney disease (ADPKD) present as cysts in both kidneys, which are enlarged . Cysts are of all sizes, small and large, and can be simple or hemorrhagic (Fig. 13.7). There is no increased risk of renal malignancy unless patient is on dialysis [33]. Extra-renal manifestations include cysts in the liver and pancreas. The disease progresses by progressively increasing number of cysts. Approximately 50% of patients with ADPKD develop renal failure from replaced renal parenchyma [33].

Imaging is important in screening first-degree relatives of people with ADPKD as genetic testing only identifies 70% of those with the disease [34]. Criteria for diagnosing ADPKD is age dependent. For high-risk patients between the age of 15 and 39 years, three cysts are required for diagnosis, for high-risk patients between the age of 40 and 59 years, two cysts are required for diagnosis, and for high-risk patients 60 years or greater, four cysts are required for diagnosis [35].

Localized Cystic Renal Disease

Localized cystic renal disease is a rare benign entity which may be mistaken for a mass of malignant potential. The disease manifests as cysts in one kidney, unilaterally. Cysts are separated by normal renal parenchyma with no capsule, distinguishing it from a cystic nephroma (Fig. 13.8) [36]. Trauma may cause bleeding and hemorrhagic product within the cysts. There are typically no cysts in other organs. Increased number of cysts may compress the intervening normal renal parenchyma which may give a more malignant appearance, thus imaging follow-up may be warranted if clear diagnosis cannot be confidently made (Fig. 13.8) [37].

Lithium-Induced Nephrotoxicity

Patients with long-term lithium use may develop nephrotoxicity manifested by acute intoxication, nephrogenic diabetes insipidus (most common and reversible), and chronic renal disease [38–40]. Imaging appearance of lithium associated chronic renal disease include normal sized kidneys with many uniformly distributed microcysts (1–2 mm in size) which are located in the cortex and medulla. On US, the microcysts may paradoxically appear as hyperechoic foci as the cysts are so small that ultrasound resolution can only detect the closely apposed walls of the cysts which reflect sound waves. The cysts are best visualized on MRI with T2-WI as the cysts are T2 hyperintense foci (Fig. 13.9) [41].

Malignant

RCC

RCC are one of the most common adult cancers, about 2–3% of all adult neoplasms [43]. Amongst RCCs, there are major histologic subtypes including clear cell RCC (ccRCC), papillary RCC (pRCC), and chromophobe RCC (chRCC). Some of the histologic features translate into distinguishable imaging features (Table 13.2). On ultrasound, RCC’s are hyperechoic compared to renal parenchyma, though less echogenic than renal sinus. Further characterization is reserved for mpMRI which can tease out secondary manifestations of histologic features. In the following section, discussion will emphasize MRI features of solid renal tumors.

Table 13.2

Image characteristics of benign and malignant solid renal tumors

Subtype	Unique imaging
Clear Cell RCC	Heterogeneous, T2 bright, Hypervascular, Intravoxel fat, Necrosis
Papillary RCC	Homogeneous, T2 dark, Hypovascular, Hemosiderin
Chromophobe RCC	Heterogeneous T2 signal, Heterogeneous enhancement
Lymphoma	Infiltrative T2 intermediate to dark, strong restricted diffusion
Urothelial Renal Mass	Centered in the renal pelvis, Infiltrative
Angiomyolipoma (AML)	Bulk fat, vascular
Lipid Poor AML	T2 dark, hypervascular
Oncocytoma	Heterogeneous T2 signal, Stellate scar, Segmental enhancement

ccRCC

ccRCC subtype is the most common RCC representing 65–80% of all RCC [44]. It is typically sporadic, but is associated with many syndromes such as von Hippel Lindau syndrome and tuberous sclerosis. Because of its potentially aggressive nature, management is also often aggressive and thus early diagnosis is important.

On histology, ccRCC are composed of cells that have cytoplasm which appear “clear” because of accumulation of cholesterol and lipids [45]. On a more macroscopic level, ccRCC are vascular tumors. MR features reflect the histology. Masses are typically T2 hyperintense, T1 hypointense and heterogeneous. Increased vascularity of ccRCC translates into avid enhancement on imaging, greater than adjacent parenchyma and also greater than other types of RCC (Fig. 13.10) [46, 47]. ccRCC tumors may bleed, seen as irregular T1 hyperintensity. The intracellular fat is reflected in IP and OOP sequences which demonstrate intravoxel fat (signal drop on OOP when compared to IP). ccRCC also restrict diffusion due to increased cellularity [47]. Because of ccRCC’s aggressive nature, larger lesions often out-grow vascular supply and have necrotic centers [46]. ccRCC’s also often contain calcifications, which indicates malignancy and may help differentiate benign and malignant masses in otherwise ambiguous lesions.

pRCC

The second most common subtype of RCC is pRCC comprising 10–15% of RCC cases [44]. There are two types (I and II). Type I is usually less aggressive than ccRCC, whereas type II pRCC are more aggresive. Pathologically, pRCC’s often contain necrosis and hemorrhage product [48]. Histologically, they have papillae which are covered by thin layer of uniform cells with scant cytoplasm, hemosiderin, and foamy macrophages [49].

Again, imaging correlates with pathologic findings. The masses are typically well-defined and homogenous and less than 3 cm in size. pRCC’s are T1 and T2 hypointense, likely from low cytoplasm content of cells. Larger lesions may contain hemorrhagic product (T1 hyperintense). Hemosiderin causes loss of signal on IP imaging compared to OOP. Rarely, intracellular lipids from foamy macrophages, translate to intravoxel fat and loss of signal on OOP compared to IP. DWI is somewhat confounding with the presence of hemosiderin and hemorrhage. On contrast enhanced images, pRCC are hypovascular and demonstrate progressive enhancement through dynamic imaging. More rarely, pRCC present as complex cysts. Lipid poor angiomyolipomas (AML) may have similar appearance to pRCC, however, they enhance avidly rather than the progressive enhancement of pRCC (Fig. 13.11) [50].

chRCC

chRCC is less prevalent compared to pRCC (4–11% of all RCC). Similar to type I pRCC, chRCC have better prognosis than ccRCC with 5-year survival rate reported to be 78–93% [51]. chRCC arise from the intercalated cells of the kidneys, much like oncocytomas. Pathologically, chRCC are well-defined lesions which present larger than other RCCs, average mass size of 7.2 cm [52].

Imaging features of chRCC are varied and less specific than other RCCs. They are peripherally located, homogeneous, typically demonstrate T2 intermediate to low intensity signal. They restrict diffusion and also enhance, although demonstrate intermediate enhancement, between pRCC and ccRCC. Calcifications are also often seen, which occur in 38% of such lesions. Sometimes, chRCC have a “tail” which extends towards the renal pelvis. Very rarely, chRCC may demonstrate segmental enhancement inversion, which is heterogeneous enhancement with some portions enhancing earlier and other portions demonstrating progressive enhancement [53]. Since chRCC’s are histologically similar to oncocytomas, imaging features are similar as well. chRCC’s may exhibit an enhancing spoke wheel central scar, approximately 30–40% of time, which can also be seen in oncocytomas [54].

Lymphoma

Distribution of lymphoma is wide spread and the genitourinary systems is the second most commonly affected site [55]. Within the genitourinary system, kidneys are involved the most. Detection is typically via imaging. CT and MRI are both sensitive in diagnosis. US is likely the first line imaging technique and may be used for follow-up, however is less specific in initial diagnosis.

On imaging, lymphoma has multiple patterns of presentation. The most common presentation is multiple tumors, seen 50–60% of the time. Other presentations include single tumors, centralized to perinephric regions, and infiltrative tumors. Lymphoma may also extend into the kidney from primary retroperitoneal location [56].

Lymphoma of the kidney is slightly greater density than renal parenchyma on non-contrast CT but enhance less than renal parenchyma thus appear as homogeneous hypodense lesion to parenchyma on contrast enhanced images. Masses can occur in both cortical and medullary regions, thus nephrogenic phase is important to acquire to not miss lymphomatous tumor [56]. On MRI, lymphoma masses are T1 and T2 hypointense. Due to the closely packed cells in lymphoma, they show avid restricted diffusion (Fig. 13.12). Similar to CT, tumors are hypoenhancing compared to renal parenchyma. On US, lymphoma is typically hypoechoic and homogeneous. Color Doppler imaging shows lesions displace normal renal vessels. Little vascularity is seen within the lesion itself [57, 58].

Several secondary signs can help distinguish lymphoma from other renal malignancies. Lymphadenopathy is a systemic disease and often presents simultaneously with retroperitioneal lymphadenopathy. In addition, lymphoma is rarely associated with renal thrombus [55].

Intrarenal Urothelial Carcinoma

Urothelial carcinoma most commonly occurs in the bladder, less commonly in the ureters, and even more rarely the renal pelvis. When in the renal pelvis, urothelial cancers tend to grow centripetally into the renal parenchyma [59]. These lesions can be confused with central RCC [60, 61]. It is clinically important to distinguish these two entities as management is drastically different.

CT and MRI are the best imaging tools for diagnosis as both morphology of tumors and intrinsic lesion characteristics that identify one from the other. Six useful morphologic features that preferentially indicate urothelial carcinoma over RCC include central location of tumor within the collecting system, focal filling in renal pelvis, preservation of renal shape, absence of cystic or necrotic, homogeneous enhancement of tumor, and extension of tumor toward ureteropelvic junction (Fig. 13.13) [59]. Of those six features, preservation of renal shape was the most reproducible sign indicating urothelial tumor [59]. Homogeneity on T2-WI and hypovascularity on all phases of dynamic sequences have also been shown to indicate urothelial origin of tumor over RCC [62].

Angiomyolipoma

AML are benign solid renal tumors which contain three elements: dysmorphic blood vessels, smooth muscle, and bulk adipose tissue. The amount of each component varies in each tumor, determining the appearance of the lesion on imaging. The presence of fat is pathognomonic. On US, the typical AML is hyperechoic. Hyperechoic masses less than 1 cm have been shown to be clinically insignificant [63], and may not need follow-up, especially if patients are low risk for RCC. On CT, AMLs are hypodense or have hypodense foci with HU comparable to bulk fat. MRI also demonstrates bulk fat which can be seen on OOP sequences separating AMLs and renal parenchyma by the India ink artifact and with signal drop out on fat suppressed imaging (Fig. 13.14).

Lipid poor AMLs, defined histologically as less than 25% fat content per high-power field, present a diagnostic dilemma as RCCs have similar appearances, especially for small masses (<3 cm) [64, 65]. On ultrasound, lipid poor AMLs are isoechoic to renal parenchyma, limiting detection and evaluation. Without fat, lipid poor AMLs have increased components of blood vessels and smooth muscle, which are both hyperattenuating compared to normal renal parenchema on CT without intravenous contrast and thus lipid poor AMLs are typically heterogeneously hyperattenuating compared to renal parenchyma, however this is not consistently true [65]. MRI features of AML may include homogeneous T2 signal compared to renal cortex and the lack of cystic degeneration or necrosis [64, 66]. These findings are similar to that of pRCC, however AMLs tend to be more vascular. Image diagnosis of lipid poor AMLs may be difficult however should be considered as a differential, especially in patients whose demographic is atypical of RCC [64]. If there is strong suspicion of a lipid poor AML, on the basis of genetic risk or patient age, needle biopsy with HMB45 staining can by quite diagnostic. In the absence of heightened suspicion of AML, larger solid renal masses are generally resected.

Oncocytoma

Oncocytomas, the second most common benign renal neoplasms, are histologically similar to chromophobe RCC and are thought to arise from intercalated cells [51]. They are well-defined and hypovascular on enhancement compared to renal cortex. On MRI, oncocytomas also share characteristics with chRCC including heterogeneous T2 signal and enhancement, and hemorrhage or microscopic lipid [54]. Oncocytomas are often characterized by a central “scar,” a central stellate region of T2 hyperintensity which does not enhance (Fig. 13.15) [54, 67]. Segmental enhancement, as described in the chRCC section, is typically a feature of oncocytoma, although rarely, chRCCs can enhance in a similar fashion. The overlapping imaging features between oncocytoma and malignant RCC are many, thus suspected oncocytomas are typically treated as malignant masses [68].

Bacterial Pyelonephritis

Although US is often used as first line imaging, bacterial pyelonephritis is not well characterized on grey-scale imaging and thus produces many false negative results, demonstrating abnormalities in only 24% of patients [69]. Some findings include changes in echogenicity, decreased in the setting of edema, or increased in the setting of hemorrhage. There may be loss of corticomedullary differentiation or foci of hypoperfusion on color Doppler imaging [70]. Use of harmonics imaging highlights patchy hypoechoic foci. Abscesses can also be seen on ultrasound as fluid collections with peripheral hyperemia which demonstrate mass effect on adjacent structures. Source for possible obstruction should be investigated, especially in the bladder (e.g. enlarged prostate).

CT with intravenous contrast in the nephrographic phase is the best to evaluate bacterial pyelonephritis. In acute pyelonephritis, renal enhancement is often patchy with wedge shaped hypo-enhancement to the papilla reflecting regions of edema, tubular obstruction and vasoconstriction (Fig. 13.16) [71]. With time, the hypo-enhancement will gradually decrease and may result in scarring or cortical thinning. Secondary signs of infection are also apparent on CT with easily visualized perinephric fat stranding or asymmetric enlargement of the kidney. Abscess are readily visible and are seen as peripherally enhancing fluid collections [72]. With the larger field of view, the full extent of abscess can be assessed.

MRI plays a smaller role in imaging bacterial pyelonephritis compared to CT as it is more expensive and time consuming without increased diagnostic benefits. Patchy edema and tubular obstruction can be seen as patchy restricted diffusion on DWI. In addition, abscesses are especially accentuated on DWI and as abscess markedly restrict diffusion. Enhancement patterns on MRI appear similar to that of CT [73].

Emphysematous Pyelonephritis and Pyleitis

Emphysematous pyelonephritis is a necrotizing form of infection, typically in diabetic or immunocompromised patients, resulting from obstruction by urinary calculi, neoplasm, or sloughed papilla. The disease is life-threatening with a high mortality rate, thus early diagnosis is imperative [74].

On radiographs, foci of radiolucency may be seen overlying and outlining the kidneys, which are ominous findings. Ultrasound demonstrates enlarged, hypoechoic kidneys with multiple shadowing hyperechoic foci of gas reflecting sound waves. Shadowing renal calculi may have similar appearances, but gas tends to produce “dirty” shadowing as opposed to clear crisp shadowing of stones (Fig. 13.17) [75]. The kidney is also typically hypervascular on color Doppler imaging.

CT provides the most complete evaluation. The kidneys are low attenuation and may contain foci of gas in a linear pattern. Fluid from necrosis and abscesses within the kidney or in perinephric spaces are readily visible. Infection can be centered around the renal parenchyma (type 1) or more extensive connecting perinephric fluid collections with the collecting system (type 2) (Fig. 13.17) [76]. Obstructive etiologies may also be evaluated at the same time.

Gas only within the collecting system is termed emphysematous pyelitis, and is less ominous than emphysematous pyelonephritis. On CT and ultrasound, gas can be seen layering in the renal pelvis. Care must be taken to exclude other causes of gas such as recent procedures [77, 78]. MRI is less favorable than CT as gas is not well seen on the modality; however, MRI may be used in circumstances to minimize radiation exposure or for patients with renal insufficiency.

Pyonephrosis

Infection can be centered around the collecting system and is referred to as pyonephrosis. On ultrasound, there is prominence of the renal pelvis which often contains debris. On CT, a prominent renal pelvis can also be seen, and also demonstrates thickened walls (>2 mm) with adjacent fat stranding. Exclusion of obstructive etiology must be performed. Urine versus pyogenic fluid often have similar HU and may be difficult to differentiate. MRI findings are similar to CT however is able to detect debris within the collecting system [79].

Xanthogranulomatous Pyelonephritis

Xanthogranulomatous pyelonephritis (XGP) is a rare chronic destructive granulomatous infection of the kidney caused by lipid-laden (foamy) macrophages. This typically occurs in women and patients with diabetes. Patients also often have obstructive renal calculi such as staghorn calculi. The most common causative organism includes Proteus mirabilis and Escherichia coli [80].

Radiographs are non-specific and only demonstrates renal calculi. On ultrasound, the affected kidney is enlarged often with a large central echogenic shadowing calculus in the renal pelvis. The kidney is often distorted with loss of normal renal architecture. CT also demonstrates an enlarged kidney with central calculus, contracted renal pelvis, and caliectasis with thinning of the cortex, or the “bear claw” sign, which is pathognomonic for XGP (Fig. 13.18). Although it may appear to be simple hydronephrosis, often, the caliectasis contains a thick inflammatory infiltrate [81]. Secondary signs of inflammation are visible as perinephric fat stranding and thickening of the renal pelvis. Delayed phase of a contrast enhanced CT often shows decreased renal function and delayed excretion of contrast. In many cases, an associated heterogenous renal mass can be confused with renal cancer. In the absence of urinary infection or associated obstruction, resection is often required to rule out malignancy.

Tuberculosis

CT and MRI are the best modalities to evaluate urinary tuberculosis (TB). The imaging findings of tuberculosis depends on the stage of the disease. The disease typically progresses from kidneys to bladder such that disease of the lower urinary tract does not occur without disease of the upper urinary tract. TB of the renal parenchyma manifests as patchy hypo-enhancement similar to bacterial pyelonephritis. The collecting system is the most common site of urinary TB. There is uneven progressive caliectasis with papillary necrosis and cortical thinning, which has a similar appearance to XGP as both are granulomatous processes, however, unlike XGP, the kidney in the setting of TB atrophies as there is increased fibrosis. The renal parenchyma atrophies completely and multiple thin-walled cysts are formed. Eventually dense calcification replaces the atrophied kidney, resulting in the so called “putty kidney” (Fig. 13.19) [82, 83].

TB in the ureters present as multifocal strictures with ureteral wall thickening and hyperenhancement which causes hydronephrosis [84]. The urinary bladder with TB appears with wall thickening. After time, there is increased fibrosis and shrinkage of the bladder and eventually dystrophic calcification [83, 85].

Urolithiasis

Urinary calculi is a common entity affecting 6% of women and 12% of men in the United States [86, 87] with incidence increasing up to the age of 60 [88]. Urinary calculi are formed by excretion and precipitation of salts including calcium, struvite, uric acid, and cysteine into the urine. These salts may become lodged throughout the urinary tract causing pain and urinary obstruction.

The composition of urinary calculi is reflected in imaging characteristics and also have treatment implications. Calcium based calculi is the most common, representing 70–80% of calculi in the US [89]. Within the category of calcium based calculi, calcium-based oxalate calculi are the most common, representing 60% of all calculi [90]. When imaged with CT, calcium based urinary calculi have the highest HU measuring up to 1700 HU [91].

Struvite calculi, 15–20% of urinary calculi, are formed by urease-producing bacteria (e.g. Proteus, Pseudomonas, Klebsiella, and enterococci). Escherichia coli, the most common organism causing urinary tract infections, however, does not produce urease [89, 92]. Urea is broken down into carbon dioxide and ammonia which raises the pH level of urine allowing carbonate to precipitate with struvite forming calculi. These calculi typically involve at least two calyces of the renal pelvis giving the appearance of antlers reflected of its namesake staghorn calculi [93]. HU of struvite are varied depending on percentage of struvite in the calculi and can range from 200 to greater than 1300 [94].

Less common calculi include uric acid calculi, which occur in the setting of gout, chronic diarrhea, or in acidic urine such as with increased body mass index and diabetes. Uric acid calculi are radiolucent on radiography but are visualized on CT with HU of <500 (Fig. 13.20) [95–97]. Cysteine calculi are also low in HU and have a ground glass appearance and may also be radiolucent but visualized on CT. Some medications, such as protease inhibitors used in HIV treatment (e.g. Indinavir) and herbal supplements can induce renal calculi formation. Indinavir related renal calculi are unique in that they are radiolucent, even on CT [98].

Calculi can be present throughout the entire urinary tract. Calculi within the calyces are typically non-obstructing and asymptomatic, although some non-obstructing calyceal calculi can present with renal colic and gross or microscopic hematuria. Stones that migrate into the ureteral pelvic junction (UPJ) which can cause obstruction and flank pain. Once through the UPJ, there are three anatomic locations of ureteral narrowing which calculi may lodge: just distal to the UPJ, at the crossing of the iliac vessels, and at the ureteral vesical junction (UVJ). The UVJ is quite narrow, resulting in obstruction of tiny 1–5 mm stones [99].

Imaging indications can be broadly divided into suspicion of stone disease versus recurrent stone disease, which are optimized with different imaging protocols. Multiple modalities are available to use including non-contrast computed tomography (NCCT), KUB, US, and MRI.

Acute Flank Pain/Suspicion of Ureteral Stone

US

The European Association of Urology (EAU) recommends initial evaluation with US before other diagnostic imaging as it can visualize the kidneys, collecting systems, parts of the ureters, and bladder to determine presence of calculi or urinary obstruction. US has 45% sensitivity and 94% specificity for ureteric stones and 45% sensitivity and 88% specificity for renal stones and increases to sensitivity of 77% and specificity of 93% in patients with acute flank pain [100–103]. With the utilization of US prior to CT, there was no significant difference in outcomes compared to the initial utilization of CT, however, radiation exposure was decreased [101].

Renal calculi appear as hyperechoic foci with sharp distinct posterior shadowing. Due to the variability of posterior shadowing of calculi and the abundance of obscuring adjacent hilar fat and peri-ureteral fat, identification of urinary on ultrasound may prove to be difficult. Utilization of color Doppler imaging can assist by demonstrating a “twinkle” artifact secondary to sonographic waves reflecting off the rough surface of the calculi (Fig. 13.21). Sensitivity for detecting calculi ranges from 61 to 90% and is heavily dependent on user.

Direct visualization of ureteral calculi is more difficult due to overlying bowel gas and retroperitoneal fat. Similar to renal calculi, ureteral calculi are seen as hyperechoic foci within the ureteral lumen and demonstrate distinct posterior shadowing (Fig. 13.21). There may also be associated ureteral wall thickening and edema. If transabdominal approach does not reveal a ureteral calculus, transvaginal or transperineal approach may be attempted to evaluate for distal ureteral calculi [104, 105].

Aside from direct visualization of calculi, US is sensitive for evaluating presence of obstructive uropathy demonstrated by hydronephrosis, hydroureter, and perinephric edema. Visualization of ureteral jets in the bladder can also confirm patency of the ureters. This may be seen on grey scale imaging as a stream of low-level echoes or as color jets on color Doppler imaging. The degree of hydration of the patient can affect the visibility of the ureteral jets and can range from less than one jet per minute to continuous flow in a healthy patient. Healthy patients can also have asymmetric jets, thus visualization of decreased jets on affected side should only be used as an adjunct tool for increased sensitivity of stone detection [106, 107].

There have been some promising studies utilizing spectral Doppler imaging and intrarenal resistive index (RI) ((peak systolic velocity-end diastolic velocity)/peak systolic velocity) to assess the hemodynamics of acute obstruction. Both absolute intrarenal RI of ≥0.70 and a difference of RI between kidneys (Δ_RI) of ≥0.08 have been shown to in acute obstructive uropathy [108–110]. This is controversial, as some studies have also demonstrated less promising results in the use of RI to predict obstruction [111–113]. This accentuates the complexity of renal obstruction and renal tissue and vascular compliance and pulse pressures, which determines RI.

There are several limitations to US. The largest is that it is operator dependent [114, 115]. Evaluation can also be limited by the patient’s body habitus, decreased mobility of patients, or inability of patients to follow directions. In addition, renal vascular calcification, calcified sloughed papilla, calcified tumor, or calcified ureteral stents may be mistaken for urolithiasis. Secondary obstructive signs such as hydronephrosis can also be misdiagnosed in the setting of parapelvic cysts. Thus, confirmation of findings with other diagnostic exams such as non-contrast CT is recommended.

NCCT

The advent of helical (spiral) NCCT for the evaluation of flank pain, has shown to be the exam yielding the highest sensitivity (>95%) and specificity for detecting urolithiasis [116]. Although radiographs have higher resolution, the high contrast between tissue types in NCCT allows several facets of urolithiasis to be assessed including detection of the presence of nearly all types of calculi, size and location of calculi, and signs of obstruction. Coronal reformatted images are also available, which increase rate of detection of stones and accurate assessment of stone size [117, 118]. In addition, NCCT is a fast exam requiring only seconds to acquire a scan. Thus, NCCT is recommended after the initial evaluation with ultrasound in order to determine the extent and location of urolithiasis.

NCCT is preferred over contrast-enhanced CT because there is increased conspicuity of urothelial calculi without the obscuration by intravenous contrast, especially in more delayed phases as contrast is excreted into the collecting system and ureters. Intravenous contrast, however, can be helpful in unique situations by defining anatomy and differentiating pelvic phleboliths versus urinary calculi.

Patients should be scanned in the prone position. This allows the posteriorly located UVJ to be in a non-dependent location which can differentiate the location of calculi lodged in the UVJ versus layering calculi in the urinary bladder.

Evaluation of NCCT should include focus on the urinary collecting system, ureters, and bladder for evaluation of presence of calculi. First, location of urinary calculi should be determined, which can change prognosis. Calculi located more proximally are associated with higher need of intervention [119]. Measurement in both axial and coronal plane should be performed to ensure maximal diameter is assessed. HU of the calculus should also be measured as this provides additional information on type of calculus as mentioned previously. Finally, investigation for signs of obstruction is important. These include hydronephrosis, perinephric fat stranding, and peri-ureteral fat stranding. Other causes of flank pain should also be assessed, especially if no calculus or findings of urinary obstruction are visible. Other causes of flank pain may include acute diverticulitis, appendicitis, rib fracture, or metastatic osseous lesions.

Conventional helical (spiral) CT uses broad range of X-ray energies. DECT is a relatively new technology which is able to assess two specific different energies of X-rays. This technology has been preliminarily shown to determine the composition of calculi by measuring the HU ratio of one energy to the other as substances absorb X-ray energies to variable degrees (Fig. 13.20) [120]. More studies are needed to optimize this technique [121, 122].

One major concern of CT is the radiation exposure to the patient, especially to younger patients. Low dose CT has been shown to have high sensitivity (97%) and specificity (95%) in detecting urolithiasis [123]. In addition, it has been shown that there is no significant difference in measurement of stone size on low-dose CT versus standard dose [124]. Effort to limit scan exposure to only necessary organs is an additional method to decrease radiation exposure.

Radiography

KUB can identify renal calculi, however is less sensitive (72%) than CT for calculi greater than 5 mm [122, 123]. Radiographs are better used for follow up than the evaluation for source of acute flank pain. Radiodensity overlying the region of the kidney, ureters, and bladder may indicate renal calculi. Limitations of radiography include the inability to locate the calculus in the anteroposterior plane unless lateral view is obtained. Not all types of urinary calculi can be seen on radiographs. Quality of radiographs is heavily dependent on overlying bowel contents, patient body habitus, size, location, and composition of stone. Thus, comparing to NCCT, it has been shown that radiography has decreased sensitivity (72%) for stones greater than 5 mm in diameter and less affective in the acute setting [125, 126].

Radiography exposes patients to radiation, however at a much lower dose than NCCT. The radiation exposure from multiple KUBs obtained are additive and may eventually equal that of NCCT if a large number are taken.

MRI

Although not the first line of imaging, MR urography can be helpful in assessing for secondary signs of obstruction. Hydronephrosis is readily visible on T2-WI as it is highly sensitive to fluid. The ureters are well-assessed throughout their entire course, especially if dilated. Calculi are diagmagnetic material and do not produce signal on MRI, thus are seen as signal voids on T1, T2, and gradient sequence, called “blooming,” within the urinary tract, which is at times difficult to visualize. MRI is beneficial as it provides abundant information on tissue without exposing patients to radiation, which may be more beneficial in pregnant or pediatric patients.

Urothelial Neoplasm

Urothelial neoplasm affects the upper urothelial tract including the renal pelvis and ureters, as well as the lower tract including the urinary bladder, urachus, and urethra. The most common histological subtype of urothelial neoplasms is urothelial carcinoma, which accounts for 90% of bladder tumors [130] and 10–15% of renal tumors [131]. Only 4% of urothelial carcinomas occur in the ureters [132]. Squamous cell carcinoma is the second most common histologic type associated with recurrent urinary tract infection followed by adenocarcinoma often in the urachal remnant, both occur mostly in the bladder [133, 134].

Urothelial carcinoma is unique in that it is often multifocal and metachronous with frequent recurrence. 2–4% of people with bladder cancer will develop renal pelvis or ureteral urothelial carcinoma and 40% of those with renal pelvis or ureteral disease will develop bladder tumors [135]. Because urothelial carcinoma can occur anywhere along the urinary tract, it is important to image the entire urinary tract for initial assessment and staging of disease and for follow-up. As such, CT and MR urography are the mainstays of imaging of urothelial carcinoma. PET/CT with fludeoxyglucose (FDG)—¹⁸F and ¹¹C choline may also be used to assess lymph node metastases in patients with urothelial carcinoma.

CT

CT Urography (CTU) utilizes intravenous contrast to assess the urinary tract during multiple time points after contrast administration and has been demonstrated to have sensitivity greater than 90% in detection of urothelial/bladder lesions in patients with hematuria [136]. Multiple differing protocols are available. In a single bolus study, several acquisitions are obtained: pre-contrast, parenchymal phase (80–90 s after injection), and urographic phase (7–9 min after injection). Urothelial carcinoma is typically hyperenhancing on earlier post-contrast phase, lending itself to be more accentuated on parenchymal phase against the walls of renal pelvis, ureters, and bladder (Fig. 13.22). The urographic phase is a delayed phase in which contrast is already excreted in the collecting systems, ureters, and bladder. Lesions will appear as filling defects during the urographic phase. Furosemide can be administered during the examination in order to increase contrast excretion and distention of the ureters for better visualization.

Single bolus requires three different CT acquisitions, which exposes patients to much radiation. The split bolus technique decreases radiation exposure by splitting the contrast bolus into two, injecting only a portion initially and the second portion 7–8 min after initial contrast administration. CT image acquisition occurs 80–90 s after the second portion is administered. This allows for simultaneous visualization of the parenchymal and urographic phase [137, 138]. If performed on a dual energy CT scanner, a virtual non-contrast CT scan can also be obtained, thus forgoing the need for pre-contrast scan. The split bolus technique decreases radiation exposure however may obscure some subtle lesions.

On imaging, urothelial carcinoma have different morphologies including papillary, sessile, and invasive. Papillary lesions, which are the most common, are frond-like and extend into the lumen of the urinary tract [139]. In the renal pelvis, tumors appear invasive which differentiates urothelial carcinoma from other renal neoplasm such as RCC. In the ureter, tumors appear as focal thickening and enhancement. CTU can also readily visualize secondary signs of urothelial tumors such as obstruction (hydronephrosis) (Fig. 13.23).

Staging is often performed with CTU, which can readily detect detects metastatic disease and local invasiveness of tumor. CTU is less effective at assessing the degree of muscle invasion of lesions due to the lack of imaging contrast between muscle layers, which hinders staging of T1 versus T2 disease [140]. However, one study showed sensitivity of 89% and specificity of 95% of detection of locally invasive disease, increasing ability to distinguish T2 versus T3 disease [137]. Extravesical and extra-ureteral extension appear as fat stranding adjacent to the tumor. This may be confused with inflammatory or infectious changes, which have a similar appearance, though is typically more diffuse rather than focal. CTU can also detect distant metastasis in the abdomen and pelvis, such as pathologic lymphadenopathy and invasive disease into the adjacent pelvic organs [139].

Annual follow up with CTU for non-muscle invasive high-risk bladder tumors is recommend by the EAU [141]. Follow up after treatment for muscle-invasive and metastatic bladder tumors are controversial and not specifically established, although regular imaging may help identify recurrent disease in a timely manner [142].

Follow up imaging after treatment of upper tract disease is recommended by the EAU based on invasiveness of primary disease. After radical nephroureterectomy, noninvasive tumors should be followed by CTU annually afterwards for a total of greater than 5 years. For invasive tumors, CTU should be performed every 6 months for 2 years, then annually for a total of greater than 5 years. If patients undergo kidney-sparing management, CTU should be performed at 3 months, 6 months, and then annually after resection [143].