27 Kidneys



10.1055/b-0034-75820

27 Kidneys

Burgener\, Francis A.

The kidneys are surrounded by perinephric fat, resulting in excellent delineation of their margins. The renal parenchyma has a relatively uniform density of 30 to 50 HU on precontrast computed tomography (CT) scans, which does not permit differentiation between the renal cortex and medulla. The attenuation of urine in the collecting system is similar to water.


Renal arteries arise posterior to the corresponding renal veins, which are usually somewhat larger. The right renal artery crosses posterior to the inferior vena cava, whereas the left renal vein crosses anterior to the aorta.


After an intravenous (IV) contrast material bolus, the attenuation in the renal cortex increases more rapidly than in the medulla, permitting differentiation between these two compartments within the first minute. After that time the density of the renal parenchyma becomes uniform again, as the renal medulla enhances more slowly than the cortex, which already depicts early contrast washout. Following an IV contrast material infusion, the renal parenchymal density increases uniformly, and differentiation between the cortex and medulla is not feasible.


The renal parenchyma is tightly invested by a rigid renal capsule composed predominantly of fibrous tissue. The capsule is rarely, if ever, visualized by CT. Because of the rigidity of the renal capsule, a subcapsular process such as a hematoma compresses primarily the adjacent renal parenchyma, which becomes flattened by the pathologic fluid collection and often assumes a lenticular shape.


Between the renal capsule and the renal fascia (perirenal fascia, Gerota fascia anteriorly, and Zuckerkandl fascia posteriorly), which is commonly seen on CT scans, lies the perirenal space, composed largely of fatty tissue. Bridging connective tissue septa connecting the renal capsule with the renal fascia may divide this space into smaller subunits. A fascia measuring ≥ 3 mm in width is an abnormal but totally nonspecific finding. It has been reported in a variety of conditions, including inflammatory, malignant, and traumatic processes, or may be caused by edema and fibrosis. The pararenal compartment is located outside the renal fascia. An anterior pararenal compartment containing the pancreas, duodenum (with the exception of the bulb), and both the ascending and descending colon is distinguished from the posterior pararenal compartment, which contains no major organs. Although these retroperitoneal compartments are anatomically well defined, an infectious or tumorous process can easily spread from one space to the other. Furthermore, pelvic disease, especially involving the rectosigmoid, may spread cephalad into the perirenal and pararenal compartments (Fig. 27.1).


CT is valuable in the detection, localization, and characterization of focal renal mass lesions. The most common renal mass in the adult is a benign cyst. Cysts may be solitary or multiple and are usually round and located in the cortex. Characteristic CT features include a homogeneous density close to water (0–20 HU), a smooth margin with sharp demarcation from the adjacent renal parenchyma, no detectable wall when projecting beyond the renal outline, and no enhancement after IV contrast material administration (Fig. 27.2). A cyst smaller than the image slice thickness may be volume-averaged, resulting in falsely high attenuation values before and particularly after contrast enhancement. Truly high-density cysts occur and are caused by proteinaceous material or “milk of calcium” in the cystic fluid, infection, or hemorrhage into the cyst (Fig. 27.3). Milk of calcium may also be found in a calyceal diverticulum (Fig. 27.4). Thin intracystic septation occasionally occurs in benign renal cysts, but other entities, such as multilocular renal nephromas, Wilms tumors, and abscesses, must be considered. The Bosniak classification is commonly used to assess cystic renal lesions (Table 27.1).

Fig. 27.1 Extraperitoneal anatomy of the left flank. Light gray area: anterior pararenal space; medium gray area: perirenal space; dark gray area: posterior pararenal space; short arrows: anterior renal fascia; long arrows; posterior renal fascia; arrowhead: lateroconal fascia.




























A


aorta


C


colon


K


kidney


LS


lesser sac


P


pancreas


S


spleen


V


inferior vena cava

Fig. 27.2 Renal cyst. A renal mass of homogeneous density close to water displacing the left kidney anteriorly is seen on this nonenhanced scan.
Fig. 27.3a–c High-density renal cyst with tiny intracystic calcification. Supine view (a). An isodense anterolateral enlargement of the left kidney containing a tiny calcification (arrow) is seen on this nonenhanced scan. Prone view (b). In this position, the tiny calcification (arrow) is moving to the most dependent portion of the kidney. Supine postcontrast enhancement (c). A well-demarcated cyst without enhancement can be differentiated from the enhanced normal renal parenchyma. The tiny intracystic calcification is located at the most dependent portion of the renal cyst.

Solid renal mass lesions are usually irregularly shaped with poor demarcation from the normal renal parenchyma (Fig. 27.5). Characteristic CT features include an inhomogeneous density that is close to the renal parenchyma (30–50 HU) and increases after IV contrast administration. Compared with the surrounding renal parenchyma, solid renal mass lesions are frequently slightly hypodense, but because of small differences in attenuation on precontrast scan, these lesions may be appreciated only after IV contrast administration, as they usually enhance considerably less than normal renal parenchyma. A solid renal mass lesion must be considered malignant until proven otherwise and requires prompt clinical workup, including surgical exploration.


Renal lesions that do not unequivocally display CT criteria of either a benign cyst or a solid tumor represent indeterminate masses. They account for about 10% of all focal renal lesions. The renal mass may be indeterminate for technical reasons, such as breathing artifacts and volume-averaging effects. Cystlike renal masses may be considered indeterminate if they demonstrate a thick wall, calcifications, multiple septa, indistinct interface with the renal parenchyma, high attenuation of the cyst content (≥ 25 HU), and/or some contrast enhancement. Complicated (hemorrhagic) cysts, abscesses, and benign and malignant cystic or necrotic tumors may all represent as indeterminate masses by CT criteria (Fig. 27.6). They correspond to types 3 and 4 in the Bosniak classification of cystic renal lesions and usually require prompt clinical workup, including percutaneous biopsy or surgical exploration.

Fig. 27.4 “Milk of calcium.” Calcium–fluid level is visible in a calyceal diverticulum.

Calcifications in a focal renal lesion occur in both benign and malignant conditions (Fig. 27.7). Peripheral curvilinear calcifications in a cystlike lesion with homogeneous, near-water-density fluid content and the absence of both a soft tissue mass and thickened (focal or uniform) wall is likely to be benign. In addition to calcified renal cysts, aneurysms and arteriovenous malformation must be considered. In hydatid (echinococcal) disease, a larger partially calcified cyst with a thin or thick wall containing daughter cysts is diagnostic. Amorphous or punctate calcifications associated with a solid or partially cystic mass are found in a variety of benign (e.g., oncocytoma) or malignant tumors (e.g., renal cell carcinomas, Wilms tumor, and metastases), tuberculosis (TB) and other granulomatous diseases, and old abscesses and hematomas (Fig. 27.8).
























































Table 27.1 Bosniak classification of cystic renal lesions

1 Simple cyst


Well-defined round mass of water attenuation


Hairline-thin imperceptible wall


No enhancement


2 Minimally complicated cyst


Cluster of cysts/septated cyst


Minimal curvilinear calcification


Minimally irregular wall


High-density content (> 25 HU)


2F Follow-up cyst


Hairline-thin septum


Wall with perceived enhancement


Intrarenal lesion > 3 cm with high density content


3 Complicated (surgical) cyst


Irregular, thickened septa


Measurable enhancement


Coarse, irregular calcifications


Irregular margin


Multiloculated lesion


Uniform wall thickening


Nonenhancing nodular mass


4 Malignant cyst


Irregular wall thickening


Solid enhancing elements


Large cystic/necrotic component

Fig. 27.5 Renal cell carcinoma. A poorly defined lesion with less contrast enhancement than the adjacent normal renal parenchyma is seen in the lateral aspect of the kidney.
Fig. 27.6 Cystic renal cell carcinoma. A well-demarcated, hypodense lesion mimicking a cyst is apparent in the lateral aspect of the left kidney on this contrast-enhanced scan.
Fig. 27.7 Calcification in renal cell carcinoma. A large mass with irregular calcifications is seen in the right kidney.

Diffuse renal parenchymal calcifications (nephrocalcinosis) occur most often in the renal medulla, especially in the renal papilla, where the largest urine concentration is attained (Fig. 27.9). Medullary nephrocalcinosis is found with medullary sponge kidney, hyperoxaluria, and conditions associated with hypercalcemia and hypercalcinuria (e.g., hyperparathyroidism, renal tubular acidosis, milk–alkali syndrome, Cushing syndrome, vitamin Dintoxication, sarcoidosis, bone metastases, multiple myeloma, and osteoporosis). Papillary calcifications are also encountered with papillary necrosis and TB.


Cortical nephrocalcinosis is rare and limited to diseases primarily involving the renal cortex (e.g., acute cortical necrosis and occasionally glomerulonephritis).


Renal calculi are readily detected by CT even if they are not calcified. Nonopaque calculi account for approximately 10% of all renal calculi and consist of uric acid, xanthine, or matrix (mucoprotein/mucopolysaccharide). Urographic differentiation from tumors and blood clots is often not possible. CT can, however, readily distinguish calculi from other nonopaque filling defects because of a difference in density. Nonopaque calculi have a CT density exceeding 50 HU, whereas tumors of all types have soft tissue attenuation values of less than 50 HU.

Fig. 27.8 Tuberculous autonephrectomy. A small, shrunken, scarred, nonfunctioning calcified left kidney is seen.

Perinephric fluid collections complicating a renal transplant are caused by lymphocele, urinoma, hematoma, and abscess formation. Lymphoceles are the most common peritransplant fluid collections, characteristically occurring within 2 to 3 weeks after transplantation. They tend to be large, may be septated, and are usually located medial and inferior to the lower pole of the transplant (Fig. 27.10). Urinomas can occur at any time after transplantation and are caused by an anastomotic leak or are secondary to a vascular injury causing a focal necrosis with subsequent leak in the urinary system. Hematomas can be differentiated in the acute stage by their higher CT density. Abscesses can be unequivocally diagnosed only if they contain gas. Transplant failure caused by rejection, acute tubular necrosis, and cyclosporine-induced nephrotoxicity cannot be reliably differentiated by CT. Nevertheless, a rapid increase in the size of a failing transplant suggests acute rejection.

Fig. 27.9 Medullary nephrocalcinosis. Diffuse medullary calcifications are evident in both kidneys.
Fig. 27.10 Lymphocele in renal transplant. A large fluid collection (arrow) is visible in the right hemipelvis after renal transplantation. The density of the lymph in the lymphocele is similar to the urine in the adjacent distended bladder.

The differentiation of focal lesions in the kidney and perinephric space is discussed in Tables 27.2 and 27.3 , respectively.













































































































































Table 27.2 Focal renal lesions

Disease


CT Findings


Comments


Renal ectopy


Fig. 27.11


Fig. 27.12


Fig. 27.13a, b


Fig. 27.14


Malpositioned kidneys are readily located and identified as functioning renal parenchyma after contrast enhancement.


In horseshoe kidneys , the lower poles of both kidneys are fused by a parenchymal or fibrous isthmus across the midline at L4–L5 between the aorta and inferior mesenteric artery. The long renal axis is medially oriented, and renal pelvises and ureters are situated anteriorly. Upper pole fusion is rare (10%). Complications include hydronephrosis secondary to ureteral pelvic junction (UPJ) obstruction, renal calculi, infection, and vesicoureteral reflux.


In longitudinal ectopy , the kidney is mal-positioned in any location from the thorax to the sacrum. Pelvic kidney is the most common location and frequently associated with vesicoureteral reflux, hydronephrosis, hypospadia, and contralateral renal agenesis. In crossed ectopy , the malpositioned kidney is commonly fused with the contralateral kidney. A large kidney with usual outline and two collecting systems on one side and an absent kidney on the contralateral side are diagnostic.


In renal fusion , the fused kidneys are located in the midline and may assume the shape of a horseshoe, disk, or pancake. Ureteral obstruction by aberrant arteries is frequently associated.


In renal malrotation , the collecting system is usually positioned anteriorly.


Differential diagnosis: A malpositioned kidney may also be caused by a large adjacent mass.


Renal duplication


Fig. 27.15


Two separate renal sinuses and pelvises are seen, separated by a parenchymal bridge.


Upper pole moiety is subject to obstruction and may simulate an upper pole mass on excretory urography when completely obstructed. Hydronephrosis and hydroureter of the obstructed upper collecting system is readily diagnosed by CT. Lower pole moiety is subject to vesicoureteral reflux.


In complete renal and ureteral duplication, the ureter draining the upper system inserts ectopically medial and below the orthotopic ureter into the bladder trigonum or urethra and may be associated with an ectopic ureterocele.


Other congenital renal anomalies are partial duplication, supernumerary kidney, and renal hypoplasia or agenesis.


Renal sinus lipomatosis/fibrolipomatosis


Fig. 27.16


Extensive proliferation of fat in the renal sinus associated with loss of renal parenchyma is characteristic. It may result in concentric encroachment of the renal collecting system (trumpetlike pelvocaliceal system on urography), but without obstruction.


Etiology: (1) normal increase of sinus fat with aging and in obesity; (2) vicarious proliferation of sinus fat with renal atrophy of any cause; (3) fibrolipomatosis induced by extravasation of urine into the renal sinus (e.g., in chronic prostatism).


Hydronephrosis


Fig. 27.17a, b


Fig. 27.18


Dilated collecting system evident as water-density structure within normal or enlarged kidney on nonenhanced images. High-density urine in obstructed system suggests pyonephrosis. After enhancement, a persistent nephrogram and delayed and decreased contrast medium excretion are characteristic. In long-standing obstruction, the kidney appears as a fluid-filled cyst with a thin rim of solid renal tissue draped around it.


Early hydronephrosis can be differentiated from an extrarenal pelvis and postobstructive uropathy by the persistent nephrogram and delayed urinary contrast material excretion after contrast enhancement.


Level of obstruction can easily be identified with CT by following the dilated collecting system and ureter to the point of obstruction. Nonopaque calculi have a CT density of at least 50 HU and can therefore be differentiated from soft tissue lesions that have a lower density. Freely mobile filling defects in the collecting system other than renal calculi include blood clots and fungus balls.


Renal cyst


Fig. 27.19


Fig. 27.20


Fig. 27.21


Solitary or multiple sharply delineated, homogeneous lesions of near-water density (0–20 HU). Wall either very thin or not detectable when projecting beyond the renal outline. No contrast enhancement. Hemorrhagic cysts may demonstrate a fluid–fluid level or hematocrit effect due to settling of red blood cells. The Bosniak classification is commonly used for the CT assessment of cystic renal lesions (see Table 27.1).


Most common renal mass in adults. Higher than water attenuation values in a renal cyst are found with hemorrhage into the cyst, contrast material leakage into the cyst (caused by either communication with the collecting system or diffusion), calcification of the cyst wall or the cyst content (milk of calcium or calcium carbonate), high protein content of cyst fluid, and infection. Partial volume averaging with normal adjacent renal parenchyma (e.g., in cysts smaller in diameter than the CT slice thickness) also results in a higher displayed attenuation value of the cyst.


Parapelvic cyst (renal sinus cyst)


Features of a benign renal cyst, but located adjacent to the renal sinus. Differentiation from an ectatic renal pelvis may require IV contrast administration demonstrating lack of enhancement of the cyst.


Occurs frequently in the fifth and sixth decade of life and is almost always asymptomatic. Very rare complications may include obstructive caliectasis and renal vascular hypertension due to compression of renal arteries.


Autosomal dominant polycystic kidney disease (ADPKD)


Fig. 27.22


Fig. 27.23


Bilateral, often markedly enlarged kidneys with lobulated contours but often not symmetrically involved. Multiple cysts of different sizes cause splaying and distorting of the collecting system and may demonstrate varying densities due to blood products of different ages. Unilateral involvement is exceedingly rare.


Also referred to as adult polycystic kidney disease. Cysts are often also present in the pancreas, spleen, and lungs. Progressive renal failure and hypertension are usually evident in the fourth decade but occasionally as early as childhood or young adulthood.


Autosomal recessive polycystic kidney disease (ARPKD)


Symmetric, slightly enlarged kidneys with numerous tiny cysts (usually 1–2 mm, occasionally larger but always < 1 cm). They represent abnormally proliferated and dilated collecting tubules and do not produce calyceal or renal pelvis distortion. After IV contrast material administration, a prolonged and increasingly hyperintense, heterogeneous nephrogram is seen with delayed and decreased urinary contrast medium excretion.


Also referred to as infantile polycystic kidney disease. Occurs in neonates and children younger than 5 y. Associated with dilated bile ducts, periportal fibrosis, and pancreatic fibrosis. Neonatal death occurs in up to 50% of cases from pulmonary hypoplasia with long–term survival improving substantially after the newborn period.


Multicystic dysplastic kidney


Fig. 27.24


Unilateral involvement consisting of a small or large single-chamber or multiloculated cystic mass, often with central or peripheral calcifications. No functional renal parenchyma is detectable after contrast administration (unlike multilocular cystic nephroma and unilateral polycystic kidney disease).


Frequent cause of palpable abdominal mass in an otherwise healthy infant or child resulting from failed fusion of the metanephros and ureteric bud. Compensatory hypertrophy of the contralateral kidney is usually present, often with an element of ureteropelvic obstruction.


Multilocular cystic nephroma (multilocular cystic renal tumor)


Fig. 27.25


Fig. 27.26


Single or multiple fluid-filled cysts measuring up to 10 cm, often replacing an entire renal pole (usually lower pole). Cysts are often separated by thick septa and sharply demarcated from the normal renal parenchyma. Peripheral and central calcifications of circular, stellate, flocculent, or granular nature in up to 50% of cases. Cyst wall and septations enhance after contrast administration.


Occurs in children younger than 5 y (M:F = 3:1) and in 40- to 70-y-old adults with strong female predominance. On ultrasound, multiple cystic masses separated by highly echogenic septa are evident.


Cystic Wilms tumor and cystic renal cell carcinoma must be differentiated. Nodular thickening of the cyst wall and/or septa may be the clue for a malignancy.


Medullary cystic disease


Fig. 27.27


Bilateral small kidneys with multiple small medullary cysts that do not extend to the renal margins are characteristic.


Rare, in the majority of cases inherited, disorder manifesting itself in adolescents and young adults with progressive renal failure.


Medullary sponge kidney


Bilateral, unilateral, or segmental ectasia of the tubules in often enlarged papilla presenting after IV contrast material administration as tubular structures radiating from the calyx into the papilla. In approximately half of the cases, small calculi measuring up to 5 mm are clustered in the ectatic tubules of the papilla.


Usually an incidental finding in asymptomatic young to middle-aged adults.


Differential diagnoses include medullary nephrocalcinosis (no ectatic tubules, calcifications beyond pyramids), renal TB (calcifications larger and more irregular), and papillary necrosis (partial or total papillary slough).


Acquired cystic disease of dialysis


Fig. 27.28


Small kidneys with largely preserved contours, as the cysts varying from 0.5 to 2 cm in diameter are mostly intrarenal. Complications include hemorrhage and development of renal adenomas and carcinomas.


Up to 50% of patients on chronic dialysis. Incidence increases with time, particularly after the third year. Cystic disease may regress after renal transplantation. Renal carcinomas are associated in 7% of patients.


Von Hippel–Lindau disease


Fig. 27.29a, b


Combination of multiple renal cysts and solid tumors (carcinomas, adenomas, and hemangiomas) characteristic. Renal carcinomas are often small, < 2 cm in size, and may occur within the cysts themselves. Involvement usually bilateral and multicentric.


Inherited (autosomal dominant) neurocutaneous dysplasia complex with onset in the second to third decade. Retinal angiomatosis, cerebellar and spinal hemangioblastomas, pheochromocytomas, pancreatic tumors and cysts, hepatic adenomas, and hemangiomas may be associated.


Renal pseudotumor


Fig. 27.30


Focal enlargement of normal renal parenchyma simulating a tumor on other imaging studies. On CT, the mass has all the characteristics of normal renal tissue, including enhancement after IV contrast medium administration.


These anomalies include:


Fetal lobulations: cortical bulges centered over corresponding calyces


Dromedary hump: in the midportion of the left kidney due to prolonged pressure by the spleen during fetal development


Column of Bertin: focal hypertrophy of the septal cortex in the midportion of the kidney causing deformation of the adjacent calyces and infundibula


Hilar lip: supra- and infrahilar cortical bulge above and below the renal sinus


Nodular compensatory hypertrophy: hypertrophied normal renal tissue secondary to focal renal scarring


Renal adenoma


Fig. 27.31


Solitary or, less commonly, multiple cortical nodules measuring by definition < 3 cm in diameter. CT appearance is similar to renal cell carcinoma of the same size, that is, homogeneous and minimally hypodense to isodense on the precontrast and markedly hypodense on the postcontrast examination.


Most common cortical lesion at autopsy. May be a precursor of a renal cell carcinoma.


Metanephric adenoma typically presents as a slightly hypoattenuating mass with little enhancement and occasionally small calcifications.


Juxtaglomerular tumor (reninoma) is indistinguishable on CT from a renal adenoma but presents clinically with marked hypertension.


Oncocytoma


Fig. 27.32


Solid 1- to 14-cm mass that is sharply separated from the cortex, does not invade the collecting system, and is rarely calcified. A central stellate, nonenhancing scar of lower density secondary to infarction and hemorrhage is characteristic but seen only in larger lesions (33%). After contrast administration, a homogeneous contrast enhancement that is only slightly less dense than the renal parenchyma is common, but occasionally poor tumor enhancement is found.


Seen in middle-aged patients, with a slight male predominance. Histologically, this benign tumor may be mistaken for a well-differentiated renal cell carcinoma with oncocytic features.


Angiomyolipoma (renal hamartoma)


Fig. 27.33


Fig. 27.34


Fig. 27.35


Fig. 27.36


Single or multiple renal masses ranging from 1 to 8 cm in diameter with attenuation values ranging from −100 HU (fat) to +150 HU (calcifications). Scattered punctate calcifications are rare (6%). Demonstration of intratumoral fat (≤ 20 HU) is characteristic, even if the tumor is composed mainly of vascular tissue, muscle, and hemorrhage, resulting in CT values > 20 HU in most parts of the lesion. After contrast administration, inhomogeneous tumor enhancement sparing only the fatty tissue and areas of necrosis is characteristic.


Occurs as an isolated lesion in middle-aged women (4:1 female predominance) or as renal manifestation in tuberous sclerosis ( Figs. 27.37, 27.38 ) , where tumors are commonly multiple and bilateral. Although the CT diagnosis of angiomyolipomas is highly suggestive by the demonstration of fatty tissue, occasionally rare tumors such as renal lipomas, liposarcomas, and Wilms tumor containing small amounts of fatty tissue cannot be absolutely excluded. Renal cell carcinomas may occasionally also contain fatty tissue and calcifications.


Renal cell carcinoma


Fig. 27.39


Fig. 27.40


Fig. 27.41


Fig. 27.42


Homogeneous or heterogeneous, irregularly shaped, and poorly demarcated mass producing an irregular or lobulated renal contour and distortion of the collecting system. The attenuation is slightly less than that of normal renal parenchyma. Less commonly, the tumor is isodense or hyperdense (e.g., after recent intratumoral hemorrhage and tumor calcifications) on precontrast scans. Rarely, renal cell carcinomas are largely to completely cystic. Calcifications occur in 20% of patients and usually are central and amorphous or peripheral and curvilinear in cystic renal cell carcinomas. Intratumoral metaplasia into fatty marrow occurs occasionally in larger lesions. After contrast administration, the nonnecrotic parts of the tumor demonstrate an unequivocal increase in density, that is, less than the surrounding normal renal parenchyma, making the tumor more apparent on contrast-enhanced scans. Tumor spread to the perinephric fat, local lymph nodes and vessels, and adjacent organs can also be depicted in more advanced stages.


Most common malignant renal tumor, accounting for > 80% of all renal primaries. Twice as frequent in men as women and rare in patients younger than 40 y (peak age 55 y). Gross hematuria (60%) and flank pain (50%) are the most common clinical presentation. Bilateral involvement in 2% of cases. CT is most valuable for both diagnosing and staging.


Robson staging system:


Stage I: tumor confined to kidney


Stage II: tumor spread to perinephric fat


Stage IIIA: tumor spread to renal vein or inferior vena cava (IVC)


Stage IIIB: tumor spread to local lymph nodes


Stage IIIC: tumor spread to both local vessels and lymph nodes


Stage IVA: tumor spread to adjacent organs (except ipsilateral adrenal)


Stage IVB: distant metastases


Medullary renal tumor


Large, ill–defined mass centered in the renal medulla with extension into the renal sinus and cortex. Contrast enhancement may be heterogeneous due to varying amounts of hemorrhage and necrosis. Renal medullary carcinoma and collecting duct carcinoma are differentiated.


Renal medullary carcinoma ( Fig. 27.43 ): Highly aggressive malignant tumor of epithelial origin occurring almost exclusively in adolescent and young adult blacks with sickle cell trait (not with hemoglobin SS sickle cell disease), with mean survival rate of 15 weeks from diagnosis. Presents as large, ill-defined, heterogeneous mass centered in the renal medulla with extension into the renal sinus and cortex and nonuniform contrast enhancement.


Collecting duct carcinoma (Bellini) ( Fig. 27.44 ): High-grade, infiltrative neoplasm centered in the renal medulla with renal sinus invasion, cortical extension, and metastases in 40% at presentation. Mean age 55 y (range 13–80 y).


Renal transitional cell carcinoma


Fig. 27.45


Fig. 27.46


Small tumors are often not detectable on precontrast scans but present as a smooth or irregular (frondlike) filling defect in the opacified renal pelvis. Contrast enhancement of the tumor itself is only subtle (8–40 HU precontrast, up to 55 HU postcontrast). Larger tumors cause hydronephrosis, obliterate the peripelvic fat, and invade the renal parenchyma and vessels, but they do not affect renal contour. Tumor calcifications are very rare.


Most common uroepithelial tumor (85%), multiple in one third of the cases. Majority (70%) of patients are men older than 60 y. Hematuria occasionally associated with flank pain is the most common clinical presentation.


Squamous cell carcinoma (15%) is frequently associated with chronic leukoplakia. Renal calculi are present in 50% of patients, and tumor calcification occurs in 10%. The prognosis is very poor, as the tumor is usually well advanced at the time of diagnosis.


Nephrogenic adenoma is an uncommon benign metaplastic response to a urothelial injury or prolonged irritation presenting as a papillary or polypoid filling defect in the renal pelvis. Malignant transformation is rare.


Wilms tumor (nephroblastoma)


Fig. 27.47


Fig. 27.48


Large, inhomogeneous mass often with central hypodense areas representing cysts, necrosis, and/or hemorrhage. Calcifications are unusual. An enhanced rim of compressed renal parenchyma (pseudocapsule) is frequently present. Rarely, a large cyst with irregularly thickened wall and septa is the dominant feature. Tumor invasion into the renal vein occurs in one third of cases. In adults, the tumor is virtually indistinguishable from a renal cell carcinoma, except for a large central necrosis, which is more typical for the latter.


Staging:


1. Tumor limited to kidney


2. Local extension into perirenal tissue, renal vein, and/or para-aortic lymph nodes


3. Not totally resectable (peritoneal implants, distant lymph node metastases in abdomen and pelvis)


4. Hematogenous metastases and/or lymph node metastases above diaphragm


5. Bilateral renal involvement


Most often in children between 1 and 5 y of age presenting usually with an asymptomatic abdominal mass. Hypertension, hematuria, aniridia, and hemihypertrophy (Beckwith–Wiedemann syndrome) may be associated. Metastases to lungs are frequent, less common to liver and lymph nodes. In contrast to neuroblastomas, bone metastases and tumor calcifications are rare.


Mesoblastic nephroma ( Fig. 27.49 ): Benign intrarenal mass in neonates with CT appearance similar to Wilms tumor, but without venous extension.


Nephroblastomatosis: Multiple nodules of primitive metanephric tissue. Benign condition with unilateral or bilateral renal involvement predisposing to the development of a Wilms tumor.


Rhabdoid tumor of the kidney


Centrally located, heterogeneous renal mass with indistinct borders and frequent central necrosis. Tumor lobules may be outlined by linear calcifications. Subcapsular crescent-shaped hematoma is associated in half of the cases.


Most aggressive renal neoplasm in childhood, typically occurring before the age of 2. May be associated with primary brain tumor of neuroectodermal origin (e.g., medulloblastoma, primitive neuroectodermal tumor [PNET]).


Renal lymphoma


Fig. 27.50


Fig. 27.51


Fig. 27.52


Homogeneous infiltrate or mass, slightly hypodense on pre-contrast and markedly hypodense on postcontrast scans. Bilateral involvement common.


Manifestations:


1. Renal enlargement caused by diffuse infiltration with maintenance of the normal renal contour


2. Multiple nodules


3. Solitary intrarenal mass


4. Retroperitoneal disease extending into the renal pelvis


5. Compression of the collecting system or vascular structures causing hydronephrosis or a nonfunctioning kidney After contrast enhancement, the lymphomatous tissue increases only slightly in attenuation.


Late manifestation of the disease, caused by hematogenous spread or direct extension from adjacent pararenal lymphoma. Absence of clinical symptoms in > 50% of patients. Leukemia can also produce bilateral renal enlargement and intrarenal masses ( Fig. 27.53 ) .


Renal metastases


Fig. 27.54


Fig. 27.55


Fig. 27.56


Solitary renal mass or, more commonly, multiple nodules of varying sizes. Metastases are usually small and do not distort the renal contour or the collecting system.


Most common renal malignancy at autopsy, but infrequently diagnosed antemortem. Lung and breast carcinomas are the most common primaries, but stomach, colon, pancreas, cervix, and gonads are other sites of origin.


Mesenchymal renal tumors (benign or malignant)


Fig. 27.57


Fig. 27.58


No characteristic features except for the demonstration of fatty tissue in lipomas and liposarcomas (see also angiomyolipoma) and the irregular peripheral contrast enhancement proceeding centrally in hemangiomas.


Very rare.


Ossifying renal tumor of infancy presents as benign calcified (80%) filling defect in the renal pelvis with poor enhancement on CT.


Renal abscess


Fig. 27.59


Cavitating mass with thick, irregular wall and liquefied center of decreased density simulating a necrotic neoplasm. After contrast administration, the wall of the abscess enhances, whereas the liquefied central part of the abscess does not. Perinephric extension and thickening of the renal fascia are common. Demonstration of gas bubbles or a gas–fluid level within the mass is virtually diagnostic but only rarely present.


The CT appearance of a renal abscess may be difficult to differentiate from a necrotic renal cell carcinoma.


Pyelonephritis, acute


Fig. 27.60


Fig. 27.61


Fig. 27.62


Fig. 27.63


Renal involvement may be unilateral or bilateral, diffuse or, more commonly, focal. Findings depend on the severity of the infection. Size of the involved kidney is normal to diffusely enlarged. On the precontrast scan, the affected renal area is isodense to slightly hypodense and poorly marginated. Occasionally, inflammatory (edematous) changes in the perinephric fat and mild thickening of both the renal fascia and the walls of the renal pelvis and calyces can be appreciated. Slight dilation of the renal pelvis and ureter is frequently also present. After contrast enhancement, a patchy inhomogeneous enhancement is evident that is, however, less than in the nonaffected part of the kidney. These hypoattenuating zones extending from the papilla into the cortex are typically wedge-shaped in the nephro-graphic phase. Other findings include poor corticomedullary differentiation after an intravenous material bolus and a striated nephrogram that may persist for an extended period of time.


Most commonly an ascending Escherichia coli infection presenting with fever, chills, and flank pain. Patients with altered host resistance (e.g., diabetes, immunosuppression), mechanical or functional ureteral or bladder outlet obstruction, including stones, and chronic catheterization are predisposed. Hematogenous route of infection accounts for 15% of cases. May occur at any age, with marked female prevalence.


Acute focal pyelonephritis is also referred to as renal phlegmon.


Emphysematous pyelonephritis( Fig. 27.64 ) is a life-threatening necrotizing infection usually in diabetics. Mottled areas of gas extending radially along the pyramids are diagnostic. Gas may also be found in the perinephric and retroperitoneal space and occasionally the renal veins.


Chronic atrophic pyelonephritis is usually associated with vesicoureteral reflux. Calyceal dilation with overlying cortical scarring, preferentially located in the polar regions, is characteristic.


Xanthogranulomatous pyelonephritis


Fig. 27.65


Diffuse or, much less commonly, focal renal enlargement with poor or no contrast excretion (global or focal). Solitary or multiple nonenhancing masses with lobulated contours and frequent extension into the perinephric space and occasionally adjacent organs are a typical presentation. A large central calculus and a pyonephrotic collecting system that may be distorted or partially replaced by the inflammatory masses are characteristically present.


Chronic suppurative granulomatous infection in a chronically obstructed kidney (usually due to nephrourolithiasis), occasionally by stricture or tumor. Most cases are associated with Proteus infections. All ages are affected (peak: fourth to fifth decade), with a 3:1 female predominance. Involvement may be diffuse (90%) or focal (tumefactive form).


Renal trauma


Fig. 27.66


Fig. 27.67


Fig. 27.68


Intrarenal (renal contusion): Focal area of decreased nephrogram with poor opacification of corresponding calyces.


Subcapsular: Lenticular defect with flattening of the adjacent renal parenchyma. On precontrast scan, the hematoma is usually hypodense, but immediately after injury, occasionally a higher density than the surrounding kidney may be found. After contrast administration, the density of the nonenhancing hematoma is always markedly decreased compared with the normal renal parenchyma.


Renal biopsies, extracorporeal shock-wave lithotripsy, and trauma are common causes. Spontaneous hematomas in the absence of bleeding diathesis should raise suspicion of an underlying malignancy or an angiomyolipoma.


Classification of renal trauma:


1. Limited to renal parenchyma: renal contusion or subcapsular hematoma without disruption of calyceal system and renal capsule.


2. Complete laceration or renal fracture with involvement of renal capsule and/or calyceal system.


3. Shattered kidney (multiple separate renal fragments) or injury to the renal vascular pedicle.


Renal infarction


Fig. 27.69


Fig. 27.70


Regional: Peripheral wedge-shaped areas of decreased density, typically between calyces and most obvious after contrast administration.


Total (renal artery occlusion): After contrast enhancement, a thin subcapsular rim of high density caused by capsular collaterals to the outer cortex surrounds a central zone of diminished density.


Caused by trauma (avulsion of the renal artery), embolism, thrombosis, and renal vein thrombosis. The latter is diagnosed by an enlarged renal vein containing a filling defect on enhanced CT scans. An exaggerated and prolonged corticomedullary differentiation may be evident in the acute stage.


Arteriovenous malformation (AVM)


Fig. 27.71


Well-defined intrarenal mass lesion with attenuation values similar to the aorta or IVC before and after contrast administration. Large feeding and draining vessels are also characteristic. Curvilinear calcifications are rare.


Congenital or acquired (trauma, biopsy, spontaneous rupture of an aneurysm, very vascular malignant neoplasm).


Intrarenal aneurysm or pseudoaneurysm of the renal artery may present similarly except for the absent feeding and draining vessels.

Fig. 27.11 Horseshoe kidney. The lower poles of both kidneys are fused by a parenchymal isthmus, with the renal pelves and ureters being situated anteriorly.
Fig. 27.12 Pelvic kidney. The enlarged kidney is located between the sacrum and urinary bladder.
Fig. 27.13a, b Crossed renal ectopy. Axial (a) and coronal (b) views showing a malpositioned left kidney located on the right side that is partially fused with the right kidney.
Fig. 27.14 Displaced right kidney by large retroperitoneal abscess. The right kidney is rotated and displaced medially by a large right retroperitoneal abscess containing a long air–fluid level.
Fig. 27.15 Supernumerary kidney. Two kidneys are seen on the right side, one on the left side. All three kidneys are functioning normally. Differential diagnosis: renal duplication where either the upper or lower pole moiety is malfunctioning.
Fig. 27.16 Renal sinus lipomatosis. Enlarged fatty areas are seen in both renal hila, especially on the left side. Note tiny punctate calcifications bilaterally in the area of the renal papillae due to hyperparathyroidism.
Fig. 27.17a, b Hydronephrosis (two cases). A large cystic area is evident in the right renal hilum caused by a ureteral pelvic junction (UPJ) obstruction (a). A dilated collecting system (arrow) of the left kidney with persistent dense nephrogram and delayed contrast excretion is characteristic (b). The hydronephrosis is caused by a large and partially thrombosed abdominal aortic aneurysm projecting anterior to the lumbar vertebra.
Fig. 27.18 Hydronephrosis in horseshoe kidney. A hydronephrosis (arrow) is seen on the right side of a horseshoe kidney evident by the medially oriented long renal axis and the anteriorly located renal pelvis.
Fig. 27.19 Renal cyst. A renal cyst (arrow) with a precontrast density similar to the adjacent renal parenchyma is seen.
Fig. 27.20 Renal cyst. A sharply delineated, homogeneous lesion of near-water density is seen within the left kidney following intravenous contrast material administration.
Fig. 27.21 Ruptured renal cyst. A large right renal cyst with poor definition on its superolateral border and obliteration of the adipose tissue in the adjacent perirenal space is seen.
Fig. 27.22 Adult polycystic kidney disease. Bilateral enlarged kidneys with multiple cysts are seen.
Fig. 27.23 Adult polycystic kidney disease. Bilateral enlarged kidneys with multiple cysts are seen. Note multiple hepatic cysts and a suggestion of small pancreatic cysts.
Fig. 27.24 Multicystic dysplastic kidney. A multiloculated cystic mass without functional renal parenchyma is apparent in the pelvis.
Fig. 27.25 Multilocular cystic nephroma. A large multiloculated mass is evident in the inferior pole of the left kidney.
Fig. 27.26 Multilocular cystic nephroma. Large septated cystic mass originating from the right kidney (arrow) occupies over half of the abdominal cavity at this level.
Fig. 27.27 Medullary cystic disease. Shrunken kidney with small cysts is seen. Findings were identical on the contralateral side.
Fig. 27.28 Acquired cystic disease of dialysis. Bilateral small kidneys with tiny cysts and a small renal cell carcinoma (arrow) in the posterior aspect of the right kidney are evident.
Fig. 27.29a, b Von Hippel–Lindau disease (two cases). Multiple bilateral cystic and solid mass lesions in slightly enlarged bilateral kidneys are seen in both patients.
Fig. 27.30 Renal pseudotumor (column of Bertin). Hypertrophy of the septal cortex (arrow) simulates an intrarenal mass lesion on urography by causing an extrinsic filling defect on the collecting system.
Fig. 27.31 Renal adenoma. A small hypodense lesion is seen in the renal cortex after contrast enhancement. On the precontrast scan, the lesion was isodense with the adjacent renal parenchyma and therefore not appreciated.
Fig. 27.32 Oncocytoma. A large solid mass with less enhancement than the adjacent renal parenchyma is seen originating from the medial aspect of the left kidney.
Fig. 27.33 Angiomyolipoma. A small, fatty lesion (arrow) is seen in the lateral aspect of the right kidney.
Fig. 27.34 Angiomyolipoma. A large, predominantly fatty lesion with mild enhancement of the nonfatty components is seen on the posterolateral aspect of the right kidney.
Fig. 27.35 Angiomyolipoma. A large, well-defined mass containing fatty foci and scattered calcifications are seen. Calcifications are rare in this condition (only 6% of cases).
Fig. 27.36 Hemorrhagic angiomyolipoma. Spontaneous rupture of an angiomyolipoma is a frequent complication resulting in a large complex renal mass with extension into the perirenal and pararenal space, as seen here on the left side.
Fig. 27.37 Tuberous sclerosis. Bilaterally enlarged and deformed kidneys containing large inhomogeneous tumor masses (angiomyolipomas) with fatty components are characteristic.
Fig. 27.38 Tuberous sclerosis. Bilateral large and deformed kidneys containing huge angiomyolipomas with considerable fatty components are seen. Note the small hamartoma in the liver (arrow).
Fig. 27.39 Renal cell carcinoma. An inhomogeneously enhancing mass is seen in the posterolateral aspect of the right kidney (arrow).
Fig. 27.40 Renal cell carcinoma. Large renal mass with hypodense areas due to tumor necrosis is evident.
Fig. 27.41 Renal cell carcinoma. A large mass with inhomogeneous enhancement is seen in the left kidney. The tumor extends into the left renal vein (arrow), which is focally enlarged and depicts filling defects.
Fig. 27.42 Renal cell carcinoma. A well-defined homogeneous lesion with minimal enhancement is seen in the lateral aspect of the left kidney, mimicking a renal cyst.
Fig. 27.43 Renal medullary carcinoma. A large right renal mass with multiple liver metastases is seen.
Fig. 27.44 Collecting duct carcinoma (Bellini). A renal mass (arrows) originating in the renal medulla and isodense to the normal renal parenchyma on this precontrast scan is seen in the left kidney.
Fig. 27.45 Transitional cell carcinoma. A large, hypodense mass is shown in the area of the renal hilum.
Fig. 27.46 Transitional cell carcinoma. A large, poorly enhancing mass lesion is seen in the left renal hilum.
Fig. 27.47 Wilms tumor. A large, inhomogeneous mass originating from the right kidney is seen.
Fig. 27.48 Wilms tumor. A large, slightly inhomogeneous, hypodense left renal mass with peripheral calcification is seen.
Fig. 27.49 Mesoblastic nephroma. The soft tissue mass (arrows) in a neonate originates from the posteriorly displaced right kidney, with the contrasted collecting system seen as two white dots just anterior to the visualized right rib.
Fig. 27.50 Renal lymphoma. Bilateral enlarged kidneys with multiple hypodense lesions are evident in this postcontrast scan. Enlarged retroperitoneal lymph nodes are also seen.
Fig. 27.51 Non–Hodgkin lymphoma. A large, hypodense, homogeneous mass is seen in the retroperitoneum extending into the renal hilum.
Fig. 27.52 Burkitt lymphoma. A large right central renal mass that is poorly demarcated against the normal renal parenchyma is seen on this postcontrast examination.
Fig. 27.53 Leukemia. A poorly defined mass in the left kidney and small peripheral nodules in the cortex of the right kidney, giving it a somewhat striated appearance, are leukemic renal manifestations.
Fig. 27.54 Renal metastases. Three poorly defined, hypodense nodules are seen in the renal cortex (metastases from bronchogenic carcinoma).
Fig. 27.55 Renal metastases. Multiple hypodense lesions of different sizes are shown in the right kidney on this postcontrast scan (melanoma metastases).
Fig. 27.56 Renal metastasis. A solitary hypodense lesion is seen in the lateral aspect of the right kidney on this post-contrast scan (metastasis from a squamous cell carcinoma originating in the hypopharynx).
Fig. 27.57 Renal angiosarcoma. A huge hypodense renal mass is seen in the left kidney displacing its noninvolved small anterior portion (arrow) anteriorly.
Fig. 27.58 Renal rhabdomyosarcoma. An infiltrating hypodense mass causing enlargement of the left kidney encircles and angulates the left renal artery (arrow).
Fig. 27.59 Renal abscess. A large renal abscess in the posterior aspect of the right kidney is seen as a hypodense lesion extending into the perirenal and pararenal spaces and psoas muscle.
Fig. 27.60 Acute pyelonephritis. After contrast enhancement, linear, radially oriented, low-density areas are seen in the renal parenchyma bilaterally.
Fig. 27.61 Focal nephritis. A larger, poorly defined, hypodense area (arrow) is evident after contrast enhancement. The patchy, inhomogeneous enhancement of the enlarged remaining kidney indicates a more widespread pyelonephritic involvement.
Fig. 27.62 Pyelonephritis. A persistent striated nephrogram is seen in the enlarged right kidney.
Fig. 27.63 Pyelonephritis. Bilateral enlarged kidneys with a patchy to striated nephrogram are shown.
Fig. 27.64 Emphysematous pyelonephritis. An enlarged right kidney depicting extensive streaky to mottled gas collections throughout the renal parenchyma with extension into the perirenal space is seen.
Fig. 27.65 Xanthogranulomatous pyelonephritis. Diffuse renal enlargement with several hypodense masses and a large calculus (arrow) in the renal pelvis is seen.
Fig. 27.66 Renal fracture. Complete transection of the right kidney is seen.
Fig. 27.67 Renal trauma. Shown here is a shattered left kidney with a large surrounding hematoma extending into the perirenal and pararenal space.
Fig. 27.68 Large renal and pararenal hematoma in a ruptured angiomyolipoma. A ruptured kidney with a huge surrounding hematoma is seen. The angiomyolipoma is not appreciated on this image.
Fig. 27.69 Renal infarction. Nonperfusion of the lower half of the right kidney. A thrombus (arrow) in the enlarged nonopacified right renal artery is also evident.
Fig. 27.70 Renal infarction. Nonperfusion of the left infarcted kidney is seen.
Fig. 27.71 Renal artery aneurysm. A large right central renal mass enhancing immediately with the same intensity as the abdominal aorta is characteristic.








































Table 27.3 Focal lesions in the perinephric space

Disease


CT Findings


Comments


Urinoma


Fig. 27.72


Localized or diffuse cystic lesion of low density with attenuation values ranging from −10 to +20 HU. Contrast extravasation into the fluid collection may be evident on late enhanced images. Long-standing urinomas may have well-defined walls. Large urinomas may dissect along tissue planes into the pelvis.


Usually associated with urinary tract obstruction, renal trauma, or iatrogenic interventions, although nonobstructive infectious and spontaneous urinomas occur.


Lymphocele


Homogeneous cystic, occasionally septated lesion with CT appearance similar to urinoma.


Develops usually 2 weeks or more after lymph node dissection or renal surgery.


Lipoma and fibroma


Small, homogeneous, well-circumscribed mass lesions originating from the renal capsule or fascia or perinephric fat.


Usually incidental findings. Benign mesenchymal tumors are even rarer than their malignant counterparts.


Liposarcoma


Variable appearance ranging from a soft tissue mass with only little adipose tissue (poorly differentiated liposarcoma) to a predominantly fatty, somewhat heterogeneous mass with irregularly thickened linear or nodular septa (well-differentiated liposarcoma) or a cystic lesion (myxoid liposarcoma). Larger tumors tend to displace rather than invade the renal parenchyma and have a smooth interface. Contrast enhancement is variable but tends to be poor.


Most common mesenchymal sarcoma originating from the perinephric fat or renal capsule and fascia. Other rare primary perinephric malignancies are malignant fibrous histiocytomas, leiomyosarcoma, and angiosarcoma.


Metastases and lymphoma


Fig. 27.73


Findings depend on histology of the primary lesion and mode of tumor spread.


Direct extension or local metastases from primary renal, adrenal, and retroperitoneal malignancies. Rarely hematogenous or lymphangitic spread from more distant organs.


Abscess


Fig. 27.74


Fig. 27.75


Fig. 27.76


Low-density mass, often with thick, irregular walls, that may enhance. Inflammatory (edematous) changes surrounding the lesion are common. Thickened renal fascia and perinephric strands may also be associated. Gas presenting as bubbles or air–fluid levels within the lesion is virtually diagnostic but only rarely present.


Usually an extension of underlying renal disease, especially a concomitant renal abscess. Diabetes mellitus and uronephrolithiasis are common predisposing factors. Other inflammatory conditions, such as pancreatitis, diverticulitis, and appendicitis, may spread into the perinephric space.


Hematoma


Fig. 27.77


Fig. 27.78


Well- (hemorrhagic cyst) to poorly defined, often inhomogeneous mass lesion that may displace the adjacent kidney. CT densities range from 80 HU (acute) to 20 HU (chronic). Rarely, a fluid–fluid level is evident, caused by the settling of cellular elements within the hematoma (hematocrit effect). No enhancement on the postcontrast scan unless acutely bleeding.


Traumatic etiologies include blunt or penetrating trauma, renal biopsy, percutaneous nephrostomy and nephrolithotomy, and extracorporeal shock-wave lithotripsy. Spontaneous (nontraumatic) etiologies include nephritis, arthritis, lupus, polyarteritis nodosa, acquired cystic disease of dialysis, renal tumors, blood dyscrasia, anticoagulation therapy, and aneurysms of the renal artery and abdominal aorta.

Fig. 27.72 Urinoma. A large, homogeneous fluid collection is seen extending from the ruptured right kidney into the perirenal and pararenal space.
Fig. 27.73 Renal cell carcinoma with local extension. A right renal cell carcinoma (R) with extension into the pararenal space (arrows), liver, and inferior vena cava (arrowheads) is seen.
Fig. 27.74 Posterior perirenal and pararenal abscess. A hypodense mass is shown in the posterior renal fossa displacing the right kidney (arrow) anteriorly.
Fig. 27.75 Anterior perirenal and pararenal abscess. A hypodense area (long arrows) is seen anterolateral to the enlarged kidney affected by xanthogranulomatous pyelonephritis. The abscess extends into the duodenum, resulting in a renoduodenal fistula containing small air bubbles (short arrows).
Fig. 27.76 Psoas abscess. A cystic mass is evident in the right psoas muscle.
Fig. 27.77 Perirenal and pararenal hematoma. A ruptured (shattered) right kidney with large surrounding hematoma extending into the perirenal and pararenal space is seen.
Fig. 27.78 Renal hematoma with perirenal and pararenal extension. A large intrarenal hematoma with hematocrit fluid level (arrows) secondary to a ruptured angiomyolipoma evident by its fatty components is seen. The soft tissue stranding in the peri-renal and pararenal fat indicates extension of the hematoma into these spaces.

Only gold members can continue reading. Log In or Register to continue

Jul 6, 2020 | Posted by in GENERAL RADIOLOGY | Comments Off on 27 Kidneys
Premium Wordpress Themes by UFO Themes