1.Urologic ComplicationsIn early reports of renal transplantation, the prevalence of urologic complications varied from 10% to25%, with a mortality rate ranging from 20% to 30% . In these patients, ureteroureterostomy orpyeloureterostomy was used to restore urinary tract continuity. Patients who undergoureteroneocystostomy, the reconstructive technique used in most active kidney transplantationprograms today, have a lower incidence of urine leak or obstruction, compared with patients whounderwent the older procedures. Approximately two-thirds of the early urologic complications (urineleak or obstruction) are apparent in the first month after transplantation and are treated by thetransplantation team. Currently, urologic complication rates are 4%8% with very low patient mortality.Urine Leak and UrinomasUrine leaks and urinomas are relatively rare complications of transplantation and usually constitute anearly postoperative problem. Extravasation of urine may occur from the renal pelvis, ureter, orureteroneocystostomy site due to ureteral necrosis caused by vascular insufficiency or increasedurinary pressures caused by obstruction. Caliceal leakage is an uncommon cause and occurs secondaryto segmental infarction in patients with accessory renal arteries or due to ligation of a polar artery.Urinomas vary in size and are usually found in the first 2 postoperative weeks between the transplantedkidney and the bladder. They may occur, however, in unexpected locations such as the scrotum orthigh.A decrease in urine output suggests that a urine leak may have occurred, and clinical signs may includefullness and tenderness around the graft, ipsilateral leg swelling, or scrotal or labial edema. Earlydetection and repair have been instrumental in reducing patient mortality.At ultrasonography (US), a urine leak or urinoma appears as a well-defined, anechoic fluid collectionwith no septations that increases in size rapidly. Drainage may be performed with US guidance, and thehigher creatinine level of the fluid compared with its serum concentration differentiates a urine leakfrom a seroma or lymphocele. Large urinomas can rupture to produce urinary ascites. They can alsobecome infected and eventually form abscesses. Radionuclide studies show extravasation of radiotracerinto an area that was initially cold. Delayed scintigrams should be obtained, since accumulation ofradiotracer may be slow. Antegrade pyelography is necessary to provide detailed information about thesite of origin of the urinoma and in planning appropriate intervention (6).Figure 1a. Urinoma from ruptured ureterovesical junction stenosis. (a) Gray-scale sonogram reveals arenal transplant that is obstructed because of a ruptured ureterovesical anastomosis and anurinoma. (b) Postvoid sonogram demonstrates a fluid collection that represents extravasated urine(arrow) and a small bladder BL). (c) Cystogram demonstrates extravasation (arrow). (Reprinted, withpermission, from reference 5.)

2. Figure 1b. Urinoma from ruptured ureterovesical junction stenosis. (a) Gray-scale sonogram reveals arenal transplant that is obstructed because of a ruptured ureterovesical anastomosis and anurinoma. (b) Postvoid sonogram demonstrates a fluid collection that represents extravasated urine(arrow) and a small bladder (BL). (c) Cystogram demonstrates extravasation (arrow). (Reprinted, withpermission, from reference 5.)Figure 1c. Urinoma from ruptured ureterovesical junction stenosis. (a) Gray-scale sonogram reveals arenal transplant that is obstructed because of a ruptured ureterovesical anastomosis and anurinoma. (b) Postvoid sonogram demonstrates a fluid collection that represents extravasated urine(arrow) and a small bladder (BL). (c) Cystogram demonstrates extravasation (arrow). (Reprinted, withpermission, from reference 5.)Small urine leaks may be treated with percutaneous nephrostomy and stent placement. Caliceal leakagecaused by infarction is treated with percutaneous nephrostomy alone. Ureteral stents must be kept inplace for 68 weeks after cessation of leakage to allow complete healing of the ureter and to preservelong-term patency. If healing is unsuccessful, reimplantation of the ureter may be required; if distalnecrosis is present, pyelocystostomy or pyeloureterostomy with the native ureter is performed (6).Urinary ObstructionUrinary obstruction occurs in approximately 2% of transplantations and almost always within the first6 months after the procedure. Obstruction of the transplanted kidney may occur at any location but ismost frequent at the site of implantation of the ureter into the bladder. More than 90% of ureteralstenoses occur within the distal third of the ureter. Narrowing at the ureterovesical junction may becaused by scarring secondary to ischemia or rejection, by technical error during theureteroneocystostomy, or by kinking. These events account for more than 50% of obstructions thatcause ureteral stricture. Less common causes include pelvic fibrosis, calculi, papillary necrosis, fungusball, clots, and compression from an extrinsic mass such as adjacent peritransplant collections.Occasionally, obstruction that develops years after transplantationespecially in patients who haveundergone multiple proceduresmay be related to adhesions, vascular insufficiency, or fibrosis. 3. Figure 2a. Hydronephrosis secondary to ureteral stricture. (a) Gray-scale sonogram demonstrates mildhydronephrosis secondary to ureteral stricture. (b)Retrograde pyelogram shows the area of narrowingat the site of ureteral implantation into the bladder (arrow). (Fig 2a and 2b reprinted, with permission,from reference5.)Figure 2b. Hydronephrosis secondary to ureteral stricture. (a) Gray-scale sonogram demonstrates mildhydronephrosis secondary to ureteral stricture. (b)Retrograde pyelogram shows the area of narrowingat the site of ureteral implantation into the bladder (arrow). (Fig 2a and 2b reprinted, with permission,from reference).The transplanted kidney is denervated; thus, the patient will not complain of typical renal colic whenobstruction occurs. Urinary obstruction manifests by a rising level of serum creatinine. Obstructionmay be difficult to differentiate from chronic rejection, since both cause rising creatinine levels. Inaddition, mild dilatation of the collecting system may occasionally be seen in cases of chronicrejection.US can be used to confirm the diagnosis of hydronephrosis; however, intrarenal edema and fibrosisassociated with rejection may prevent the normal hydronephrotic response. Some transplant recipientsmay have substantial obstruction but little or no renal dilatation. Mild to moderate dilatation of thetransplanted pyelocaliceal system and ureter may occur secondary to a full bladder. In all cases, whenthe patients bladder is full, the bladder should be emptied and the transplant imaged again. In addition,a denervated, transplanted collecting system has no tone; thus, any transient episode of hydronephrosismay cause a persistent appearance of mild dilatation. The single renal graft is responsible for excretingthe entire urine output from the transplant recipients body, and, over time, increasing output mayexacerbate pelvocaliectasis. Studies have attempted to differentiate obstructive fromnonobstructivepyelocaliectasis by using the resistive index. Extrapolation of these results from nativeto transplanted kidneys has not, however, been entirely successful. US also demonstrateslymphoceles,hematomas, abscesses, and urinomas that may cause ureteral obstruction. Any echogenicity within adilated collecting system is usually clinically significant.Scintigraphy may demonstrate urinary obstruction. In a patient with early partial obstruction, goodperfusion and prompt uptake of the radiotracer may be seen; however, in a patient with functionallysignificant hydronephrosis, radioactivity is retained in the collecting system. Delayed images (obtained24 hours after injection) are useful for differentiating an obstructed ureter from a dilated but 4. unobstructed ureter, since an unobstructed system shows clearance into the bladder. Diureticrenography has proved useful for determining the functional significance of dilated collecting systems.Conventional clearance times (furosemide clearance t1/2>20 minutes ) can be used in the assessment ofurinary tract patency.Excretory urography is only infrequently successful for locating a urinary obstruction, and the site isusually best determined with an antegrade contrast material examination. The superficial anteriorposition of the allograft allows easy access for antegrade pyelography performed with real-time USguidance. The Whitaker test is helpful in equivocal cases. The combination of normal results from theWhitaker test and antegrade pyelography virtually excludes the presence of obstruction.Percutaneous nephrostomy is used to relieve obstruction and allow the deployment of other radiologicinterventions such as ureteral stent placement and balloon ureteroplasty. Balloon dilation ofposttransplantation ureteral strictures produces an overall success rate of ureteral dilatation in 90% ofcases, with the best results obtained in fresh surgical strictures and the poorest in chronic ischemicstrictures or areas of periureteral fibrosis. Strictures of the middle and upper ureters result mostcommonly from ischemic or periureteral fibrosis and may require surgical intervention. High balloonpressures of 1012 atm or greater are usually needed for successful dilation, and the balloon is leftinflated for 20 minutes or until balloon waisting has disappeared. After dilation, a 10-F stent is left inplace for only 10 days. In the immunocompromised transplant recipient, the risk of infection precludeslong-term stent placement unless a totally internal, double pigtail stent is used. Recurrences mostcommonly develop within the first year after transplantation.Figure 3a. Hydronephrosis relieved by stent placement.(a) Gray-scale sonogram reveals severehydronephrosis resulting from narrowing at the ureterovesical anastomosis. Obstruction was relievedby stent placement. (b)Sonogram obtained after placement of a retrograde stent (arrow) demonstratescomplete resolution of the hydronephrosis.Figure 3b. Hydronephrosis relieved by stent placement.(a) Gray-scale sonogram reveals severehydronephrosis resulting from narrowing at the ureterovesical anastomosis. Obstruction was relievedby stent placement. (b)Sonogram obtained after placement of a retrograde stent (arrow) demonstratescomplete resolution of the hydronephrosis. 5. Figure 4a. Dilation of a ureteral stenosis. Sequence of fluoroscopic images (ac)demonstratesplacement of a JJ stent across a midureteral stricture.Figure 4b. Dilation of a ureteral stenosis. Sequence of fluoroscopic images (ac)demonstratesplacement of a JJ stent across a midureteral stricture.Figure 4c. Dilation of a ureteral stenosis. Sequence of fluoroscopic images (ac)demonstratesplacement of a JJ stent across a midureteral stricture.Peritransplant Fluid CollectionsPeritransplant fluid collections have been reported in up to 50% of renal transplantations and includeurinomas, hematomas, lymphoceles, and abscesses. The clinical significance of these collections islargely determined by their size, location, and possible growth. In the immediate postoperative period,small hematomas or seromas manifesting as crescenticperitransplant collections are almost expected.Their size should be documented at baseline examination, since any increase in size may warrantintervention. Growing collections may be indicative of urine leak, abscess, or vascular injury. Differenttypes of peritransplant fluid collections can be partially differentiated based on the time interval aftertransplantation. Urinomas and hematomas are most likely to develop immediately after transplantation, 6. whereas lymphoceles generally occur 48 weeks after the surgical procedure. The sonographiccharacteristics of peritransplant fluid collections, however, are entirely nonspecific, and ultimately,diagnosis may be made only with percutaneous aspiration.HematomasHematomas are common in the immediate postoperative period, but they may also developspontaneously or as a consequence of trauma or biopsy. They are usually small and resolvespontaneously. Large hematomas can displace the transplanted kidney and produce hydronephrosis.At US, hematomas demonstrate a complex appearance. Acute hematomas are echogenic and becomeless echogenic with time. Older hematomas even appear anechoic, more closely resembling fluid, andseptations may develop. Similarly, at computed tomography (CT), the appearance of a hematoma alsois time dependent. An acute hematoma has high-attenuation components, and older hematomas containliquefied and serous portions of intermediate attenuation . At magnetic resonance (MR) imaging, anacute hematoma can show high signal intensity with both T1-weighted and T2-weighted pulsesequences. At scintigraphy, hematomas demonstrate a cold defect.Figure 5a. Subcapsular hematoma in a patient who sustained blunt trauma to the abdomen whileplaying a sport. (a) US image demonstrates an isoechoicsubcapsular fluid collection (arrows). (b) CTscan shows a heterogeneous crescenticsubcapsular collection in the transplanted kidney secondary tohematoma (arrows).Figure 5b. Subcapsular hematoma in a patient who sustained blunt trauma to the abdomen whileplaying a sport. (a) US image demonstrates an isoechoicsubcapsular fluid collection (arrows). (b) CTscan shows a heterogeneous crescenticsubcapsular collection in the transplanted kidney secondary tohematoma (arrows).Diagnostic aspiration can be performed to rule out abscess formation. However, percutaneous drainageof the entire fluid collection is often neither efficacious (due to its multiloculated nature) nor advisablebecause of the self-limited nature of the complication and risk of infection.Lymphoceles 7. Lymphoceles are the most common peritransplant fluid collections, with a prevalence of 0.5%20%.They may develop at any time, from weeks to years after transplantation. However, they are usually anearly complication, occurring within 12 months after transplantation. Lymphoceles are caused byleakage of lymph from surgically disrupted lymphatic channels along the iliac vessels or from thelymphatics of the transplanted kidney. Risk factors include inadequate ligation of the lymphaticchannels across the iliac vessels, administration of heparin, and possibly increased lymphatic flowsecondary to edema of the lower extremities. These fluid collections usually occur medial to thetransplant, between the graft and the bladder .Lymphoceles are the most common fluid collection that causes transplant hydronephrosis. Patients witha failing allograft may develop ipsilateral lower extremity edema caused by compression of the femoralvein. In rare cases, lymphoceles may develop in the scrotum and lymphatic drainage may occurthrough the wound.At US, lymphoceles are anechoic) and may have septations. Similar to other peritransplant fluidcollections, they can become infected and can develop a more complex appearance . At CT,lymphoceles have variable characteristics and are usually sharply circumscribed. Their CT attenuationvalues are typical of those of water and usually lower than those of recent hematomas and abscesses.Radionuclide and MR imaging studies are helpful for excluding the presence of urine and blood,respectively.Figure 6. Lymphocele. US image demonstrates mild hydronephrosis of the transplanted kidney. Theanechoic area represents a lymphocele (L) adjacent to the kidney.Figure 7. Lymphocele. Sonogram of another patient shows a multilocular fluid collection (arrows)that surrounds the renal transplant. The collection proved to be a lymphocele. 8. Figure 8. Infected lymphoceles. US image demonstrates a complex echogenic fluid collection(arrows) adjacent to the transplanted kidney.Small lymphoceles are monitored sonographically, and large ones, if they grow or causehydronephrosis, should be drained. Aspirated fluid should have a creatinine content equal to that ofserum, and the cell count and differential may show relatively few white blood cells with apredominance of lymphocytes. Results of Gram stain and culture of the fluid should be negative.Lymphoceles commonly recur after simple percutaneous or surgical drainage. Permanent resolution oflymphoceles may require prolonged catheter drainage and transcatheter instillation of sclerosing agentssuch as povidine-iodine, absolute alcohol, or doxycycline (17). Repeated aspirations run the risk ofinfecting an otherwise sterile fluid collection. However, success rates of up to 97% have been achievedsafely and effectively with percutaneous transcathetersclerotherapy (17). If a lymphocele becomesinfected, external drainage and antibiotic treatment are needed. Surgical treatment of a sterile fluidcollection involves removal of a generous window of peritoneum for marsupialization. Thetransplanted kidney effectively becomes an intraperitoneal structure. Future leakage is thereforeresorbed in the peritoneal cavity. Retrograde pyelography helps identify the course of the transplantedureter before marsupialization, since the ureter could be displaced anteromedially and injured when theperitoneal window is constructed.Abscesses and InfectionMore than 80% of renal transplant recipients suffer at least one case of infection during the first yearafter transplantation. Early diagnosis of and intervention for infectious diseases can help prevent loss ofgraft function and improve patient outcome.Infections that occur in the first weeks after transplantation, such as pneumonia, surgical woundinfections, and urinary tract infections, are similar to those that typically develop innonimmunocompromised patients who have undergone surgery. Infections with opportunisticpathogens and cytomegalovirus often develop 16 months after surgery, and infections common in thegeneral population are seen after 6 months. Patients frequently have multiple infections, andimmunosuppressive medications, indwelling catheters, and frequent glycosuria are all risk factors.Peritransplant abscesses are an uncommon complication and usually develop within the first few weeksafter transplantation. These abscesses may be caused by pyelonephritis or bacterial seeding of alymphocele, hematoma, or urinoma. Acute bacterial nephritis, renal abscess, or perinephric abscessmay occur.Patients may have few signs or symptoms of infection because of their immunosuppressed state. Theymay present with fever of unknown origin, pain, or symptoms related to the pressure of the abscess onthe transplanted system. In a febrile transplant recipient, any peritransplant fluid collection must bepresumed to be infected. Acute pyelonephritis can mimic acute graft rejection, and their imagingappearances may be the same.The sonographic appearances of infections and abscesses are quite variable. Focal pyelonephritis mayappear as focal areas of increased or decreased echogenicity. These findings are nonspecific and canrepresent infarction or rejection. Intrarenal masses are infrequently visualized and are also 9. sonographically nonspecific. They may represent primary renal cell carcinoma orposttransplantationlymphoproliferative disorder. Abscesses have a complex, cystic, nonspecificappearance at US; however, at CT, they manifest with gas, which serves to differentiate them fromother collections. In emphysematous pyelonephritis, gas in the parenchyma of the renal graft producesan echogenic line with distal reverberation artifacts. This finding can be confirmed with abdominalradiography or CT. Any echogenicity within a dilated collecting system is usually clinically significant.Highly echogenic, weakly shadowing masses within a transplanted collecting system are fairly specificfor fungus balls). The presence of low-level echoes in a dilated pyelocaliceal system in a febrile patientsuggests pyonephrosis. Papillary necrosis results in sonographic changes in the calices, and intravenousor retrograde pyelography is the definitive study for diagnosing this condition. Retrograde pyelographymay also demonstrate distortion of the calices, a feature seen in tuberculosis of the renal transplant.Gallium-67 citrate and indium-111tagged leukocyte studies are helpful for diagnosing infections thatdevelop 1 month or more after graft healing is complete .Figure 9. Perinephric abscess. US image demonstrates a loculatedperinephric fluid collection withcomplex sonographic features (arrow). The collection proved to be an infected urinoma.Figure 10a. Fungus ball of the transplanted kidney. (a)US image demonstrates a soft-tissue echogenicmass(m) in the renal pelvis of a transplanted kidney. (b)Retrograde pyelogram shows filling defects(arrows) within the renal pelvis. These findings proved to be a fungus ball. (Fig 10a and 10b reprinted,with permission, from reference 5.) 10. Figure 10b. Fungus ball of the transplanted kidney. (a)US image demonstrates a soft-tissue echogenicmass(m) in the renal pelvis of a transplanted kidney. (b)Retrograde pyelogram shows filling defects(arrows) within the renal pelvis. These findings proved to be a fungus ball. (Fig 10a and 10b reprinted,with permission, from reference.)Figure 11. Hydronephrosis secondary to a fungus ball. Color Doppler US image demonstrates anechogenic mass (m) in the transplanted kidney that is causing hydronephrosis. The mass proved to be afungus ball.Figure 12. Renal transplant tuberculosis. Retrograde pyelogram demonstrates a renal transplant withirregular margins from renal tuberculosis. (Reprinted, with permission, from reference).Abscesses may be treated with either US- or CT-guided percutaneous drainage. Both intrarenal andextrarenal abscesses usually respond to external drainage and systemic antibiotics.Vascular ComplicationsRenal Artery StenosisRenal artery stenosis occurs usually in the first year after transplantation. The stenosis may be locatedbefore the anastomosis (because of atherosclerotic disease in the donor vessel), at the anastomosis 11. (secondary to vessel perfusion injury, faulty suture technique, or reaction to suture material), or afterthe anastomosis (due to rejection, turbulent flow from kidney malposition, or arterial twisting, kinking,or compression). Approximately half of renal artery stenoses occur at the anastomosis, and end-to-endanastomoses have a threefold greater risk of stenosis than end-to-side anastomoses.About 80% of patients with end-stage renal disease are hypertensive, and after renal transplantationtwo-thirds of this group experience a reduction in hypertension. In patients with persistenthypertension, renal artery stenosis may not be considered as a cause owing to concomitant graft failure.Several clinical scenarios should prompt a search for stenosis: (a) severe hypertension refractory tomedical therapy, (b) hypertension and the presence of an audible bruit over the graft,and (c)hypertension associated with unexplained graft dysfunction.Color Doppler US demonstrates stenotic segments as focal areas of color aliasing due to increased flowvelocity. These areas can be selectively evaluated with duplex Doppler techniques to characterize andgrade the flow disturbance. Doppler criteria for significant stenoses include (a) focal frequency shiftsgreater than 7.5 KHz (when a 3-MHz transducer is used) or velocities greater than 2 m/sec, (b) avelocity gradient between stenotic and prestenotic segments of more than 2:1, and (c)marked distaldisturbance (spectral broadening). In the renal parenchyma, tardus-parvus waveform abnormalities canbe observed.MR angiography can be used to diagnose renal artery stenosis in renal transplants. MR angiographyhas the advantage of requiring either no contrast material or a gadolinium chelate that is notnephrotoxic. Renal scintigraphy and time activity curves show reduced perfusion in transplants withcomplete vascular obstruction and renal artery stenosis. This finding is nonspecific, however, as it maybe seen with other causes of parenchymal failure, including graft rejection and urinary obstruction.Figure 13. Renal artery stenosis. Maximum intensity projection (MIP) image of a 35-year-old patientwith recurrent severe hypertension who underwent a second renal transplantation shows severeproximal stenosis (arrow) in the renal artery of the first transplant. Notice the severe decrease in theperfusion of the first transplant.Surgical correction of graft renal artery stenosis is usually successful, but it is associated withsubstantial morbidity. Primary treatment of graft renal artery stenosis by means of percutaneoustransluminal angioplasty with or without stent placement results in good intermediate-term patency andis associated with significant early improvement in blood pressure and creatinine level. Because of itslow level of morbidity, relatively modest cost, and effectiveness, percutaneous transluminalangioplasty is accepted as the initial treatment of choice. Clinical success rates resulting in substantialinitial improvement or cure have been reported in 73% of patients. Decrease in hypertension may beseen in 1 day, and the prevalence of periprocedural complications is substantially lower than thatassociated with surgical repair. Up to 20% of stenoses may require repeat dilation for maximumsuccess. 12. Figure 14a. Percutaneous transluminal angioplasty of a renal artery stenosis. (a)Angiogram showsnarrowing of the proximal renal artery (arrow). (b) Another angiogram shows a catheter placed acrossthe area of stenosis. (c) Angiogram obtained after angioplasty was performed shows restoration of anear normal arterial lumen.Figure 14b. Percutaneous transluminal angioplasty of a renal artery stenosis. (a)Angiogram showsnarrowing of the proximal renal artery (arrow). (b) Another angiogram shows a catheter placed acrossthe area of stenosis. (c) Angiogram obtained after angioplasty was performed shows restoration of anear normal arterial lumen.Figure 14c. Percutaneous transluminal angioplasty of a renal artery stenosis. (a)Angiogram showsnarrowing of the proximal renal artery (arrow). (b) Another angiogram shows a catheter placed acrossthe area of stenosis. (c) Angiogram obtained after angioplasty was performed shows restoration of anear normal arterial lumen.InfarctionRenal artery thrombosis may result from hyperacute rejection, anastomotic occlusion, arterial kinking,or intimal flap. Segmental infarcts in the renal transplant may be focal or diffuse and may occur as partof rejection or as a result of an unassociated vascular thrombosis. Vasculitis may induce smallsegmental infarcts.Patients with renal transplant infarction present with absence of urinary output and often with swellingand tenderness over the graft and anuria. Although the graft itself is denervated, the inflammationwithin the transplanted kidney may incite an inflammatory response in the adjacent visceralperitoneum, with local pain in this location. 13. At US, a segmental infarct appears as a poorly marginated, hypoechoic mass or a hypoechoic masswith a well-defined echogenic wall. If the infarction is global, the kidney will appear hypoechoic andbe diffusely enlarged. At color or power Doppler imaging, segmental infarcts appear as wedge-shapedareas without color flow in , although these findings may also be seen in severe pyelonephritis ortransplant rupture. In total vascular obstruction, there is no perfusion to the transplanted kidney, and noarterial or venous blood flow is seen in the graft at US. At technetium-99m dynamic radionuclidestudies, a photopenic region may be seen. However, these findings are not specific, since hyperacute oraccelerated acute rejection can have similar clinical, Doppler US, and scintigraphic features.Figure 15. Infarct of a renal graft. Power Doppler US image demonstrates segmental loss of perfusionin the transplanted kidney (arrows), a finding compatible with infarct.CT can be used to detect perfusion deficits in the renal graft parenchyma, but it is generally notemployed in patients with elevated creatinine values because of the risk of compromising renalfunction. If any doubt exists as to the nature of the US findings, angiography or MR angiography maybe performed. MR angiography is increasingly used to screen for vascular abnormalities in renaltransplants. Phased-array surface coils provide excellent signal-to-noise information that permits rapidacquisition of high-quality images without the use of potentially nephrotoxic agents. Dynamicenhanced MR imaging can be useful for diagnosing both segmental and global infarctions as well asrenal artery thrombosis. In addition, MR imaging has been helpful for demonstrating small infarctscaused by iatrogenic drug-induced vasculitis.Figure 16. Infarct of a renal graft. CT scan demonstrates segmental hypoattenuation (arrow) in thetransplanted kidney, a finding that proved to represent an infarct. 14. Figure 17a. Occlusion of a graft renal artery with lower pole infarction in a 38-year-oldpatient. (a) Nontargeted MIP image reveals one graft renal artery that is normal. However, a total ofthree graft renal arteries were anastomosed to the external iliac artery, and nonvisualization of two ofthe three arteries indicates perioperative thrombosis. This vascular anatomy could not be ascertainedwith Doppler US. (b) Another MIP image demonstrates the venous anatomy.(c) Contrast materialenhanced three-dimensional MIP image demonstrates perfusion to the upper renal pole with lack ofperfusion to the lower pole, a finding that indicates lower pole infarction from arterial thrombosis.Figure 17b. Occlusion of a graft renal artery with lower pole infarction in a 38-year-oldpatient. (a) Nontargeted MIP image reveals one graft renal artery that is normal. However, a total ofthree graft renal arteries were anastomosed to the external iliac artery, and nonvisualization of two ofthe three arteries indicates perioperative thrombosis. This vascular anatomy could not be ascertainedwith Doppler US. (b) Another MIP image demonstrates the venous anatomy.(c) Contrast materialenhanced three-dimensional MIP image demonstrates perfusion to the upper renal pole with lack ofperfusion to the lower pole, a finding that indicates lower pole infarction from arterial thrombosis.Figure 17c. Occlusion of a graft renal artery with lower pole infarction in a 38-year-oldpatient. (a) Nontargeted MIP image reveals one graft renal artery that is normal. However, a total ofthree graft renal arteries were anastomosed to the external iliac artery, and nonvisualization of two ofthe three arteries indicates perioperative thrombosis. This vascular anatomy could not be ascertainedwith Doppler US. (b) Another MIP image demonstrates the venous anatomy.(c) Contrast materialenhanced three-dimensional MIP image demonstrates perfusion to the upper renal pole with lack ofperfusion to the lower pole, a finding that indicates lower pole infarction from arterial thrombosis. 15. Figure 18a. Complete occlusion of a graft renal artery with allograft infarction in a 47-year-old patientwith elevated serum creatinine levels. (a) Axial T1-weighted breath-hold gradient-echo image revealsperipheral high signal intensity involving the renal cortex (arrow), a finding compatible withhemorrhage. The patient had cortical necrosis proved at surgery. (b) Axial T2-weighted breath-holdshort inversion time inversion recovery image demonstrates peripheral low signal intensity(arrow). (c) MIP image, obtained during the arterial phase of three-dimensional contrast-enhanced MRangiography, demonstrates complete occlusion of the graft renal artery beyond its origin(arrow). (d) Contrast-enhanced three-dimensional MIP image demonstrates lack of a corticalnephrogram with a peripheral rim sign (arrow), an appearance that indicates total infarction of thekidney.Figure 18b. Complete occlusion of a graft renal artery with allograft infarction in a 47-year-old patientwith elevated serum creatinine levels. (a) Axial T1-weighted breath-hold gradient-echo image revealsperipheral high signal intensity involving the renal cortex (arrow), a finding compatible withhemorrhage. The patient had cortical necrosis proved at surgery. (b) Axial T2-weighted breath-holdshort inversion time inversion recovery image demonstrates peripheral low signal intensity(arrow). (c) MIP image, obtained during the arterial phase of three-dimensional contrast-enhanced MRangiography, demonstrates complete occlusion of the graft renal artery beyond its origin(arrow). (d) Contrast-enhanced three-dimensional MIP image demonstrates lack of a corticalnephrogram with a peripheral rim sign (arrow), an appearance that indicates total infarction of thekidney.Figure 18c. Complete occlusion of a graft renal artery with allograft infarction in a 47-year-old patientwith elevated serum creatinine levels. (a) Axial T1-weighted breath-hold gradient-echo image revealsperipheral high signal intensity involving the renal cortex (arrow), a finding compatible withhemorrhage. The patient had cortical necrosis proved at surgery.(b) Axial T2-weighted breath-holdshort inversion time inversion recovery image demonstrates peripheral low signal intensity(arrow). (c) MIP image, obtained during the arterial phase of three-dimensional contrast-enhanced MR 16. angiography, demonstrates complete occlusion of the graft renal artery beyond its origin(arrow). (d) Contrast-enhanced three-dimensional MIP image demonstrates lack of a corticalnephrogram with a peripheral rim sign (arrow), an appearance that indicates total infarction of thekidney.Figure 18d. Complete occlusion of a graft renal artery with allograft infarction in a 47-year-old patientwith elevated serum creatinine levels. (a) Axial T1-weighted breath-hold gradient-echo image revealsperipheral high signal intensity involving the renal cortex (arrow), a finding compatible withhemorrhage. The patient had cortical necrosis proved at surgery.(b) Axial T2-weighted breath-holdshort inversion time inversion recovery image demonstrates peripheral low signal intensity(arrow). (c) MIP image, obtained during the arterial phase of three-dimensional contrast-enhanced MRangiography, demonstrates complete occlusion of the graft renal artery beyond its origin(arrow). (d) Contrast-enhanced three-dimensional MIP image demonstrates lack of a corticalnephrogram with a peripheral rim sign (arrow), an appearance that indicates total infarction of thekidney.Figure 19. Multiple cortical infarctions from drug-induced vasculitis in a 42-year-old patient. Earlycontrast-enhanced three-dimensional MIP image reveals a large upper pole infarction with multiplesmaller focal cortical areas of signal loss, findings compatible with small infarctions.Percutaneous angiographic interventional techniques may be valuable in treating infarctions and renalartery thrombosis. Early diagnosis and treatment are vital for allograft salvage. Depending on the causeand duration of the occlusion, thrombolytic therapy may prolong survival.Arteriovenous Fistulas and PseudoaneurysmsPercutaneous biopsy is commonly performed in transplant recipients when rejection is suspected.Arteriovenous fistulas and pseudoaneurysms are occasionally seen after graft biopsies. Gross hematuriais seen after 5%7% of biopsies and is usually self limiting; however, massive or persistent hematuriamay occur.Color and duplex Doppler US easily demonstrate arteriovenous fistulas. Arteriovenous fistulas andpseudoaneurysms appear as localized areas of disorganized color that extend outside the confines of thenormal vessel. This appearance is caused by perifistula vibration and is detected with the more 17. sensitive color Doppler units. Arteriovenous fistulas also appear as abnormal high-velocity turbulentflow isolated to a single segmental or interlobar artery and paired vein that produces aliasing on colorDoppler images. The feeding artery shows a high-velocity low-resistance waveform, and the drainingvein demonstrates arterialization.Figure 20a. Arteriovenous fistula. (a) Color Doppler US image demonstrates a highly vascularlesion. (b) Color duplex Doppler image shows the classic waveform of an arteriovenous fistula, withhigh velocities and low impedance.Figure 20b. Arteriovenous fistula. (a) Color Doppler US image demonstrates a highly vascularlesion. (b) Color duplex Doppler image shows the classic waveform of an arteriovenous fistula, withhigh velocities and low impedance.Figure 21a. Arteriovenous fistula. (a) Duplex Doppler US image of the lower pole segmental arteryshows increased velocity and decreased resistive index.(b) Duplex Doppler US image of the adjacentvein shows arterialization of flow, a finding consistent with arteriovenous fistula.Figure 21b. Arteriovenous fistula. (a) Duplex Doppler US image of the lower pole segmental arteryshows increased velocity and decreased resistive index.(b) Duplex Doppler US image of the adjacentvein shows arterialization of flow, a finding consistent with arteriovenous fistula. 18. On gray-scale US images, pseudoaneurysms appear as simple or complex renal cysts, but with colorimaging, highly vascular intracystic flow is seen. Pseudoaneurysms with a narrow neck and no venouscommunication demonstrate a classic machinelike to-and-fro Doppler spectrum at their necks. Thoseassociated with arteriovenous fistulas exhibit a high-velocity low-resistance spectrum at their necks,with minimally pulsatile high-velocity flow in the draining vein. When the degree of perifistulavibration limits US assessment of the vascular anatomy, MR imaging enables evaluation.Figure 22. Arteriovenous fistula following transplant biopsy. A color Doppler study in a 41-year-oldhypertensive patient with a bruit audited over the renal allograft revealed tissue vibration. Because ofmarked tissue vibration, it was difficult to interrogate the transplant vasculature. Non-targeted MIPimages during the arterial phase of contrast-enhanced three-dimensional MR angiography reveal afocal severe stenosis of the graft renal artery beyond its origin (arrow). The transplanted renal venoussystem is enhancing during the early arterial phase along with the iliac vasculature and inferior venacava. The cortical nephrogram is very faint due to the marked arteriovenous shunting.Figure 23. Arteriovenous fistula. Contrast-enhanced three-dimensional MR angiogram demonstratesthe renal artery and veins simultaneously, an appearance suggestive of fistula formation. The diagnosiswas confirmed at angiography (not shown).Most complications after biopsy are treated conservatively, and most pseudoaneurysms resolvespontaneously. If, however, a pseudoaneurysm demonstrates progressive enlargement or unusual size(more than 2 cm in diameter), intervention is warranted. Selective transvascular catheterization may beused. The size and location of the arteriovenous fistula or pseudoaneurysm determine which embolicagent to use. For example, a large arteriovenous malformation is more easily treated with steel coils,since particulate matter such as absorbable gelatin sponge (Gelfoam) may pass through the fistulouscommunication and embolize the systemic circulation. Peripheral lesions may be difficult to catheterizeselectively, but a flow-directed detachable balloon can be delivered to the site. Microcatheter systemsmay also be helpful for superselective embolization of small, peripheral feeding vessels. In treatment oftransplant-related arteriovenous fistulas (unlike that of peripheral arteriovenous fistulas), occlusion ofthe proximal bleeding vessel is sufficient.Renal Vein ThrombosisRenal vein thrombosis is an unusual complication of transplantation; it occurs in less than 5% ofpatients and usually in the first postoperative week. Renal vein thrombosis is heralded by an abruptcessation of urinary function and swelling and tenderness over the graft. Hypovolemia, venouscompression from a peritransplant fluid collection, dysfunctional anastomosis, and slow flowsecondary to rejection or other allograft disease can also precipitate renal vein thrombosis. Anincreased prevalence of renal vein thrombosis in left lower quadrant allografts has also been attributed 19. to compression of the left common iliac vein between the sacrum and the left common iliac artery(silent iliac artery compression syndrome.At gray-scale US, renal vein thrombosis may manifest with an enlarged kidney. Venous flow isreduced or absent, and there is increased resistance on the arterial side, often resulting in reverseddiastolic flow on Doppler images. MR venography helps confirm this complication in transplants.Figure 24. Renal vein thrombosis. Duplex Doppler image demonstrates reversal of flow in diastole(arrows) in the transplanted kidney due to renal vein thrombosis secondary to deep venous thrombosis.Figure 25a. Iliac venous compression from a lymphocele in a 39-year-old patient with right lowerextremity edema. (a) MIP image produced from subtracting the arterial phase data from the equilibriumphase data demonstrates a normal renal vein and poor visualization of the external iliac vein due tocompression. (b) Axial source image (from a two-dimensional time-of-flight MR venographic study)helps confirm that the external iliac vein (solid arrow) is compressed by the underlying lymphocele(open arrow).Figure 25b. Iliac venous compression from a lymphocele in a 39-year-old patient with right lowerextremity edema. (a) MIP image produced from subtracting the arterial phase data from the equilibriumphase data demonstrates a normal renal vein and poor visualization of the external iliac vein due tocompression. (b) Axial source image (from a two-dimensional time-of-flight MR venographic study)helps confirm that the external iliac vein (solid arrow) is compressed by the underlying lymphocele(open arrow). 20. Early recognition of renal vein thrombosis is crucial because the allograft may sometimes be salvagedby prompt thrombectomy. Even with prompt diagnosis, however, graft infarction may develop, and atransplant nephrectomy is usually performed to prevent secondary infection.Calculous DiseaseKidney transplant recipients, compared with the general population, are at increased risk for developingurinary calculi and approximately 1%2% develop a clinically significant stone. Persistent secondaryhyperparathyroidism is seen in 38%77% of end-stage renal disease patients after transplantation. Inthe first year after transplantation, 15% of patients may be hypercalcemic, which increases the risk ofrenal stonesThe diagnosis of urinary calculi is suspected when renal function suddenly deteriorates. The patientdoes not experience typical renal colic because the transplanted kidney is denervated.US, radionuclide imaging, and contrast material studies are all useful diagnostic methods. Percutaneousnephrostomy tube placement is valuable because it provides low-pressure drainage and allows renalfunction to stabilize. Antegrade pyelography can then be used to give exact definition of the collectingsystem and position of the stone .Figure 26a. Renal transplant calculus in a 34-year-old patient with hematuria. (a) US imagedemonstrates hydronephrosis with a shadowing echogenic focus seen in the upper middle renal pole(arrow). (b) US image of the distal ureter shows an echogenic focus with shadowing (arrow) a findingconsistent with an obstructing calculus.Figure 26b. Renal transplant calculus in a 34-year-old patient with hematuria. (a) US imagedemonstrates hydronephrosis with a shadowing echogenic focus seen in the upper middle renal pole(arrow). (b) US image of the distal ureter shows an echogenic focus with shadowing (arrow) a findingconsistent with an obstructing calculus.Most stones can be removed with endourologic techniques. Upper tract stones are best treated bymeans of percutaneous nephrostolithotomy. Cystoscopy with electrohydraulic lithotripsy is appropriatefor treating bladder stones.Neoplasms 21. Prolonged immunosuppression following renal transplantation places the transplant recipient at about100 times the normal risk for developing cancer. The average reported prevalence of malignancy inthese patients is 6% (38), with cases consisting predominantly of skin cancers and lymphomas. Thedegree of immunosuppression and its duration are both important factors in the development ofmalignancy. The frequency of urologic tumors such as prostatic adenocarcinoma and germ cell tumorsof the testis does not appear to be increased in this population. However, the prevalence of renaladenocarcinoma may be increased, with 90% of the tumors occurring in the native kidney and 10%occurring in the transplanted kidney (39). One reason for the increased risk of renal adenocarcinoma isthat approximately half of the patients who undergo hemodialysis because of chronic renal failuredevelop acquired renal cystic disease and 9% develop tumors (40). Patients with longer use ofhemodialysis are at greater risk for developing acquired cystic disease. Fortunately, less than 1% ofthese patients develop malignant tumors that metastasize. In addition, patients with a significant pastexposure to cyclophosphamide have an increased risk for developing of urothelial tumors (41);although cyclophosphamide is less commonly used now because of the availability of cyclosporin A,there are many renal transplant patients with a history of cyclophosphamide exposure.A complete urologic evaluation for gross hematuria is recommended in all renal transplant recipients.Intravenous pyelography may be useful if there is good transplant function, although it will not provideinformation about the native kidney. US or CT of the native and transplanted kidneys provides morecomplete information, and a solid heterogeneous enhancing mass that may be cystic is often identified.Cystoscopy with retrograde pyelography of all present kidneys and ureters is advisable.Figure 27. Renal transplant adenocarcinoma. CT scan shows a cystic mass (arrow) arising from therenal transplant that proved to be renal cell carcinoma.Transplant glomerulopathy and recurrence of preexisting glomerulonephritis frequently causemicrohematuria often associated with proteinuria. However, since these patients have an increased riskof developing neoplasms, a complete urologic work-up is advisable.Development of renal adenocarcinoma in the transplanted kidney is uncommon, with the majority ofmalignancies related to skin cancers and lymphomas. Malignancy in the transplanted kidney is treatedby total removal of the renal graft and cessation of immunosuppression. Urothelial malignancies canlikewise be treated in a standard fashion. In the presence of immunosuppression, intravesicalinstillation of Calmette-Gurin bacillus is not recommended.Gastrointestinal and Herniation ComplicationsGastrointestinal complications may occur in transplantation patients. The most common of thesecomplications is gastrointestinal hemorrhage due to peptic ulcer (42). Prevalence of the complicationsmay vary with use of an intraperitoneal or extraperitoneal approach in placement of the allograft (43).Postoperative adhesions may lead to intestinal obstruction. Herniation of bowel through a transplantperitoneal defect may lead to compromise of the intestine or of the transplant itself (Fig 28). Urinaryobstruction from obturator herniation of the ureter may also occur (44). Pseudomembranous colitissecondary to overgrowth of Clostridium difficle in patients receiving antibiotic therapy is anothercomplication that can be seen in renal transplant recipients. A typical accordion sign secondary tomassive edema of the intestinal wall is highly suggestive of the diagnosis on CT images of theabdomen. 22. Figure 28. Renal transplant herniation. CT scan demonstrates multiple distended small bowel loopsaround the transplanted kidney, findings compatible with obstruction. Small bowel had herniatedthrough the peritoneal defect related to the renal graft, a diagnosis that was surgically proved.PosttransplantationLymphoproliferative DisorderImpaired immune surveillance and the oncogenic effects of immunosuppressive therapy itself may becausative factors of the posttransplantationlymphoproliferative disorder (PLTD). An association withEpstein Barr virus is usually demonstrated. PLTD complicates 8% of transplantations and is diagnosedat a median of 80 months after transplantation. The liver, brain, and lung are more common sites ofinvolvement than the gastrointestinal tract. PLTD lesions are polymorphic collections of B cells butmay evolve into forms indistinguishable from non-Hodgkin lymphoma. If there is involvement of thesmall intestines, patients often have generalized disease.Figure 29a. Posttransplantationlymphoproliferative disease in a 25-year-old renal allograft recipientwho presented with abdominal pain. (a) Contrast-enhanced CT scan demonstrates circumferentialthickening of the jejunum (arrows). (b)Contrast-enhanced CT scan obtained at a lower level showsencasement of the superior mesenteric artery by lymphadenopathy (arrowheads), in addition to thejejunal thickening (arrow).Figure 29b. Posttransplantationlymphoproliferative disease in a 25-year-old renal allograft recipientwho presented with abdominal pain. (a) Contrast-enhanced CT scan demonstrates circumferentialthickening of the jejunum (arrows). (b)Contrast-enhanced CT scan obtained at a lower level showsencasement of the superior mesenteric artery by lymphadenopathy (arrowheads), in addition to thejejunal thickening (arrow). 23. Figure 30. Posttransplantationlymphoproliferative disease in a kidney transplant recipient whopresented with fever. Contrast-enhanced CT scan demonstrates a necrotic mass in the pelvis posteriorto the transplanted kidney (arrows).ConclusionsTransplantation is currently one of the accepted treatments of irreversible kidney disease.Improvements in surgical techniques and more sophisticated, potent immunosuppressive drugs haveresulted in remarkable advances in survival of patients and renal grafts. Nevertheless, substantialcomplications occur in both the immediate postoperative period and later. Imaging has a critical role inthe evaluation of these complications, and interventional radiologic techniques are often successfullyapplied to their treatment.