The genitourinary system

Kidney and urinary tract

 

Anatomy

Kidney
The kidneys (Fig. 13) are located in the retroperitoneum and measure approximately 12 cm (height), 6 cm (width) and 4-5 cm (depth). The renal surfaces are usually smooth, but fetallobulation may persist for life. The kidneys move with respiration; the cranio-caudal excursion may be as much as 10 cm. The renal pelvis is normally within the confines of the kidney, but it may also be extrarenal. The size of the pelvis depends in part on the state of hydration. At ultrasonography the parenchyma is echopoor whereas the renal pelvis and the surrounding sinus tissue (mostly fat) is echorich. The arcuate vessels when seen mark the location

	Figure 14. Relations of a transplant kidney. The graft artery may also be anastomosed end to end to the internal iliac artery.
	Figure 15. Enhanced CT of a normal renal transplant in the right iliac fossa.

of the cortico-medullary junction. At CT it is not possible to distinguish between cortex and medulla on unenhanced exposures, whereas on images taken during the first 60 seconds after the contrast medium has reached the kidney there is a clear demarcation between medulla and cortex; during the excretion phase the attenuation of the two areas is again the same. On T2-weighted MRI the renal parenchyma is bright whereas the medulla has lower signal intensity than the cortex on unenhanced T1 weighted images.

The transplanted kidney

The transplanted kidney does not differ from the kidney in situ with one exception: the location. Normally the graft artery is anastomosed end-to-end to the internal iliac artery or end-to-side to the external iliac artery (Fig. 14). The graft vein is anastomosed to the external iliac vein. It is placed in either the right or left iliac fossa just beneath the skin. Often only the upper two-third is covered by peritoneum. Its location just beneath the skin makes the allograft quite suitable for ultrasonographic examination whereas the underlying iliac bones are an obstacle to good urographic visualization. The location just under the skin makes is possible to differentiate between medulla and cortex at ultrasonography; the medulla is slightly less echogenic than the cortex. Its presentation at CT and MRI is similar to that of kidneys in situ (Fig. 15).

Ureter
The ureters course along the psoasmuscles from the renal pelvis, pass over the common iliac vessels, and enter the bladder deep in the bony pelvis dorsolaterally. Visualization of the normal ureter requires in the majority of patients intraluminal contrast.

Bladder
The urinary bladder is best examined when it is full, at which time it fills the anterior part of the pelvis. The top of a filled bladder may extend into the abdomen. Normally the bladder contains between 200 and 500 ml. The bladder wall is thicker in men than women and decreases from 2 cm to 2 mm during filling. In males the bladder is located ventral to the anterior wall of the rectum with the seminal vesicles posterior. The outlet of the bladder (e.g. neck) is separated -from the membranous urethra by the prostate. In females the uterus and vagina are located behind and underneath the bladder and the urethra, whereas the salpinges and the ovaries are located supero-laterally to the empty bladder. The upper one third of the bladder is intraperitoneal.

Urethra
The male urethra (Fig. 16) consists of four parts: pars prostatica in which the ejaculatory ducts empty on either side of the posteriorly located verumontanum; pars membranacea, the shortest part, is the part of the urethra, which transverses the urogenital diaphragm, and is followed by pars bulbosa and pars pendula. Taken together the prostatic and membranous parts are defined as the posterior urethra while the bulbous and pendular portions are known as the anterior urethra.
The female urethra is 2 to 3 cm in length and is located anterior to the vagina. It is surrounded by the internal and the external sphincter.

Physiology

The kidney has several functions including excretion of metabolic pro ducts and foreign substances ("waste products"), regulation of body fluid osmolality and volume, regulation of electrolyte balance, regulation of

Figure 16.Diagram of the male urethra and genitals.

Figure 17. The nephron. The kidney is divided into cortex, medulla and papilla. The blood enters the glomerulus (G) through the afferent arteriole and leaves for the vasa recta (VR) through the efferent arteriole. The filtered component passes through PCT (proximal convoluted tubule), PST (proximal straight tubule), tDL (thin descending limb of the loop of Henle), tAL (thin ascending limb of the loop of Henle), TAL (thick ascending limb of the loop of Henle), DCT (distal convoluted tubule), CCD (cortical collecting duct), MCD (medullary collecting duct), PCD (papillary collecting duet) and out into the calyx.

acid-base balance, and production and secretion of hormones, The kidney forms concentrated urine as a mechanism for relieving the body of waste materials (Fig, 17). This is accomplished by filtration of the blood at the glomerulus, resulting in a protein-free ultrafiltrate of plasma. The kidneys are perfused by one-fourth of the cardiac output, resulting in a renal blood flow of 1,250 ml per min. The glomerular filtrate averages 125 ml per min, which then through reabsorption of water is reduced to the normal urine output of about l ml per min. Approximately two-thirds of the ultrafiltrate volume is reabsorbed by the proximal tubule by a process linked to the active secretion of hydrogen ions and the active reabsorption of sodium, glucose, amino acids, and other solutes ("obligatory" reabsorption). Isotonicity of the fluid in the proximal tubule with the plasma is maintained as the cells of the proximal tubule are freely permeable to water. The counter-current multiplier system of the loop of HenIe then acts to create a high solute concentration in the medulla by active transport of sodium out of the ascending limb of the loop, resulting in a high osmotic gradient between the medulla and the collecting ducts descending through it. The cells in the descending limb have a high permeability for water, whereas the cells in the ascending limb are impermeable to water. The gradient, in conjunction with antidiuretic hormone secreted by the posterior lobe of the pituitary, allows water to diffuse from the collecting ducts into the medulla and results in a concentrated - so called mature - urine. From the collecting ducts the final 15 % of water absorption is achieved (“facultative” reabsorption). Body acid-base balance is maintained by the ability of the kidney to secrete hydrogen by the formation of titrable acid and excretion of ammonium and its ability to reabsorb bicarbonate selectively in exchange for hydrogen. The kidney is also instrumental in erythropoiesis, being the chief site of either the activation or production of erythropoietin. It also produces renin and 1,25-dihydroxyvitamin D3' Parathyroid hormone also acts on the distal tubule to conserve calcium.

After formation by the kidney, urine is delivered to the bladder by the collecting system and ureter. The calyces function independently and asynchronously in transmitting urine to the renal pelvis. While the location of a pacemaker for coordinated peristalsis is not precisely known, it is felt that the first propagating wave begins in response to urine distending the renal pelvis, although in some kidneys the activity can originate in the upper infundibulum. This wave then passes down the ureter in a coordinated fashion via an electrical impulse that passes through connecting smooth muscle cells in the ureteral wall. As one segment of the ureter contracts to propel the urine bolus caudad, another immediately below relaxes to accept the bolus, this sequence repeating until the bolus reaches the bladder into which it is expelled as a jet (Fig. 18). Peristaltic waves are inhibited as pressure in the bladder rises and by ureteral distension.

Figure 18. CT of the bladder demonstrating a jet (arrow) of contrast medium entering the bladder from the ureter (arrowhead).

The micturition reflex are is parasympathetic and derived from the second through fourth sacral cord segments. The external sphincter has a somatic innervation. Receptors in the bladder wall initiate the micturition reflex via afferent fibers in the arc in response to bladder distention. This voiding reflex can then be inhibited or facilitated by activity originating in the cerebral cortex and extending down the spinal cord to the sacral level. During voiding, the bladder detrusor contracts and actively funnels the bladder neck; the sphincters surrounding the membranous urethra then relax, allowing complete expulsion of the bladder content. Between voiding, the intravesical pressure normally remains at a low level because of the reflex arc by the inhibitory effect of the central nervous system as well as the elastic properties of the bladder smooth muscle. Urinary continence is maintained by the internal and intrinsic sphincters combined.

Pathology

Prerenal pathology
The kidneys are commonly affected by disorders of the aorta, renal arteries, and renal veins. Hypertension is a frequent concomitant of renal artery disease - both as a cause and as an effect. Disorders that affect the renal artery and its major branches include atherosclerosis, fibromuscular

	Figure 19.Arteriosclerosis. Arteriogram demonstrating arteriosclerosis in the lower abdominal aorta and a stenosis (arrow) of the left renal artery dose to the aorta.
	Figure 20. Fibromuscular dysplasia. Arteriogram demonstrating several narrowings in the right renal artery of a young woman.

hyperplasia, arteritis, neurofibromatosis, aneurysms, arteriovenous malformations, embolic disease, and thrombosis.

Renal artery stenosis
In atherosclerosis deposition of lipid material on the intimal surface leads to a secondary reaction within the intima. Arteriosclerosis is primarily a problem of the elderly (Fig. 19). Fibromuscular hyperplasia is term that encompasses several' disorders characterized by multiple fibrosing lesions in main and segmental vessels. It typically occurs in young females (Fig. 20). Among the protean manifestations of neurofibromatosis are renal artery stenosis and renovascular hypertension. Two characteristic lesions are seen in patients with neurofibromatosis: 1) stenosis of one or both renal arteries, and 2) unilateral or bilateral aneurysms in the renal artery or its branches. The aorta and renal arteries may be involved in inflammatory processes that result in marked narrowing. One such disorder, Takayasu's arteritis, occurs most frequently in young females.

Hypertension
Hypertension is reported to affect from 7% to 20% of the adult population. An exact prevalence is, however, unknown, mainly because of differences in the study populations and the diagnostic criteria. Among the rare secondary causes of hypertension renovascular disorder is the most frequent. The prevalence depends not only on the source of the study population but also on the definition of hypertension in that population and on its severity. The prevalence of renovascular hypertension in a hypertensive population with diastolic pressure between 90 and 104 mmHg is probably less than 1%, whereas in a population with a diastolic pressure above 125 mmHg the prevalence is reported to about 30%. With such a low prevalence in the largest group of patients, screening of all hypertensive patients for renovascular hypertension with either scintigraphy, intravenous urography, or digital angiography is not advisable owing to the low number of true positives, the cost and the unacceptably high false-positive rate. Before the patient is referred for an imaging examination, some selection must take place. Patients with a diastolic pressure above 110 mm Hg, young patients, those with a sudden rise in blood pressure independent of age, and patients with a poor response to therapy should be examined further. The captopril-enalpril renogram appears to be the most cost-effective procedure for screening those patients. Understanding the effects of angiotensin-converting enzyme inhibition on the kidney distal to a stenosis and appreciating the potential effect of sodium balance or antihypertensive medications are crucial in anticipating the putative changes in the radionuclide studies of the renovascular bed following angiotensin-converting enzyme inhibition (Fig. 21).

 

Figure 21. The effect of angiotensin converting enzyme inhibition on glomerular perfusion and filtration rate in renal artery stenoses.

Normally, renin secretion is stimulated by extracellular fluid volume contraction, reduced pressure in the baroreceptor of the afferent arteriole, diminished sodium delivery to the macula densa, and influence of cathecholamines or prostaglandins. A negative feed back loop also exists such that angiotensin II itself, reduces the production of renin. Renovascular hypertension appears to be dependent on renin secretion from the juxtaglomerular apparatus from the underperfused stenotic kidney and is partially maintained by participation of the contralateral kidney, which demonstrates an abnormal pressure-natriuresis relationship in which a new set-point of sodium homeostasis is attained at a higher level of arterial pressure. Angiotensin-converting enzyme inhibition acts to interrupt the renin-angiotensin-aldosterone system pathway by preventing the conversion of the decapeptide angiotensin I to the octapeptide angiotensin II such that both the vasoconstrictor-hemodynamic and aldosterone-stimulating effects of angiotensin II are blocked. Hence, angiotensin-converting enzyme inhibition acts as a pharmacological probe for investigating the role of angiotensin II in the pathophysiology of renovascular hypertension. In addition, the converting enzyme also serves to degrade vasodilatory prostaglandins and bradykinins, such that enzyme inhibition may result in the enhancement of the tissue levels of these vasodilatory substances. The rationale for captopril- and enalpril-stimulated radionuclide

Figure 22. Captopril scintigraphy. a) Without captopril. b) With captopril. Captopril abolishes the uptake of99mTc DMSA in the right kidney (arrowheads) (PA-image) causing so-called medical nephrectomy. Subsequent angiography showed a stenosis of the right renal artery.

studies is that the angiotensin-converting enzyme inhibitor removes the angiotensin Il -dependent efferent arteriolar resistance, which results in a reduction in transcapillary forces and, therefore, reduces renal function in the kidney distal to stenosis. When renal perfusion is reduced, as seen in patients with renal artery stenosis, the transcapillary pressures that maintain the forces to drive glomerular filtration are sustained by a preferential increase in efferent arteriolar resistance. The increased efferent arteriolar resistance is maintained via angiotensin Il. Captopril and enalpril act to block the formation of angiotensin Il and consequently remove postglomerular forces maintaining filtration; thus, the glomerular filtration rate of the affected kidney decreases. The decrement in individual kidney function may then be noninvasively assessed using conventional radionuclide studies (Fig. 22). The hippuran renogram after captopril or enalpril has been reported to be highly predictive of the blood pressure response to angioplasty or reconstructive surgery with a sensitivity of 96 % and specificity of 95 %. In the 1970's intravenous urography and simple renography were popular for screening a hypertensive patient, but these modalities are no longer used due to poor sensitivity and specificity. Doppler ultrasonography demonstrating hemodynamic changes may be useful in very experienced hands, but as a routine examination the sensitivity and specificity are less than that for captoprilenalpril renography. In some places central vein renin assay is used for the diagnosis of renal artery stenosis. The role of MR angiography is

Figure 23. Wedge-shaped photon deficient area in the left kidney due to an infarct demonstrated during 99mTc DMSA scintigram.

promising, but unsettled regarding screening. A major drawback is the expense. Conventional or digital radiographic angiography is still needed for definitive demonstration of the lesion. However, it should be kept in mind that only after correction of the stenosis is achieved and the blood pressure has become normal, can the diagnosis of renovascular hypertension be made with certainty.

Emboli and thrombi
Emboli or in situ thrombosis can result in acute obstruction of the renal artery or its branches. Failure to restore renal blood flow within a few hours after renal artery occlusion usually results in infarction and loss of function. Intravenous urography and nuclear medicine will show absent function or delayed function if the obstruction is incomplete (Fig. 23). A rim-like nephrogram ("cortical rim-sign") may be seen on enhanced CT or angiography due to collateral circulation. However the cortical rim sign may also be seen in renal vein obstruction, acute tubular necrosis (vasomotor nephropathy) and cortical necrosis. Ultrasonography is often normal in the acute stage; in the ensuing days the size decreases and the kidney becomes more echogenic. Both Doppler ultrasonography and angiography (Fig. 24) will show absence of flow.

Renal artery aneurysm
Renal artery aneurysm may impress the renal pelvis and mimic a parapelvic cyst on intravenous urography and ultrasonography. Color

Figure 24. Multiple infarcts in a transplanted kidney shown at arteriography. Estimated original outline of the graft (---).

Doppler ultrasonography, enhanced CT and angiography will confirm the diagnosis.

Renal arteriovenous fistula
A renal arteriovenous fistula may be congenital (arteriovenous malformation) or acquired. Causes of the latter include rupture of a renal artery aneurysm, blunt trauma, penetrating injuries (e.g. renal biopsy). The typical presenting sign are a bruit, hypertension, hematuria, and signs of high output congestive heart failure. Intravenous urography and ultrasonography are rarely helpful, although pyeloureteral "notching" from collaterals is sometimes noted on the urogram. Dynamic CT, nuclear medical angiography (first passage scintigraphy) and Doppler ultrasonography may be diagnostic. Selective renal arteriography is definitive and demonstrates early venous filling with dilatation of each feeding artery and draining vein. Embolization may be attempted at the time of angiography. MRI will demonstrate signal void on both T1-and T2-weighted spin-echo images due to fIowing blood, but MRA is much more sensitive and graphic, and the vascular images can be projected in any plane as well as in 3D.

Renal vein thrombosis
The patient with acute renal vein thrombosis typically presents with flank pain, hematuria, fever, and proteinuria. Signs of the nephrotic syndrome may appear in the subacute phase. Renal enlargement is detected by many imaging studies. Whether there is opacification at intravenous urography and accumulation of radioactivity on scintigrams depends on the degree of obstruction and the extent of collateral venous circulation, which is usually better in the left kidney. Intravenous urography and direct pyelography may show notching of the ureter by periureteric collaterals. CT may demonstrate a thrombus in the renal vein and/or inferior vena cava and perinephric venous engagement ("cobwebbing"). Ultrasonography will show nephromegaly and decreased echogenicity due to edema. Renal arteriography demonstrates prolongation of arterial and capillary flow, stretched vessels, a decreased nephrogram, and non-visualization of the renal vein. Clot visualization with renal phlebography is superior, but invasive procedures are no longer called for in renal vein thrombosis unless thrombolysis is attempted, which is unusual. At present, MRA is probably the most sensitive, accurate and best test, but lack of availability is a major drawback.

Renal pathology

Anomalies
Renal agenesis is often an incidental radiological finding. A major clue is the characteristic compensatory hypertrophy of the contralateral kidney. If this is lacking one should search for an ectopic kidney. A nonvisualizing kidney on urography caused by renal agenesis can be confirmed by ultrasound or CT. Ultrasonography can evaluate the renal fossae, but CT is more effective in evaluating the lower abdomen for a small ectopic kidney (Fig. 25). Renal anomalies, especially agenesis, are associated with a significant incidence of seminal vesicle anomalies, and in the female, with utero-vaginal anomalies. This should be kept in mind during ultrasonographic examination.

Fusion anomalies of the kidney are often asymptomatic. Intravenous urography will show the abnormal axis of fusion and delineate the ureters

	Figure 25. Normal sized ectopic kidney above os sacrum. The kidney is also rotated.
	Figure 26. Intravenous urography demonstrating crossed renal ectopy. The "left" kidney is located below the right kidney.

(Figs. 26 and 27). Horseshoe kidneys are recognized on ultrasonography by the extension across the spine. CT, MRI and scintigraphy readily identify both horseshoe kidneys and renal ectopy. Very graphic visualization is produced by arteriography (Fig. 28).

In renal dysplasia there is no kidney parenchyma, usually just a collection of cysts. Renal dysplasia is non-functional and thus not seen by urography or scintigraphy. Calcification in cyst walls is sometimes recognized on KUB, however. CT can identify the variation of renal dysplasia that does not display multicystic changes as a small mass of tissue in the renal fossa. Ultrasonography will show absence of a normal kidney and will identify a typical multicystic dysplastic kidney. There is no renal pelvis, but there may be a rudimentary ureter.

	Figure 27. A horseshoe kidney is easily demonstrated at intravenous urography. The renal axes intersect inferiorly.
	Figure 28. A horseshoe kidney is well outlined at digital subtraction angiography.
	Figure 29. Simple renal cyst. Ultrasonography reveals an anechoic cyst with dense echoes in the posterior wall. There is acoustic enhancement deep to the lesion.

Cysts
Simple cysts are the most common renal mass. They have been detected more readily since the advent of ultrasound and CT, and may be found in more than 50% of patients over the age of 50 years. The ultrasound criteria for a benign cyst include the absence of internal echoes, smooth, sharply defined walls and acoustic enhancement beyond the posterior wall proportional to the fluid content (Fig. 29). Refraction lines at the edges of the cyst are typical, as is the absence of flow on color Doppler ultrasonography. The CT criteria for a benign cyst include homogenous attenuation value near the density of water, imperceptible cyst wall, smooth interface with renal parenchyma, and lack of enhancement following intravenous contrast injection (Fig. 30). When these criteria are met, the diagnosis of a simple cyst is accurate in 93 % - 98 % of cases. In those cases not meeting the strict criteria for ultrasound or CT, needle aspiration or enhanced MRI should be considered to establish the final diagnosis (Fig. 31). MRI is extremely sensitive to vascularity and has detected small occult tumors in the wall of renal cysts. Unlike CT, it is not unusual to visualize cyst walls with MRI. Scintigrams obtained with a renal parenchymal agent such as 99mTc-glucoheptonate or 99mTc-dimercaptosuccinic acid demonstrate an area of absent activity that persists through the dynamic (blood pool) and static (parenchymal) phases.

Figure 30. Simple renal cyst in a left kidney demonstrated at enhanced CT. Homogenous low-attenuating process, which does not enhance after administration of intravenous contrast (apparent unsharpness at cyst-kidney interface is due to volume averaging).

Bleeding into a cyst produces a "hemorrhagic cyst" which may be difficult to differentiate from a renal carcinoma on imaging studies, although it is usually possible to do so.

Adult polycystic kidney disease
In adult polycystic kidney disease, which is inherited as an autosomal dominant condition, the cysts may occur anywhere along the nephron. Approximately 90% of patients have a positive family history. Cysts may be diagnosed by imaging from approximately the age of 20 years, while they are still asymptomatic. Ultrasonography demonstrating multiple cysts in a patient with positive family history is diagnostic. The patients often present with symptoms like pain, urinary tract infection, hematuria and hypertension most commonly in the fourth or fifth decade, although, rarely the cysts may be obvious at birth. The median age for end stage renal failure is in the late fifth decade. Cysts are easily detected by ultrasonography, CT and MRI using the criteria for cysts. Intravenous urography demonstrates enlarged kidneys with smooth or irregular contours (Fig. 32) and multiple radiolucensies on nephrotomography ("swiss-cheese"). The pyelocalyceal system is usually splayed and deformed by the multiple cysts. Bleeding into cysts occurs very often and are best diagnosed by MRI demonstrating cysts containing hemorrhagic fluid with mixed signal intensity and a fluid-level on both T1-weighted and T2-weighted sequences. Fine curvilinear calcifications - probably a residual of intracystic bleeding - can be diagnosed at CT (sometimes on KUB) and they do not signal malignancy (Fig. 33). The frequency and

a	Figure 31. Simple renal cysts demonstrated at MRI The patient had one cyst in each kidney. a) T1-weighted image. b) T2-weighted image. MRI clearly delineates renal cysts. On T1-weighted images the content is signal poor often with a clearly delineated wall, whereas on T2weighted images it is signal intensive, sometimes with edge enhancement.
b
	Figure 32. Adult autosomal dominant polyeystic kidney disease demonstrated at intravenous urography. Both kidneys are enlarged with irregular contours. The pyelocalyceal systems are splayed and deformed.
	Figure 33. Adult autosomal dominant polycystic kidney with multiple parenchymal calcifications on unenhanced CT. The patient is on replacement therapy due to end-stage renal failure.

number of calcifications increases with age. As many as 40-80% of all patients with adult polycystic kidney disease have hepatic cysts. In many cases the live r cysts may be larger and more numerous than the renal cysts. Also the frequency of detectable hepatic cysts increases with age of the patients. After the start of replacement therapy (dialysis or transplantation) the size of the polycystic kidneys decreases.

Medullary sponge kidney
Medullary sponge kidney ("tubular ectasia") is a sporadic disorder of developmental origin. The collecting ducts (Bellini) in the distal renal pyramids and papillae become dilated; small cysts which usually communicate with the collecting ducts and in which calculi frequently form, are occasionally se en in the medulla in the more severe cases. Medullary sponge kidney is usually bilateral but may be unilateral and/or segmental. It is often an incidental finding in intravenous urography. Plain films show clusters of small calculi in the distribution of the papillae or medulla. Intravenous urography is diagnostic and shows linear dilated collecting tubules ("streaks" or "brush" appearances), some of which contain calculi (Fig. 34). Neither ultrasonography, CT nor MRI add anything.

Acquired cystic disease
Acquired cystic disease refers to cystic formation in the cortex and medulla in patients with end-stage renal failure treated with intermittent hemodialysis. It is most frequently seen in patients with glomerulonephritis and the cysts often disappear when the patient receives a functioning

a	Figure 34. Medullary sponge kidney (tubular ectasia). a) Nephrogram. b) Excretory phase. lntravenous urography shows multiple distinct collections of contrast material in dilated papillary collecting ducts ("brush effect") and punctuate calcifications in the same locations.
b
	Figure 35.Acquired cystic disease. Enhanced T1 weighted MRI demonstrating solid lesion (arrow) anteriorly in the left kidney due an erythropoetin producing tumor. The parenchyma is signal poor; compare it with the image of a normal kidney obtained with the same TR/TE sequence shown in Fig.11. .
	Figure 36. Renal variants (pseudotumors), which may simulate a tumor

graft. Ultrasonography shows haphazardly dispersed small cysts, usually less than 3 cm in size, some with hemorrhage or calcification. The kidneys demonstrate increased echogenicity which is presumably due to the underlying renal parenchymal disease and may become very large. CT and MRI show small cysts scattered throughout the cortex and medulla. Contrast enhances non-cystic tissue on both CT and MRI (Fig. 35). Patients with acquired renal cystic disease are at risk for the development of renal cell carcinoma.

Pseudo tumor
One of the most common space-occupying lesions in the kidney is the hypertrophied column of Bertin, which is an infolding or double thickness of healthy renal cortex, most characteristically separating the superior from middle pole calices. Other so-called pseudotumors include the prominence of the lateral renal margin secondary to the splenic impression ("dromedary hump") and the hilar lip, which often occurs superior to the hilus, secondary to focal hypertrophied parenchyma (Fig. 36). Focal parenchymal hypertrophy adjacent to an area of scarring from previous inflammation is another cause for a pseudotumor. The diagnosis

Figure 37. Angiomyolipoma. CT without (upper row) and with (lower row) intravenous contrast medium applied and bone settings (left column) and soft tissue setting (right column) of window and level. The angiomyolipoma (arrows) had attenuation values similar to that of fat. At Ultrasonography it was hyperechoic.

is well established with renal scintigraphy showing normal accumulation of the tubular cell seeking 99mTc DMSA. CT and especially MRI can also be used for the diagnosis in indeterminate cases, whereas ultrasonography is usually of limited value.

Adenoma
Renal adenomas are slow-growing, solid parenchymal epithelial tumors that originate in mature tubular cells and are thought to be pre-malignant. Cystic areas and calcifications can occur. Lesions less than 3 cm are usually benign, but the final classification is based on histology and clinical behavior rather than on size.

Angiomyolipoma
Angiomyolipomas (hamartomas) contain varying amounts of smooth muscle, blood vessels and mature fat cells. Demonstration of fat by CT (Fig. 37) (negative attenuation values [-15 or lower]) or MRI (fat suppression sequence) within the tumor is nearly pathognomonic of it an angiomyolipoma, although there have been a few cases of fat-containing renal cell carcinoma. On the other hand some angiomyolipomas contain undetectable amounts of fat or have the fat masked by hemorrhage and are therefore not diagnosed until after removal. Sonography is non-specific and reveals a hyperechoic mass. Surgery is unneccesary in the vast majority of the cases.

Figure 38. Oncocytoma (arrowheads) in the left kidney at enhanced CT. Centrally a scar (arrow) was found. The findings are only suggestive of oncocytoma.

Oncocytoma
Oncocytomas are epithelial neoplasms believed to originate from the proximal collecting tubules. These tumors are characteristically benign, but due to their solid nature can not be definitely categorized as benign prior to surgery. A central scar demonstrated at ultrasonography, CT (Fig. 38) or MRI is suggestive of, but not pathognomonic. Because a renal cell carcinoma may mimic an oncocytoma completely, conservative surgery (i.e. partial nephrectomy) is rarely justified.

Renal ceil carcinoma
Renal cell carcinomas occur most commonly in the sixth decade and are often detected incidentally. Depending on the initial imaging study further evaluation by at least one other study is usually required. Symptoms, when present, are usually non specific; e.g. hematuria, flank pain and a palpable tumor may occur in adult polycystic kidney disease as well as in renal cell carcinoma. Intravenous urography typically shows renal enlargement with a well-circumscribed or occasionally irregular mass. Five% - ten% will show calcification, which if central or diffuse is extremely suspicious. The kidney is often rotated on its axis and/or displaced (Fig. 39). Tomograms obtained during the nephrogram phase show a lucent or inhomogenous mass whose interface with the adjacent renal parenchyma may be smooth or irregular. When the mass extends beyond the renal contour a thick or irregular wall can sometimes be discerned. CT, MRI and ultrasonography can all be used in establishing the nature of a renal mass more precisely. Demonstration of a solid mass is indicative of a renal cell carcinoma until another diagnosis has been proven. CT is excellent for both

	Figure 39. Renal cell carcinoma in the upper pole of the right kidney. The collecting system is displaced and the upper pole is occupied by a mass.
a	Figure 40. Renal cell carcinoma. a) Tumor in the lateroposterior part of the left kidney. b) Tumor in the anterior part of the right kidney slightly dislocating the liver. Both the contrast enhancing wall and the inhomogenous enhancement of the les ion exclude the possibility of a simple cyst.
b
	Figure 41. Recurrent renal cell carcinoma. The process (arrows) in the left renal bed does not enhance and its appearance is not reminiscent of any normal abdominal structure.
	Figure 42. Renal cell carcinoma. Mixed hyper- and hypoechoic mass (arrows) in the upper pole.

diagnosis and staging. The CT criteria for renal malignancy include heterogeneous tissue with an attenuation value near to that of renal parenchyma, contrast enhancement, irregular interface with surrounding parenchyma, and areas of calcification (Fig. 40). Secondary spread to regional lymph nodes and extension into the renal vein are clear signs of a malignant tumor. At most institutions CT is used as the primary modality to stag e renal carcinoma prior to treatment because of its diagnostic accuracy, and its ability to detect local extension, regional lymph node involvement, and distant metastases as well as to evaluate the contralateral kidney. CT is also best for evaluating the renal bed for recurrent tumor (Fig. 41). Ultrasonography can also be used for the diagnosis of a solid mass (i.e. sound absorption) and thereby exclude the presence of a cyst. Common ultrasonographic patterns are a hyperechoic somewhat

Figure 43. Renal cell carcinoma in the lower pole of the right kidney at MRl. T1-weighted image after application of intravenaus contrast - gadodiamide (Omniscan). There is central necroses.

attenuating mass (Fig. 42) and a complex mass containing echo-poor, relatively transsonic areas that represent foci of liquefaction necrosis. Ultrasonography may also be used for excluding a tumor in the opposite kidney and extension into the perinephric space. MRI demonstrates an inhomogenous, enhancing mass. The T1-weighted and T2-weighted signals vary with the composition of the tumor (Fig. 43). MRI appears to be the most sensitive and most accurate method of diagnosis in renal cell carcinoma and detecting venous extension. However, because of its expense, lack of universal availability and because CT and ultrasonography are also very accurate, it is usually reserved for special situations, i.e. patients with very complicated lesions, or those who can not receive iodinated contrast medium. Renal angiography is seldom necessary anymore for diagnosis.

Lymphoma
Imaging techniques demonstrate renal involvement in approximately one-third of patients with systemic lymphoma. Renal lymphoma can present as a mass, as multiple, unilateral or bilateral masses, as diffuse infiltration with renal enlargement or as infiltration into the sinus or the perinephric space. Retroperitoneal adenopathy is nearly always present. Leukemic and myelomatous infiltration causes renal enlargement.

Metastases
Metastases to the kidney are usually associated with primary neoplasms of the lung, breast, stomach, cervix, colon, and pancreas. Differentiation from a primary renal malignancy is sometimes suggested by the infiltrative, poorly defined pattern of metastases or bilaterality, but in general this differentiation is unreliable, and needle biopsy is required for diagnosis.

Infection
Acute pyelonephritis is usually caused by bacteruria resident in the gastrointestinal and genital tracts. Underlying systemic diseases and conditions of altered host resistance predispose to renal infection. Imaging studies are unnecessary in most adult patients with typical clinical signs who respond to medical therapy. If an imaging examination is indicated, ultrasonography is often preferred at the initial imaging procedure because of its ability to demonstrate calculi, hydronephrosis, intrarenal or perinephric abscesses. Subtle parenchymal changes associated with infection, as well as extrarenal spread, are more consistently demonstrated by CT than by ultrasonography and include patchy area of underperfusion, small, dense nephrographic foci and perinephric edema. 99mTc-glucoheptonate or 99mTc dimercaptosuccinic acid scintigraphy is also useful, because localized infections appear as focal defects, often before they can be seen with CT or ultrasonography. Hydronephrosis and ureteral obstruction is demonstrated on delayed images.

Emphysematous pyelonephritis is a very serious condition which is due to extensive necrosis and gas formation caused by gram-negative organisms. Gas in the renal parenchyma (and sometimes in the perinephric space and in the pyelocalyceal system) may be seen on plain film or CT. Ultrasonography show increased echogenicity with blurred acoustic shadowing due to reverberations of sound in the gas medium. Intrarenal gas is readily seen on CT scans.

Severe pyelonephritis, if inadequately treated or unresponsive to antibiotics may lead to the formation of a chronic occult infection or a renal abscess. Intravenous urographic findings include obliteration of the ipsilateral psoas stripe, diffuse enlargement or a focal mass, and deformity of the pyelocalyceal system. Ultrasonographically, a renal abscess appears as hypoechoic or anechoic mass with fluid- fluid (or fluid-debris) level and distal acoustic enhancement. The wall may appear as an echogenic rim. Unenhanced CT scans show low attenuation within the abscess cavity. The wall enhances, but the centre does not. The findings at MRI are similar. Pus is signal intensive on T1-weighted and

	Figure 44. Bilateral reflux nephropathy. Clubbed calyces with overlying reduction of parenchyma in a 17 year old female with increasing serum-creatinine and hypertension.
	Figure 45. Right-sided reflux nephropathy. 99mTc DMSA scintigraphy is more sensitive than intravenous urography for depicting scars or active parenchymal disease since it only mirrors active tubular cells. Oblique views are of great importance for the detection of small scars.

T2-weighted images. A perinephric abscess has similar imaging features, but its location is extrarenal.

Chronic pyelonephritis is an interstitial, nonsuppurative nephritis. The inflammatory process originates in the medulla from retrograde ascent or in the cortex from antegrade or blood-borne infection and involves the pyramids, the cortex, or both, producing cortical scars and calyceal deformities. It rarely occurs in patients with a normal urinary tract. It may be due to vesico-ureteral reflux (reflux nephropathy - a residual of intrarenal reflux in infancy), obstruction, sickle cell disease and analgesics. Urographic findings include unilateral or bilateral small kidneys. In reflux nephropathy calyceal clubbing, and adjacent cortical scarring is found (Fig. 44). Intravenous urography often underestimates the extent of renal scarring compared to renal scintigraphy (Fig. 45). In obstructive nephropathy the whole kidney is involved. Ultrasonography shows focal parenchymal atrophy and areas of fibrosis. CT demonstrates scarring with irregular renal margins.

Xanthogranulomatous pyelonephritis is a complication of chronic inflammation that is believed to represent an inadequate acute inflammatory response in an obstructed, infected, and ischemic kidney. The renal parenchyma is replaced by yellow tumor-like masses containing lipidladen histiocytes. In the diffuse form plain films commonly demonstrate a radiopaque staghorn calculus in an enlarged kidney. Intravenous urography shows an absent or decreased nephrogram and absent, decreased and/or delayed opacfication of the pyelocalyceal system. Ultrasonography demonstrates renal enlargement with parenchymal replacement by multiple anechoic or hypoechoic masses surrounding the pyelocalyceal system, which usually contains stones. Pyonephrosis may be present. CT shows an enlarged kidney with a contracted renal pelvis which usually contains a staghorn calculus and replacement of renal sinus fat by fibrosis. The parenchyma is replaced by low-attenuation masses representing xanthoma, cavities, and dilated calyces. Extrarenal extension into the perinephric and paranephric spaces, psoas muscle, and adjacent viscera is commonly present. In about 10 to 20 % of cases xanthogranulomatous pyelonephritis is segmental. A proteus organism is usually found in the urine.

Renal tuberculosis is usually secondary to hematogenous spread from a pulmonary focus. Although gross morphologic changes are typically more severe in one kidney, microscopic lesions are invariably present in both. Progressive disease is associated with tuberculoma formation and antegrade destruction of the medulla, pyramids, and papillae with cavities. Healing of these lesions is accompanied by interstitial fibrosis, parenchymal calcification, cortical scarring, stricturing of infundibula and calyces, and hydronephrosis. Extrarenal extension (e.g. perinephric or psoas abscess and fistulas to small intestine or colon) is not uncommon. The findings on plain films, intravenous urography and pyelography reflect the bilateral, but asymmetric distribution of active renal infection and sequelae of healing (Fig. 46). These include absent, decreased or delayed excretion of contrast material, localized caliectasies with minor irregularity of the calyces, papillary necrosis with irregular or moth-eaten calyces and occasional filling of adjacent medullary parenchymal abscesses, amputation of the tips of calyces and infundibula,

Figure 46. Tuberculosis. Retrograde pyelography was performed since no contrast medium was excreted during intravenous urography. Typical changes with medullary-papillary cavitation, moth-eaten calyces and pipe stem ureter.

hydronephrosis, a parenchymal mass or abscess that does not communicate with pyelocalyceal system, cortical scarring, linear, ring and/or amorphous parenchymal calcifications, and autonephrectomy resulting in an enlarged reniform sac filled with caseous material or an atrophic fibrotic calcified kidney. Imaging modalities otherthan intravenous urography and retrograde pyelography are non-specific in renal tuberculosis. Depending on the stage of the disease, the findings on ultrasonography and CT resemble those of papillary necrosis and xanthogranulomatous pyelonephritis. Involvement of the ureter bladder and/or internal genitalia is quite common in patients with renal tuberculosis. Alternating strictures and dilatation may give the ureter a "corkscrew" or "beaded" appearance. More extensive infiltration can produce a rigid "pipe stem" ureter (Fig. 46).

Papillary necrosis
Papillary necrosis is believed to be due to localized ischemia. It is especially frequent in diabetes mellitus and analgesic abusers. Less common associations include hypotension, renal vein thrombosis, obstruction, sickle cell disease, and sickle cell trait. Intravenous urography remains the best imaging modality for demonstrating the various stages of

Figure 47. Renal papillary necrosis due to analgesic abuse. Irregular calyces with central contrast defects (= necrotic papillae) and backflow of contrast into the collecting tubules (pyelotubular backflow). A necrotic papilla obstructs outflow from the renal pelvis.

 

Figure 48. Nephrocalcinosis secondary to Alport's disease. Chronic calcifications outlining the contracted kidneys.

papillary necrosis. The findings include decreased opacification of the affected calyces, contrast material surrounding the separated necrotic papilla - central separation produces a ring sign while marginal separation produces a claw sign - , a single contrast -filled cavity within a papilla, a convex irregular calyx which becomes a "blunt" calyx with healing, hydronephrosis due to obstruction of the ureter by necrotic tissue or a calculus, punctuate or ringshaped papillary calcification due to calcification of one or more necrotic papillae. Because of its relatively poor spatial resolution, ultrasonography is generally not diagnostic in the early stages of papillary necrosis. The resolution of CT and MRI is not great enough to show papillary changes, but retrograde pyelography can provide this information (Fig. 47), if the urogram is indeterminate.

Nephrocalcinosis
Nephrocalcinosis is a form of metastatic or dystrophic calcification in the renal parenchyma. It can be secondary to hypercalcemic and hypercalcuric states, hyperoxaluria, medullary sponge kidney cortical necrosis, adult polycystic kidney disease chronic nephrosclerosis and chronic glomerulonephritis (Fig. 48). CT is the best modality to diagnose tiny calcifications, whereas more gross calcifications may be seen on plain films. Calcifications within or close to the genito-urinary tract may have many causes (Fig. 49).

Medical disease
The kidney is involved in numerous pathologic conditions. Some like lupus erythromatosus are systemic, while others like glomerulonephritis are localized to the kidney. The so-called "medical" diseases of the kidney involve primarily the renal parenchyma as distinct from the collecting system and tend to be bilateral. The kidneys may be enlarged, normal in size, or small. Since many of these diseases resemble each other radiologically the role of imaging in patients with such renal disease and/or renal failure is not to make a specific histological diagnosis, but Figure 49. Etiology of calcifications within or dose to the genito-urinary tract on KUE.

	Figure 49. Etiology of calcification within or close to the genito-urinary tract on KUB.
	Figure 50. End-stage renal failure. Ultrasonogram demonstrating a small contracted kidney (arrows) with high echogenicity and loss of corticomedullary boundary.

to exclude surgical renal disease, namely, obstruction. A renal biopsy may in most cases be needed to establish a definitive diagnosis. The medical diseases include vasomotor nephropathy (formerly termed acute tubular necrosis), cortical necrosis, glomerulonephritis, Good pastures syndrome, periarteritis nodosa, sclerodermia, Wegener's granulomatosis, systemic lupus erythromatosus, acquired immune deficiency syndrome (AIDS), diabetes mellitus, sickle cell disease, amyloidosis, multiple myeloma, hemophilia, and radiation nephritis. Every patient in renal failure should have a screening ultrasonography. Because ultrasonography of the kidney is independent of renal function, hydronephrosis can be excluded. However, up to 25 % of patients with hydronephrosis do not have underlying obstruction, and approximately 4% of patients with obstruction do not develop hydronephrosis due to a low glomerular filtration rate. Diuresis renography can not be used confirm or exclude the occurrence of obstruction in patients with a glomerular filtration below 10-15 ml/min x 1.73m2. The normal renal cortex is less echogenic than the liver or spleen. Most parenchymal disease are characterized sonographically by increased cortical echogenicity with general preservation of corticomedullary boundaries, but these may be lost in severe cases (Fig. 50). Iodinated contrast media (urography, CT, angiography) should be avoided in patients with diminished renal function, since contrast agents may further depress the renal function. MRI may be helpful in the future, but it is too soon to be sure. Periarteritis nodosa is an exception for the limited use of imaging in medical diseases. Renal

Figure 51. 131I hippuran renography of renal transplants. The 5 min. images as well as the histogram show good uptake in and excretion from the graft in the right side, whereas there is only a very slow uptake in the left sided graft. The latter is undergoing chronic rejection, whereas the one in the right side has recently been transplanted.

angiography demonstrates microaneuryms and irregular arteries and areas of decreased perfusion distal to occluded vessels.

Transplantation
Renal transplantation has been a routine procedure at many institutions for three decades. The failing allograft can present a complex and confusing diagnostic problem. The clinical presentation of fever and tenderness of the renal graft is non-specific. Initially one will exclude any overt mechanical problem such as hydronephrosis, urinoma, lymphocele etc. that can be remedied by imaging-guided intervention or surgery. However, these complications cause less that 5 % of graft dysfunction. This is the reason why most attention is directed to the interplay of the interstitial processes causing the decrease in renal function, and why radionuclide studies, which can quantify perfusion and function, have assumed an important role in the management of renal transplants (Fig. 51). The most commonly adopted procedures are perfusion studies and renography. Nuclear medical examinations can with high certainty exclude pathology and should be the primary imaging tool for monitoring post-operative renal transplants. Ultrasonography can yield an anatomic record of the renal allograft, but except for Doppler imaging, no conclusions can be drawn about any aspect of renal function. Duplex and color Doppler imaging permit simultaneous evaluation of vascular flow from the main renal artery through the arcuate arteries. All other imaging is supplementary to nuclear medical examinations and ultrasonography in renal transplants. CT offer a significant anatomic imaging value because it can demonstrate the kidney and perinephric anatomy whereas ultrasonography cannot because of technical factors such as bowel loops, surgical sutures, osseous structures and so forth. MRI in evaluation of the allograft for parenchymal disease is an area of current interest. Only time will show whether it is valuable, but preliminary studies have indicated that MRI is able to give both information about perfusion and function, as does nuclear medical examinations, as well as very fine anatomic details.

Trauma
The kidney is the most frequently injured organ in blunt abdominal trauma. The choice of imaging depends on the patient's clinical condition, the severity of trauma and the possibility of multiple involvement. In a patient who presents with hematuria following relatively minor flank trauma it is appropriate to begin with an intravenous urography. In a moderately or severely injured patient - whenever possible - contrast-enhanced CT should be the initial imaging procedure, since it depicts the extent of renal and perinephric injury and may demonstrate injuries of other abdominal viscera. Ultrasonography is not helpful in the acute situation and only causes the appropriate examination and treatment of a traumatized patient to be delayed. The usefulness of ultrasonography is limited because it is often impossible to perform properly due to the trauma (pain, ileus, wounds etc.). In the most severe injuries there may not be time for any pre-operative imaging.

Intravenous urography will demonstrate whether there are one or two functioning kidneys. A renal contusion or intrarenal hemorrhage appears as a localized decrease in intensity of the nephrogram or as an intrarenal mass with splaying of the collecting system. Extravasation of opacified urine indicates a lacerated collecting system, which is often associated with a serious parenchymal injury (but does not always mean surgery). It must be kept in mind that asymmetric opacification can be due to pre-existing disease. If the patients is in shock at time of injection, the kidneys may not opacify or there may be a persistent nephrogram without opacification of the collecting system. In a patient who has sustained relatively mild trauma and is clinically stable, further imaging is usually

Figure 52. Posttraumatic renal hematoma involving on the right kidney (probably sub-capsular). Upper level: No contrast has been administered. Lower level: after intravenous contrast medium administration. The attenuation value of the haematoma (arrows) is higher than of the renal parenchyma before administration of contrast medium but lower after contrast was given.

unnecessary if the intravenous urography is normal. On the other hand, abnormal intravenous urogram may warrant further evaluation by means of CT. Intrarenal and extrarenal hematomas (Fig. 52), disruption of the renal parenchyma, perfusion defect and extravasation of contrast laden urine or blood into the perinephric and paranephric spaces are readily demonstrated by CT. Leakage of urine implies laceration of the collecting system and/or renal parenchyma, which often is self-limited, but sometimes requires stenting or even open surgery. A locally decreased or striated nephrogram indicates local contusion. In some patients with renal pedicle injuries, only a rim of cortical tissue is opacified. This indicates occlusion of the renal artery and perfusion through collaterals.

Postrenal pathology
Duplication of the renal collecting system is the most common urological anomaly and easily diagnosed on urography when renal function of both the upper and lower segments is preserved. When complete, reflux into the lower collecting system commonly occurs, and an ectopic ureter with or without associated ureterocele often obstructs the upper collecting system. Obstructed duplication may be suspected on the urogram when there is downward displacement of the lower calyces and an insufficient number of them, the so-called "drooping lily" sign. Ultrasound is a good method to demonstrate the dilated upper collecting segment, which is seen as a cystic structure just superomedial to the normal renal parenchyma, but ultrasound can not determine whether there is obstruction. For this purpose diuresis renography may be used to distinguish between

Figure 53. Ureteroceles. Mild dilatation of both distal ureters with bulbous protrusion into the bladder. The lucent rim surrounding the ureteroceles is mucosa elevated by the intravesical portion of the dilated ureters.

obstructive and non-obstructive dilatation, if there is sufficient function in the ectopic segment. Duplication of the contralateral collecting system is a helpful sign, since renal duplication is bilateral in 15% of the cases, and partial duplication is even more frequent.

A simple or non-ectopic ureterocele (Fig. 53) is usually associated with a non-duplicated ureter. On intravenous urography a so-called cobra-head deformity representing the dilated distal ureter surrounded by a uniformly thin rim of lucent epithelium is seen. Simple ureteroceles are also easily demonstrated by ultrasonography and CT.

Urothelial tumors
Most urothelial neoplasms are malignant. Transitional cell carcinoma, the most common, occurs most often in older men. Squamous cell carcinoma and mucinous adenocarcinoma are much less common. The various imaging techniques (intravenous urography, pyelography (Figs. 54-55), contrast-enhanced CT (Fig. 55), MRI and ultrasonography (Fig. 56)) demonstrate an irregular filling defect in the renal pelvis, often associated with obstructive hydronephrosis or mucosal irregularity. Severe hydronephrosis or infiltration of the parenchyma by tumor commonly results in nonvisualization on intravenous urography or contrast-enhanced

	Figure 54. Small pelvic tumor (arrowheads) demonstrated during retrograde pyelography.
a	Figure 55. Large pelvic tumor demonstrated by retrograde pyelography (a) with the patient positioned at various angles and by CT (b).
b
	Figure 56. Pelvic tumor (arrows). Ultrasonography shows an echo-poor mass within the echo-rich pelvis.
	Figure 57. Urothelial tumor in the lower ureter at retrograde pyelography.

CT. Retrograde pyelography is needed in most renal pelvic or calyceal filling defects to better characterize the lesion and to obtain tissue by means of brush biopsy. The appearance of ureteral tumors is similar to that of upper tract urothelial neoplasms (Fig. 57).

Infection
Pyelitis and ureteritis are chronic inflammations of the uroepithelium and suburoepithelium, often resulting in cysts. Intravenous urography shows multiple round eccentric fillings defects related to the pyelocalyceal

Figure 58. Ureteritis cystica. Intravenous urography reveals multiple round filling defects in the pelvis and upper part of the ureter.

system or the ureteral wall (Fig. 58).

Pyonephrosis (purulent material in the obstructed pyelocalyceal system) is usually secondary to an underlying congenital anomaly, stricture or calculus, which in turn leads to hydronephrosis, urine stasis and infection. Plain films may show an enlarged renal outline, an opaque calculus, or an abnormal gas collection. Intravenous urography typically shows a decreased or absent nephrogram and poor visualization of the pyelocalyceal system; because of the poor diagnostic yield, this study is generally omitted, when pyonephrosis is suggested. Retrograde pyelography shows blunted, irregular calyces sometimes with evidence of papillary necrosis. Filling defects representing necrotic tissue or purulent material can sometimes be seen in the pyelocalyceal system and ureter. Ultrasonography typically shows a dilated pyelocalyceal system containing echogenic fluid and/or a shifting fluid-debris level. Radiopaque and non-radiopaque calculi can often be identified. Failure to visualize the proximal ureter suggests that there is an obstruction of the ureteropelvic junction. CT shows multiple coalescing low-attenuation, urine filled spaces containing fluid-debris or contrast-debris. CT can detect even minimally opaque calculi. Perinephric extension of the inflammatory process is more reliably detected by CT than by other imaging modalities. MRI does not seem to add anything. Changes of xanthogranulomatous pyelonephritis can be superimposed on long-standing pyeonephrosis.

	Figure 59. Pouch stone (arrow) formed around a metal suture. Foreign bodies (e.g. metal sutures which are not covered with mucosa) within the urinary tract may act as a nidus around which calculi can be formed.
	Figure 60. Staghorn stone in the left renal collecting system (arrows) and in the lower left ureter (arrowheads) with hydronephrosis in the right kidney due to a small stone, which can not be seen on this urogram. The urogram was taken 3 hours after administration of the contrast medium. No excretion of contrast medium is seen on the left side.
	Figure 61. Nephrotomogram demonstrating a calculus (arrows) in the renal pelvis. It was not seen on the plain film. The kidney has also a dromedary hump.
a	Figure 62. Large stone in the left renal pelvis on KUE (a) and after administration of intravenous contrast medium (b). The stone does not totally obstruct the outflow from the renal pelvis. The contrast medium partly obscures the stone.
b

Calculi
It is estimated that 2-3 % of the population develop urinary calculi. Men are affected twice as often as women. Approximately 10% of stones are caused by an identifiable metabolic abnormality such as hyperparathyroidism, but most are idiopathic. Chronic infections and/or foreign bodies (Fig. 59) can also cause stones. The incidence of calculi is unusually

a	Figure 63. Renal pelvic calculi (arrows). a: Large staghorn calculus. b: Small pelvic calculus. At ultrasonography calculi are highly echogenic and show sharp acoustical showing.
b

high in certain geographic regions. The clinical significance of urinary calculi lies in the accompanying symptoms and sequelae. Increased intraluminal pressure in the collecting system secondary to a calculus causes pain and can result in perforation of a calyceal fornix with leakage of urine and/or contrast material into the renal sinus and perinephric soft tissues. This so-called pyelosinous backflow is usually self-limited if the urine is sterile. Approximately 90% of upper urinary tract calculi are radiopaque and therefore potentially visible on plain films (Fig. 60). Tomography may be helpful in visualizing poorly opaque stones (Fig. 61). The factors that determine whether or not calculi will be detected are respiratory motion, overlying gas and feces, size and position of the calculus and technical quality of the film. On intravenous urography, an opaque calculus may be more, less or equally opaque as the surrounding opacified urine (Fig. 62). When obstruction is present, the collecting system proximal to the calculus is dilated. If there is a filling defect in the pyelocalyceal system and no opaque calculus is seen on the plain film,

Figure 64. Stricture in the lower ureter following ureteroseopy demonstrated at intravenaus urography. Such strictures may be found months after a patient has undergone ureteroseopy.

blood clot or neoplasm must be considered as a differential diagnosis. Ultrasonography can be helpful, but is highly operator-dependent and some patients have minimal obstruction. The combination of KUB and ultrasonography works very well when dilatation is present, but the middle third of the ureter can be a problem. Ultrasonography is indicated in patients in whom intravenous urography fails to demonstrate the collecting system and in patients with markedly impaired renal function. A renal calculus appears sonographically as an echogenic focus with sharp acoustical shadowing (Fig. 63). CT is extremely sensitive in detecting calculi, but is usually reserved for patients in whom the diagnosis is in doubt. On CT, calculi usually exhibit very high attenuation values. The complications of calculus disease such as hydronephrosis and retroperitoneal pathology are clearly depicted by CT. MRI does not give further information.

Obstruction
Obstruction to antegrade flow of urine may occur at any level from the renal collecting tubules to the distal urethra (Fig. 64). The urographic manifestations of acute obstruction are normal or enlarged kidneys, an obstructive nephrogram (Fig. 65), mild to moderate dilatation of the pyelocalyceal system which may be visualized best on delayed films, and

Figure 65. Obstructive nephrogram on the left side due a ureteral calculus. The renal parenchyma on the left is still opacified by contrast medium, whereas it has already been excreted on the right side.

pyelosinous backflow secondary to small forniceal ruptures of the calyces. The classic urographic sign of long-standing obstructive hydronephrosis is a dilated collecting system. Other characteristic urographic findings include the crescent sign, a thin curvilinearopaque line, which represents reoriented, dilated tubules that are arranged parallel to the calyceal surface rather that perpendicular to it; a negative pyelogram, representing a dilated pyelocalyceal system filled with unopacified urine seen against a background of opacified parenchyma; the rim sign, a thin rim of opacified parenchyma seen during the parenchymal phase, often seen in patients with marked parenchymal atrophy secondary to longstanding severe obstruction; layering of contrast medium in the erect position, a consequence of lost peristalsis, and total absence of excretion. The worst cases will result in renal atrophy. The quality of the nephrogram and opacification of the collecting system vary with the degree of residual functional impairment. Intravenous urography is also excellent for evaluating the results of corrective surgery for pyeloureteral obstruction (Fig. 66). Because ultrasonographic visualization of the collecting structures is independent of renal function, hydronephrosis is readily demonstrated by ultrasonography (Fig. 67) even when there is no

a	Figure 66. Urogram before (a) and after (b) Anderson Hynes pyeloplasty for uretero-pelvic junction obstruction. After surgery the renal pelvis is much smaller and the form of the calyces has nearly normalized.
b
	Figure 67. Hydronephrosis. Ultrasonography shows a dilated, fluid-filled (echo poor) collecting system.
a	Figure 68. Hydronephrosis due to ureteral calculus. Immediately after administration of contrast medium there is pa or parenchymal opacification (a - right kidney), whereas 24 hours after the administration both opacification of the parenchyma and the pelvis (b - right kidney) may be found. The slight excretion on the left side 24 hours later is probably due to reabsorption of contrast medium through pyelosinous reflux on the right.
b

visualization on intravenous urography. It should be remembered that ultrasonography can be normal in patients with acute obstruction in whom dilatation of the collecting has not yet occurred. A full collecting system from overhydration can be mistaken for hydronephrosis. Ureteral jets will be diminished or absent. While CT readily demonstrates

	Figure 69. Hydronephrosis due to cervical carcinoma. Sagittal T1-weighted image after administration of contrast shows the ureter (arrows) as a dilated, elongated, low signal intensity column.
a	Figure 70. Diuresis renogram. a) Classic diuresis renogram responses when the frusemide is injected 20 min. after the radiopharmaceutical. The response (bottom left) is equivocal. In such cases it may be an advantage to repeat the study and inject the frusemide 15 min. before the radiopharmaceutical b) Diagram showing conversion of equivocal (F +20) washout to obstructive or non-obstructive patterns on F - 15 diuresis renograms.
b
a	Figure 71 a, b. No obstruction at diuresis renoscintigraphy. There is a good response to the Lasix injection on both sides. Lasix was injected 20 min. (arrow) after 99mTc MAG3.
b

hydronephrosis, it is usually obtained to determine the etiology and extent of pathology rather than as a screening examination (Fig. 68). CT clearly depicts retroperitoneal lesions, a frequent cause of ureteral obstruction. Hydronephrosis is also well demonstrated on both T1 and T2-weighted MRI. The dilated collecting system appears as a cluster of communicating low-intensity structures within the renal parenchyma, which has a more intense signal on T1-weighted images and the ureter is seen as a dilated, elongated, low signal intensity column (Fig. 69). While retroperitoneal pathology is readily detected by MRI, calcium-containing calculi are very low signal and may go undetected against a T1-weighted background. With a T2-weighted pulse sequence where urine is bright, stones may, however, stand out very clearly. While intravenous urography provides more precise morphologic information, nuclear medicine has a number of important advantages in the management of the patient with

a	Figure 72 a, b. Obstruction at diuresis renoscintigraphy. There is absence of response to Lasix on both sides. A/so in this case Lasix was injected 20 min. (arrow) after 99mTc MAG3.
b

urinary obstruction. It can give information about whether the hydronephrosis is obstructive or non-obstructive. It is especially useful in patients with possible stenosis of the ureteropelvic junction. In equivocal cases, the use of furosemide (Lasix) either before or during the examination ("diuresis" renography) can help to clarify many cases (Figs. 70-72).

Retroperitoneal fibrosis
Although the cause of retroperitoneal fibrosis is uncertain, it is a known complication in patients taking methysergide and has been alleged to be related to several other drugs (such as ß-blockers). Occasionally a specific cause can be identified e.g. an aortic aneurysm with perianeurysmal fibrosis or a retroperitoneal tumor with a marked desmoplastic reaction. Retroperitoneal fibrosis usually occurs between L5 and S2 and generally

Figure 73. CT in a patient with retroperitoneal fibrosis reveals a dense soft tissue attenuation mass surrounding the aorta. This mass extended from L2 to L5.

involves both ureters at this level. The intravenous urogram demonstrates varying degrees of ureteral obstruction and typically shows medial deviation of one or both ureters. In periureteral fibrosis the fibrotic reaction is limited to the periureteral tissues and the affected ureter may not be deviated. The fibrotic mass can be demonstrated by CT (Fig. 73), MRI and ultrasonography.

Trauma
The ureters are well protected in the retroperitoneal paraspinal region and are seldom traumatized in blunt abdominal trauma. On the other hand, partial or complete disruption of the ureter can result from penetrating injuries such as knife or bullet wounds. Iatrogenic injuries can result from instrumentation or surgery. Provided adequate renal function is preserved, intravenous urography may demonstrate narrowing or disruption of the ureter; if renal function is diminished, direct pyelography may be needed to evaluate adequately the injured segment. CT, ultrasonography and MRI give information about the surroundings.

Pathology of the lower urinary tract

Hematuria can be a sign of many urinary tract diseases (Fig. 74). However, it may also occur in the absence of demonstrable disease ("essential hematuria"). Terminal or initial hematuria points towards disease in the bladder trigone and/or urethra, whereas uniform (total) hematuria is more indicative of disease in the upper urinary tract or the rest of the bladder. Erythrocytcylinduria is found in medical renal disease e.g. glomerulonephritis. Patients with mixed hematuria should probably undergo cystoscopy, but beyond this the need for imaging and if SD what

Figure 74. Various causes of hematuria. Treatment with anticoagulants can also cause hematuria

type of examination is often debated. Hitherto intravenous urography has been the most frequently performed examination in those cases, but there is a clear tendency that ultrasonography is no w preferred in many countries as the initial examination. While ultrasonography may detect renal parenchymal tumors earlier than urography, it is important to remember that urography is more sensitive in detecting tumors of the renal pelvis and ureter.

Diverticula
Diverticula are acquired (usually) or congenital (rarely) outpouchings of the bladder wall. They may range from very small to so large that they press on other pelvic organs. The wall of a diverticulum is often smooth in contrast to the irregular trabeculated bladder wall. Approximately one fourth of all diverticula contain calculi and in approximately 3 % a malign ant tumor may be present. Two important investigations for the diagnosis of diverticula are ultrasonography which demonstrates an echo-poor outpouchings (Fig. 75), and cystography, which quantifies the degree of diverticular emptying. As with unenhanced CT and MRI it is important to demonstrate the neck of the diverticulum in order to avoid the wrong diagnosis of a perivesical fluid collection. At intravenous urography

	Figure 75. Bladder diverticulum. It is of utmost importance to demonstrate the neck of the diverticulum in order to distinguish it from a fluid collection with no connection to the bladder.
	Figure 76. Trabeculated bladder with diverticula. Due to outflow obstruction (BPH) a spiral metallic prosthesis has been inserted in the prostatic urethra. There are also metal clips outside the genito-urinary tract (large bowel anastomosis from previous sigmoid resection).

(Fig. 76), enhanced CT (Fig. 77) and enhanced MRI, contrast medium is found in the outpouching confirming the presence of a diverticulum. Intravenous urography often overlooks non-filling diverticulae or those located on the anterior bladder wall, but cystography will demonstrate them. Frequently the pelvic ureter will be medially displaced. Urethral diverticula occur most frequently in females. They may be so large that they elevate the bladder base, giving the impression of a "female prostate". The primary examination is voiding urethrography, but sometimes ultrasonography during micturition has been reported to be successful.

Figure 77. Bladder diverticula filled with contrast medium. Urothelial cancer in the upper left part of the bladder.

Tear-drop bladder
At intravenous urography a so-called tear-drop or pear-shaped bladder is sometimes seen. This special configuration of the bladder is due to compression from extravesical processes. The possible causes can be revealed at ultrasonography, CT and MRI and include hematoma, abscess, urinoma, hypertrophy of the iliopsoas muscle, lymphoma, tumor, fibrosis, bilateral iliac aneurysms, occlusion of the vena cava and pelvic lipomatosis.

Urachus
Urachal remnants can be seen in all degrees ranging from a tiny elongation of the anterior upper contour of the bladder to a fistula extending to the umbilicus. A tumor may arise in the residual tissue. CT is the best modality to demonstrate a urachal tumor since it very often contains very gracile calcifications anterosuperiorly to the bladder.

Infection
In simple cystitis no changes are found with the various imaging modalities, but in severe cystitis one can find a slightly diminished bladder capacity with a thick bladder wall and mucosal edema at ultrasonography, CT and MRI and sometimes on intravenous urography. In chronic cystitis the bladder shrinks and the wall thickens. Bilharzia causes chronic cystitis and mucosal edema as well as thickening of the distal ureter including the vesicoureteral orifices. With time thin linear calcifications may develop in the bladder ureters and even renal pelves. Calcifications may also be due to tuberculosis, but most frequently these are found in the seminal vesicles seminalis, and ampullae of the vasa deferentia.

Figure 78. Bladder stone. Ultrasonography shows an echorich process in the upper part of the bladder with acoustic shadowing.

Calculi
Bladder calculi are indicative of residual urine since they very rarely develop in a bladder which can be completely emptied. Some stones (e.g. uric acid) do not contain calcium and together with very small calcium containing stones they may be overlooked at conventional roentgenography, but they can be seen at ultrasonography (Fig. 78) and CT.

Neurogenic bladder
Residual urine including maximal bladder volume is easily determined by ultrasonography. Residual urine can also be measured at nuclear medicine. The main cause of incomplete bladder emptying is bladder outlet obstruction, but neurogenic diseases often cause residual urine, which is also a consequence of vesicoureteral reflux. Urodynamic evaluation and cystography are complementary examinations in the evaluation of patients with neurogenic diseases and are often performed simultaneously (video urodynamics). Cystography gives information about the bladder neck and vesicoureteral reflux.

Trauma
In connection with trauma lesions may involve the bladder and the male urethra. Rupture of bladder and the urethra in a patient who is not severely injured is properly diagnosed by cystography (Fig. 79) and urethrography, respectively, showing contrast outside the natural lumen. In case of a multitraumatized patient CT should be performed as the primary examination since it gives information about the surroundings (Fig. 80) and the relations to bones. While intraperitoneal bladder rupture should be operated promptly, a conservative attitude toward the management of extraperitoneal bladder rupture is sometimes justified. Disruptions of the

	Figure 79. Extraperitoneal bladder rupture. Cystography shows bladder rupture secondary to a pelvic fracture.
	Figure 80. Extraperitoneal bladder rupture. Contrast medium around the bladder 10 hours after intravenous urography, which showed only slight elevation of the bladder. A fracture of the symphysis was obvious on one of the subsequent sections. It was impossible to perform ultrasonography adequately due to pain.

posterior urethra are usually managed by initial cystostomy and delayed second stage repair in order to reduce the incidence and severity of late complications like stricture and impotence.

Bladder hernia
Bladder hernia, which occurs most commonly in the inguino-serotal area, is diagnosed equally well by all modalities. Therefore the least expensive modality - ultrasonography - should be used as the primary modality. Sometimes it may be necessary to perform cystography to demonstrate the outline of the hernia to the surgeon. In the 1970's colpocystourethrography was frequently performed in females with incontinence

	Figure 81. Artificial sphincter. A plainfilm should be taken both during infiated and defiated phase. If the fluid contains contrast medium, the integrity of system may be studied.
	Figure 82. Urethral stricture verified by urethrography.

and/or genital hemia for diagnosis and planning oftreatment. Its value was severely questioned in the 1980's but now the examination is reserved for rare cases of recurrent incontinence.

Artificial sphincters
Plain radiographs are excellent for control of the placement and evaluation of mechanical malfunctioning artificial sphincters (Fig. 81) and other prostheses. Urethrography may be necessary if intraurethral erosion is suspected. Diagnosis of fluid accumulation including infection and abseesses around the artificial material requires ultrasonography and/or CT.

Urethral stricture
Stricture (stenosis) of the urethra, urethral trauma and urethral tumors are the urethral diseases most frequently investigated radiologically. Strictures occurs almost exclusively in males, are readily diagnosed by urethrography demonstrating luminal narrowing (Fig. 82), and in adults, are nearly always acquired (e.g. infection, post-cystoscopy lesion, trauma, catheter). Urethrography should be performed in patients in whom urethral fistulas are suspected. Problems with urethral catheterization (except for BPH) are also an indication for urethrography. Most urethral neoplasms occur in the anterior urethra of the male and are usually imposed on long standing strictures. Squamous cell carcinoma is by far the most common type. Urethral tumors are much less common in women, are not related to a stricture, and can be of any cell type.

a	Figure 83. Bladder tumor. Ultrasonography may detect tumors as small as 10 mm (a). Normally the echogenicity of bladder tumors is moderate (b). On (b) one can also see a balloon catheter (b) and portions of a hypertrophic prostate (p).
b
	Figure 84. Bladder tumor at vesicoureteral junction (lower part) causing hydronephrosis (upper part).

Tumor
Ninety percent of all bladder tumors arise in transitional epithelium. Cystoscopy with biopsy is the most sensitive method of detecting bladder tumors, but imaging must be done for staging. Ultrasonography, CT and MRI each have their advantages. Ultrasonography can also recognize some bladder tumors, but it often overlooks low grade papillomatosis, very small tumors « 10 mm), and tumors in trabecular bladders. At abdominal or transrectal ultrasonography localized thickening and/or protrusion in the bladder lumen is found (Fig. 83). The echogenicity of bladder tumors is moderate. It is very important that before an ultrasonographic examination the bladder be well filled, because a folding of the wall should not be interpreted as a tumor. It is often difficult to differentiate between small to moderate sized bladder tumors and

	Figure 85. Bladder tumor. There is a filling defect arising from the right bladder wall.
a	Figure 86.Bladder tumor. a. Sagittal T1-weighted image demonstrating a tumor in the bladder base. b. Same as (a) after administration of gadodiamide. Only slight increase in signal intensity of the tumor. c. T2-weighted image of a signalpoor tumor at the ureterovesical junction causing dilatation of the ureter (different patient than a and b).
b
c

trabeculation of the wall. In some institutions transurethral ultrasonography is still used, since it gives a clearer image of the tumor and may demonstrate invasion. However, transurethral ultrasonography requires anesthesia and cystoscopy and is thus invasive. In patients in whom two to three consecutive cystoscopic controls have revealed no recurrence of bladder carcinoma, abdominal ultrasonography of a well filled bladder has proved to be sufficient both from disease controlling and economical aspects. Ultrasonography of bladder tumors should always include examination of the kidneys (Fig. 84). The role of intravenous urography in the work-up of bladder carcinomas is limited to control of the upper urinary tract, especially the ureters. It has been shown in comparative studies that intravenous urography overlooks approximately one-third of all bladder tumors (Fig. 85). In contrast to both CT and ultrasonography it is not possible with intravenous urography to distinguish between adherent blood clots, non radiopaque calculi and bladder tumors. Overlying gas may sometimes be confused with an intravesical lesion on intravenous urography, but not with ultrasonography, CT or MRI. MRI is excellent for evaluation of the rare urethral tumors. The main indication for CT (Fig. 77) is not the diagnosis of bladder tumor or degree of bladder wall invasion, but diagnosis of extravesical spread e.g. iliac nodes and extension outside the bladder wall. MRI and clinical staging are complementary for staging urinary bladder cancer; in superficial tumors, clinical staging, including deep transurethral biopsy, is the best technique. For invasive tumors, MRI is the best technique (Fig. 86). In the determination of local tumor growth and the detection of bone marrow infiltration MRI is superior to CT. For the detection of lymph node involvement, CT and MRI are equal. A limitation of all staging procedures is the determination of extent of tumor growth within the muscle layer of the bladder wall (differentiation between stages T2 and T3a). It seems likely with endorectal coils or phased-array multicoils and paramagnetic contrast media MRI may soon be able to solve the problem of differentiating stage T2 from stage T3 tumors. A limitation of MRI is its difficulty in differentiating between tumor and acute edema resulting from transurethral resection or biopsy. Even with endorectal coils and intravenous contrast medium it remains impossible to differentiate the two stages. Therefore, staging of urinary bladder cancer should start with MRI, followed by clinical staging.

	Figure 87. Ileal urinary conduit. Diagram demonstrating a bladder substitute (conduit) made from part of ileum and anastomosed to the ureters (Bricker procedure).
	Figure 88. "Pouchography" ("loopography") demonstrating leakage (arrows) at the anastomoses between the ileal loop and the urethra.

Enteric neo-bladder
In cases of muscular invasion (but without extravesical spread) or of congenital or acquired atrophic bladders, total cystectomy is often performed. A bladder replacement is made by parts of the bowel. There are several types of "bowel bladders" each with their advantages and disadvantages (Fig. 87). The radiologist is involved in postoperative control

a	Figure 89. Renal artery stenoses before (a) and immediately after (b) percutaneous transluminal renalangioplasty.
b

of these urinary reservoirs or conduits. Evaluation for urinary leakage in the first days after surgery and later on determination of capacity, stenoses or reflux are some of the indications for imaging. Cystography ("pouchography", "loopography", etc.) is the appropriately primary imaging modality in these cases (Fig. 88).

Intervention

Angiographic interventions

Percutaneous Transluminal Renal Angioplasty (PTRA)
Since the first report of renal artery percutaneous angioplasty in 1978 the method has rapidly become accepted as the treatment of choice for most patients with renovascular hypertension. Transluminal angioplasty is simply designed to enlarge the lumen of a stenotic artery (Fig. 89). Since atheromatous material is not compressible, it must be fractured and pushed

a	Figure 90. Stenosis of arterial anastomosis of transplant before (a) and months after (b) percutaneous transluminal angioplasty. The dilatation improved the flow (and function) considerably.
b

off the intima of the renal artery. The arterial media is also split and the adventitia is stretched beyond its elastic recoil. The atheromatous plaque is forced into the medial portion of the artery. The adventitia remains intact, the media heals by fibrosis, and there is re-endotheliazation over the tears in the intima. A similar process of controlled injury also occurs with nonatherosclerotic stenosis (Fig. 90). The intima is disrupted and the lesions are split or stretched beyond their point of elastic recoil. The overall technical success rate for percutaneous transluminal renal angioplasty is generally reported as 80-90%. Obviously the number, type, location and experience of the radiologist contribute significantly to the success or failure of the procedure. Complications of renal artery percutaneous transluminal angioplasty may be considered as general complications such as adverse contrast medium reaction or problems at the puncture site, or specific to percutaneous transluminal renal artery, such as a rupture, dissection, embolus, or thrombosis of the renal artery.

Embolization
Percutaneous transcatheter embolization of the renal artery or of the vesical branches of the internal iliac artery is used in a variety of situations. It may be used in cases where renal ablation without surgery is desired or where arrest of bleeding from the kidney or the bladder is needed. Embolization is also effective for treatment of arteriovenous fistulas and

Figure 91. Percutaneous stone dislodgement from the mid ureter to the renal pelvis with a balloon catheter. In the pelvis ESWL was applied.

aneurysms. Much less commonly percutaneous transcatheter thrombolysis can be performed for arterial or venous thrombosis, but the usual treatment for these conditions is medical (anticoagulants, etc.).

Vein sampling
Selective renal vein sampling provides a method of measuring the renin level being secreted by each kidney.

Non-angiographic interventions

Nephrostomy
Percutaneous nephrostomy is the single most valuable interventional technique in uroradiology. It relieves obstruction of the urinary tract and provides access to the collecting system for a variety of diagnostic and therapeutic procedures. The indications include: 1) Relief of obstruction (preserve renal function, treatment of infection, relieve pain), 2) Urinary diversion (heal leak or fistula), 3) Diagnostic study (antegrade pyelography, Whitaker test, biopsy or brushing for biopsy), 4) Removal of solid material (stone (Fig. 91 ), foreign body), 5) Access forureteral intervention (stricture dilation, stenting, ureteral occlusion), 6) Infusion of chemolytic agents, and 7) Access for nephroscopy. The procedure may be guided with fluoroscopy, ultrasonography (Fig. 92) or CT; the combination of ultrasonography (guidance) and fluoroscopy (control incl. placement) is the best. Either trocar technique or the Seldinger technique may be used. With some experience and adequate equipment the success

Figure 92. Percutaneous nephrostomy. Under continuous real-time ultrasonographic guidance a posterior calyx is punctured using either a trocar or Seldinger technique. The tip of the needle is easily seen (arrow).

Figure 93.Steps in percutaneous stent placement. After access to the renal collecting system is gained through a nephrostomy, which has been in place for one to two weeks a straight guide wire is passed through the region of ureteral obstruction and into the bladder. After dilatation a double-pigtail catheter is straightened and passed over the guide wire. The pigtail catheter is advanced by a pusher until one end is in the bladder and the other in the renal pelvis. When the guide wire is removed from the catheter, the pigtail catheter acquires its desired shape. A nephrostomy catheter is left in the pelvic cavity until it has been documented that the stent functions properly.

rate is above 95 %. The most common complications are related to bleeding, urine extravasation and infection.

Balloon dilatation and stenosing
With the nephrostomy catheter providing access to the collecting system interventional procedures can be performed in the ureter. This direct approach avoids problems associated with transversing the urethra, bladder, and ureterovesical junction. Ureteral stents may be placed to bypass obstruction (Fig. 93), to heal a ureteral leak or fistula, or to prevent stricture formation. In patients in whom a stricture has already occurred angioplasty balloon catheters may be used to dilate the stricture. Balloon dilatation of urethral strictures via the direct route is now a routine procedure at many institutions. Complications of ureteral or urethral stricture dilation are rare. The most untoward event is perforation of the ureter or urethra. However, these usually heal without sequelae. Because serious complications are so unlikely, percutaneous stricture dilatation is often undertaken as the initial procedure. If it fails, surgery is not compromised. During the recent years special urethral stents (endoprothesis) have been developed for both acquired urethral strictures and prostatic obstruction (Fig. 76). They are inserted using either fluoroscopic or endoscopic guidance.

Drainage
Both renal and non-renal retroperitoneal abscesses are particularly well suited to percutaneous drainage. They can usually be approached posteriorly during guidance with CT or ultrasonography such that peritoneum, bowel, and other organs are not transversed. In most patients percutaneous drainage results in cure and surgery can be avoided. The response to percutaneous abscess drainage is seen within the first 24 to 48 hours. The complications of percutaneous abscess drainage include bleeding, spread of infection into a previously uninfected space, and exacerbating bacteremia or sepsis during manipulation.

Biopsy
Percutaneous biopsy has become a common radiological procedure. Using a variety of imaging modalities cutting needles provide tissue for histological evaluation. Aspiration needles provide material for cytopathology and may be used to diagnose the primary tumor, but they are commonly used to confirm the presence of metastases when the primary tumor has been diagnosed previously. Fine needle histology biopsies can also be obtained. They are used to diagnose the occurrence of a primary tumor. Gross needle biopsy (18-20G) is used primarily for renal biopsy in patients suspect of having a medical renal disease in order to obtain enough tissue for immunological diagnosis. The most common complication of biopsy is bleeding. In about 60 % of patients undergoing medical renal biopsy perinephric bleeding occurs, but it is rarely necessary to treat (transfusion, surgery) it. Arteriovenous fistulas occur in many patients but in nearly all patients they close within the next days. If persistent, they can be embolized. Tumor seeding can not be excluded, but it occurs rarely.

Ureteral occlusion
In patients with urinary leakage, which does not stop following urinary diversion, ureteral occlusion can be performed either by inserting a balloon in the ureter or injecting embolizing drugs.

Henrik S. Thomsen and Howard M. Pollack