MRI of the Kidneys, Ureters, and Urinary Bladder

Normal Features

Normal kidneys measure approximately 10 to 14 cm in length. Renal axes tilt medially at the upper poles with anteromedial rotation (according to the position of the hilum) and the kidneys extend from the T12–L1 to the L3 levels ( Fig. 6.3 ). The kidneys are cloaked in a sheath of retroperitoneal fat with interdigitating fibrous septa capped by the adrenal glands. A barely perceptible linear hypointensity encircles the retroperitoneal fat—Gerota’s fascia—an important landmark in staging RCC ( Box 6.1 ).

BOX 6.1

Renal Cell Carcinoma (RCC) Staging

Primary Tumor (T)

T0: no evidence of primary tumor

T1: tumor ≤7 cm limited to kidney

T2: tumor >7 cm limited to kidney

T3: tumor extends into major veins; invades adrenal gland or perinephric tissues not beyond Gerota’s fascia

T3a: tumor invades adrenal gland or perinephric tissues not beyond Gerota’s fascia

T3b: tumor extends into major renal veins or IVC below diaphragm

T3c: tumor extends into major renal veins/IVC above diaphragm

T4: tumor invading beyond Gerota’s fascia

Regional Lymph Nodes (N)

N0: no regional lymph node metastasis

N1: metastasis in a single regional lymph node

N2: metastasis in >1 regional lymph node

Distant Metastasis (M)

M0: no distant metastasis

M1: distant metastasis

Robson Staging System

Stage I (T1 or 2, N0, M0): tumor confined to kidney

Stage II (T3a, N0, M0): tumor spread to perinephric fat confined with renal fascia; possible ipsilateral adrenal involvement

Stage IIIA (T3b–3c, N0, M0): tumor spread to renal vein, inferior vena cava or both

Stage IIIB (T1–T3a, N1–N3, M0): tumor spread to local lymph nodes

Stage IIIC (T3b–T3c, N1–N3, M0): tumor spread to local vessels and lymph nodes

Stage IVA (T4, any N, M0): tumor spread to adjacent organs (except ipsilateral adrenal gland)

Stage IVB (any T & N, M1): distant metastases

American Joint Committee on Cancer System

Stage I: T1, N0, M0

Stage II: T2, N0, M0

Stage III: T1–T2, N1, M0 or T3a-c, N0–N1, M0

Stage IV: T4 or any T, N2, M0 or any T, any N, M1

Normal kidneys exhibit corticomedullary differentiation characterized by moderately greater fluid content in the medulla, relative to the cortex ( Fig. 6.4 ). The kidneys enhance avidly with earlier enhancement of the renal cortex during the arterial phase, reiterating the corticomedullary pattern—the renal cortical phase for our purposes. Within 60 to 90 seconds contrast perfuses the medullary renal parenchyma, resulting in global renal parenchymal enhancement—the parenchymal phase.

The renal collecting system is generally biconcave or flat, and excreted urine demonstrates water signal. Occasional flow voids in T2-weighted images sometimes simulate renal calculi. The collecting system urothelial lining appears as inconspicuous linear hypointensity, exhibiting no discernible enhancement.

Anomalies and Pseudolesions

Congenital anomalies of the kidneys and urinary tract afflict 3 to 6 per 1000 live births, although only a few common developmental anomalies and pseudolesions ( Box 6.2 ) are worth mentioning before discussing pathologic renal lesions. Renal and collecting system embryogenesis is a complex process following a series of steps necessary for the execution of subsequent developmental steps. Incomplete or absent interfacing of the ureteric bud (primordial collecting system and ureter) and metanephric blastema (primordial renal parenchyma) results in renal agenesis and/or a number of other potential parenchymal and ureteral/collecting system anomalies.

BOX 6.2

Common Renal Developmental Anomalies and Pseudolesions

Inductional

Renal agenesis

Renal hypoplasia

Supernumerary kidney

Positional

Renal ectopia

Malrotation

Fusional

Horseshoe kidney

Crossed fused ectopia

Pancake kidney

Structural

Fetal lobulation

Prominent column of Bertin

Hilar lip

Positional anomalies include ectopia and malrotation. Embryonic growth results in a relative ascent of the kidneys during the fourth through eighth week of gestation, ultimately positioned between the first and third lumbar vertebrae. Underascent occurs far more commonly than overascent, and the ptotic kidney ranges in position from the true pelvis to the iliac fossa and anywhere below the expected location centered at the L2 level ( Fig. 6.5 ). Contralateral renal anomalies, such as renal agenesis or ptosis, frequently coexist.

Concomitant medial rotation along the longitudinal renal axis, during ascent, orients the ureteropelvic junction (UPJ) medially. Nonrotation or incomplete rotation leaves the UPJ facing anteriorly, and renal calyces in the medial segment of the kidney lie medial to the renal pelvis ( Fig. 6.6 ). Overrotation results in a posteriorly facing UPJ.

Renal fusion anomalies generally incur positional and rotational derangements. Medial renal fusion results in a solitary discoid lump of renal tissue in the pelvis, referred to as “pancake kidney.” Crossed fused renal ectopia represents the sequela of embryologic renal fusion with the relatively normally positioned kidney dragging its fused counterpart across the midline, resulting in a single ipsilateral S-shaped renal mass with two separate moieties and normal bilateral ureterovesical junctional positioning ( Fig. 6.7 ). Horseshoe kidney is the most common renal anomaly reflecting midline fusion of the metanephric blastema. Ascent is arrested at the level of the inferior mesenteric artery ( Fig. 6.8 ). Coexistent anomalies, such as UPJ obstruction and duplication anomalies, conspire with the geometric and rotational distortion and urinary stasis to lead to complications, including stone formation and infection.

Structural anomalies incur no risk of complications and deserve mention only to prevent misdiagnosis. Fetal lobulation persists in 5% of adults with a smooth undulating outer renal contour conforming to the position of the renal pyramids. Smoothly marginated indentations conform to the edges of renal pyramids with normal appearance and thickness of underlying parenchyma (≥14 mm), excluding the possibility of an underlying mass or scarring. The column of Bertin potentially simulates a renal mass, but represents invagination of normal renal cortical tissue into the renal sinus, usually occurring at the upper polar/interpolar junction and averaging 3.5 cm in size ( Fig. 6.9 ). The hilar lip represents fusion of medial renal lobes, usually occurring in the upper pole and potentially protruding and distorting the renal sinus. Signal characteristics and enhancement identical to the adjacent renal parenchyma, occurring in the expected location, confirm the presence of normal functional renal tissue in cases of renal anomalies.

Focal Lesions

Focal renal lesions are encountered every day in clinical practice in cross-sectional imaging studies—the vast majority of which are incidental, and many indeterminate. Thirteen percent to 27% of abdominal imaging studies incidentally detect a renal lesion. Whereas many of these lesions are incompletely characterized, the overwhelming majority of these lesions are simple or minimally complicated cysts with no malignant potential. Establishing true cystic etiology eliminates the need for further workup and/or follow-up. The presence of solid components implies malignancy, which usually mandates surgical resection ( Fig. 6.10 ).

Most renal cysts are simple in appearance with fluid signal characteristics (T2 hyperintensity and T1 hypointensity), no enhancement, septation, wall-thickening, or nodularity. However, simple cysts occasionally experience complications in the form of hemorrhage, infection, rupture, etc. As such, these benign, nonneoplastic cysts are referred to as “complicated cysts,” to distinguish them from complex/neoplastic cysts, which demonstrate some element of solid tissue. Signal alterations alone pose no risk of malignancy, although they often challenge interpretation. The most common signal alteration occurs as a result of hemorrhage, resulting in T1 hyperintensity and T2 hypointensity. Proteinaceous contents induce a similar appearance.

Other complicated cystic lesion features pose greater diagnostic difficulty. Superimposed infection and trauma induce reactive wall thickening, which overlaps with the appearance of cystic neoplasms (especially RCC, clear cell type). These neoplasms often harbor more complex features with mural nodularity and solid components. In an effort to stratify renal lesions based on the likelihood of malignancy, Bosniak developed a predictive classification system (for computed tomography [CT]) to guide management ( Table 6.2 ). Although not specifically adapted for MRI, this scheme illustrates the range of imaging complexity of renal lesions and offers management guidance. Although the MR inconspicuity of calcification precludes factoring it into the classification scheme, it generally applies to magnetic resonance (MR) findings—replacing intensity changes for density changes.

TABLE 6.2

Bosniak Classification Scheme for Cystic Renal Lesions

Bosniak Category	Imaging Features	Management
I	Thin wall; no septa, calcifications, or solid components, water features; no enhancement	No follow-up
II	Few thin septa with less than or minimal enhancement; fine calcification or focal thick calcification; homogeneous high-density sharply marginated lesion (<3 cm) with no enhancement	No follow-up
IIF	Multiple thin septa with less than or minimal enhancement; thick or nodular calcification; no enhancing soft tissue components; high-density lesions (>3 cm) with no enhancement	Observe
III	Thickened irregular or smooth walls or septa with enhancement	Surgery
IV	Same features as III with enhancing soft tissue components	Surgery

Solid lesions include benign and malignant neoplasms. Macroscopic fat is the only finding that connotes a benign etiology—AML. After excluding AML, renal infection and infarction, rare benign neoplasms (such as oncocytoma), and solid tissue (enhancement) effectively equals malignancy. Unless clinical findings raise the suspicion of inflammatory or vascular etiology, the presumptive diagnosis is malignancy until proved otherwise. Because biopsy results are notoriously confusing, solid renal lesion management involves either percutaneous ablation or surgical pathologic diagnosis and treatment. Because very small lesions (<1 cm) challenge the resolution of imaging methods, limiting diagnostic confidence, imaging surveillance preempts potentially unnecessary surgery ( Table 6.3 ).

TABLE 6.3

Management Scheme for Solid Renal Lesions

Size	Presumptive Diagnosis	Management
Large (>3 cm)	Renal cell carcinoma	(Partial) Nephrectomy ∗
Small (1–3 cm)	Renal cell carcinoma	(Partial) Nephrectomy ∗
Very small (<1 cm)	Renal cell carcinoma, oncocytoma, angiomyolipoma	Active surveillance

∗ Ablative treatment is an option in the appropriate clinical setting.

Cystic Lesions

Using the combination of heavily T2-weighted images to detect fluid hyperintensity in postcontrast images to exclude enhancement confirms cystic etiology. T1-weighted sequences depict hemorrhagic cysts with variable hyperintensity, and postcontrast images exclude enhancement. Ninety percent of all renal cystic lesions are simple cysts ( Fig. 6.11 ). Hemorrhage, debris, and infection complicate renal cysts. If there is an increasing number of cystic lesions (and renal enlargement), consider the possibility of polycystic disease. Cystic lesions prevail in other inherited diseases, such as von Hippel–Lindau (VHL) disease and tuberous sclerosis (TS) (with assorted solid lesions, discussed in the section “Solid lesions with ball morphology”). Developmental etiologies include multicystic dysplastic kidney and calyceal diverticulum. Acquired conditions, such as renal cystic disease of dialysis and lithium therapy, present with renal cystic lesions. RCC (clear cell types) dominates the cystic neoplastic category; consider multilocular cystic nephroma (MLCN) in the appropriate demographic categories (young males and middle-aged females), with herniation into the renal pelvis.

Simple Renal Cyst

The simple renal cyst is ubiquitous, with a prevalence of up to two thirds of the population, and increasingly prevalent with age. Renal cysts detach from the parent renal tubule and become self-enclosed; continued fluid secretion distends the cavity, resulting in an isolated cystic structure. Ongoing fluid secretion accounts for continued growth of simple renal cysts (≤5% per year), despite the lack of neoplastic or autonomously regenerating cells. Therefore careful attention to imaging features is paramount in excluding neoplasm.

The contents of the simple renal cyst—free water protons—account for its appearance: extreme T2 hyperintensity and T1 hypointensity with no enhancement. If even visible, the cyst wall is uniformly smooth with no perceptible enhancement in postcontrast images ( Fig. 6.12 ). Size varies from millimeters to over 10 cm. Cysts are stratified into three different categories based on their location: 1) exophytic, 2) parenchymal, and 3) parapelvic ( Figs. 6.13 and 6.14 ). Because most renal cysts arise from the cortex (although some develop from the medulla), most renal cysts are exophytic and/or intraparenchymal (see Figs. 6.12 and 6.13 ).

Renal cyst complexity assumes many forms, which fall into two major categories—morphologic and signal-related. Morphologic derangements include deviation from simple sphericity and/or septation; signal derangements deviate from simple fluid characteristics with evidence of hemorrhage or debris ( Fig. 6.15 ). Occasional fluid-fluid levels depict layering hematocrit ( Fig. 6.16 )—a relatively infrequent manifestation of a hemorrhagic cyst. Signal alterations from hemorrhage present the greatest challenge to interpretation; precontrast hyperintensity limits the ability to detect augmented T1 signal from enhancement (see Fig. 6.15 ). Fibrinous septations from previous infection generally measure less than 2 mm in thickness with no other evidence of complexity to suggest neoplasm ( Fig. 6.17 ). As long as no enhancement beyond minimal linear septal or wall enhancement is present, simple cystic etiology is confirmed.

Careful scrutiny of these features is critical, because a minority of clear cell RCC (less than 10%) is mostly cystic. In Bosniak’s terms, the discrimination of types II and IIF lesions from understated type III lesions bears close inspection. Usually, a solid enhancing component differentiates RCC from a nonneoplastic cyst—especially with the benefit of subtractions. When subtractions are not available and signal alterations limit assessment of enhancement, rely on ROI measurements compared with a reference standard (see Figs. 6.2 and 6.15 ). Other etiologies are not realistic considerations, except under specific circumstances. For instance, with multilocularity and when herniating into the renal pelvis, consider multilocular cystic nephroma (MLCN) in the appropriate demographic setting (young males or middle-aged females). Infectious cysts—renal abscesses and echinococcal cysts—require a suggestive history.