**6.1. Vascular complications**

*5.2.2.4. Lymphocele*

40 Current Issues and Future Direction in Kidney Transplantation

with a lymphocele.

*5.2.3. Vesicoureteral reflux*

Lich-Gregoir technic [74].

months [75].

**6. Other urological complications**

Lymphoceles are lymph collection from the iliac lymphatic vessels of recipient or graft hilum that accumulates between the transplanted kidney and bladder. It results from surgical disruption of lymphatics and usually occur 4 to 8 weeks following transplantation [62, 70-72]. Usually these are small in size and asymptomatic; however, when large can cause hydro‐ nephrosis or lower extremity edema and may require drainage [33]. US shows an anechoic collection with fine septa within it, usually inferior to the region between the kidney and bladder (figure 12). Scintigraphy demonstrates a photopenic area which does not fill up with tracer on delayed images [73]. CT shows well defined round or oval collection of 0–20 HU. On

**Figure 12.** A minimal complex fluid collection around the graft extending to the pelvis, with fine septa, consistent

It seems to have a greater incidence in patients whom extravesical cystoureteral anastomosis was performed. However the clinical relevance is still not established, with a slightly increase in risk of infection. Cysto-uretrogram can easily make this diagnosis. Many technical modifi‐ cations has been proposed to reduce the vesicoureteral reflux and urine leakage like modified

**•** Ureteral necrosis: more common in the distal ureter and caused by a tight submucosal tunnel or vascular ischemia or rejection. It is a cause of urinary leak and is common in the first 6

MR images, an homogeneous and often minimal complex collection is depicted.

Vascular complications (VC) after renal transplantation are the most frequent type following urological complications, seen in less than 10% [81]. Early VC includes renal artery or vein thrombosis, lesions to the iliac vessels and cortical necrosis. Delayed complications mainly include renal artery stenosis, arteriovenous fistula and rarely pseudo-aneurysm. They have a high associated morbidity and mortality. Although DSA remains the gold standard for vascular complications, US with Doppler is the screening method for assessing blood supply of a kidney graft [49, 82]. MRI with angiography (MRA) has been used more often to confirm US diagnosis of vascular abnormalities in renal transplants [31]. With this combination, radionuclides are scarcely used to evaluate graft vascular complications.

#### *6.1.1. Early vascular complications*

Usually occurs in the first week post transplantation. Renal artery and vein thrombosis are generally related to the position of the graft, to a long vessel, to surgical techniques (anasto‐ mosis of the arteries), or to compression, e.g. hematoma compressing the renal vein. Renal vein thrombosis can also be secondary to extent of a thrombus in the iliac vein.

Arterial thrombosis is rare in the early transplant period. US and MRI show complete absence of flow in the main transplant renal artery and intrarenal arteries, no flow in the parenchyma with CD or PD (Figure. 13), and no parenchymal perfusion detectable at MRI. MRI can also demonstrate absence of renal artery enhancement. Occlusion of a lobar artery or a pedicle artery leads to a focal well-defined area of infarct, which consequences are dependent to the extension of this area [25]. In the ischemic area, the renal cortex has appearance of a wedgebased hypoechoic mass with echogenic walls, and no signal on CD [31]. MRI can better delimitate the zone of infarct. MRI and CT show a non-enhancing area with enhancing capsule. Scintigraphy may also be used to confirm arterial occlusion (Figure 14).

Renal vein thrombosis is a frequent cause of loss of the renal graft, occurring in 4-6% of the transplants in adults [83]. It´s a difficult diagnosis because it begins in the venules within the renal parenchyma, and initially, large veins remain normal [84]. Characteristic features of renal vein thrombosis include a dilated transplanted renal vein containing a thrombus with absent venous flow (Figure 15); lack of venous outflow that causes a very high resistance to arterial

**Figure 13.** Acute renal artery thrombosis. (A) Gray-scale US shows gas within the collecting system (arrows). (B) Ab‐ sence of signal at PD.

inflow; there may be no diastolic flow (RI = 1) or even diastolic flow reversal (Figure 16) [84]; absence of venous signals in the graft at CD or PD; decrease in the arterial sign at CD of the peripheric arteries [25]. These are non-specific findings, also present in ATN and rejection. Clinical and biochemical findings should take them apart. MRI can demonstrate the extent of the thrombus, but they must not delay the surgical approach.

#### *6.1.2. Vascular thrombosis — Artery / vein*

Lesions to the iliac or renal allograft vessels may occur during the transplantation and are associated with multiple arteries donors, anatomic variations, recipients ateromathosis, thrombophilia, obesity and other chronic diseases. They can lead to a non viable graft. Artery dissections, perforation, pseudoaneurysms, and thrombosis are the most common type of these complications [25]. Sonographic evaluation of such these lesions in the immediate posttransplant period may be limited and MRI/MRA might be necessary.

**6.2. Late vascular complications**

(A)

(B)

detected in the site of the anastomosis.

Renal artery stenosis (RAS) is the most common VC. Stenosis can occur within a few months, most often caused by trauma to the donor's or recipient's vessel during clamping, or it may be delayed for few years, in which case atherosclerosis is usually the cause [84]. Kinking of the renal artery may cause a similar clinical condition, leading to an erroneous suspicion of RAS.

**Figure 14.** A and B: 99mTc-DTPA renal scintigraphy. Photopenic area in the left iliac fossa. Absence of arterial blood flow and of glomerular filtration in the transplanted kidney. Radionuclide angioscintipraphy performed with 99mTc-DTPA.

Imaging in Kidney Transplantation http://dx.doi.org/10.5772/55074 43

The photon deficiency and no uptake of radioactivity at the site of the graft indicate non-viability.

The patency of the renal artery should be performed in patients with severe hypertension refractory to medical therapy or with hypertension combined with either an audible bruit or unexplained graft dysfunction [50]. It usually occurs in the anastomosis or in the proximal donor artery, related to the surgery technique, media and intima injuries, and atherosclerosis, both from the donor or the recipient. They can occur in a short or long segment, multifocal or unifocal involvement. Flow disturbances resulting from a tight anastomosis are most readily

Cortical necrosis is extremely rare but severe. It can be secondary to a long cold ischemic time or rejection. Diagnosis is difficult because in the initial phase, arteries and veins remain patent. US can show a globular and heterogeneous graft with decrease in the CD sign of the cortical arteries. RI is elevated and progresses to absence of diastolic flow. Focal, patchy or diffuse zones of necrosis are better demonstrated by MRI. Biopsy is necessary to exclude rejection [25].

**Figure 14.** A and B: 99mTc-DTPA renal scintigraphy. Photopenic area in the left iliac fossa. Absence of arterial blood flow and of glomerular filtration in the transplanted kidney. Radionuclide angioscintipraphy performed with 99mTc-DTPA. The photon deficiency and no uptake of radioactivity at the site of the graft indicate non-viability.

### **6.2. Late vascular complications**

inflow; there may be no diastolic flow (RI = 1) or even diastolic flow reversal (Figure 16) [84]; absence of venous signals in the graft at CD or PD; decrease in the arterial sign at CD of the peripheric arteries [25]. These are non-specific findings, also present in ATN and rejection. Clinical and biochemical findings should take them apart. MRI can demonstrate the extent of

**Figure 13.** Acute renal artery thrombosis. (A) Gray-scale US shows gas within the collecting system (arrows). (B) Ab‐

Lesions to the iliac or renal allograft vessels may occur during the transplantation and are associated with multiple arteries donors, anatomic variations, recipients ateromathosis, thrombophilia, obesity and other chronic diseases. They can lead to a non viable graft. Artery dissections, perforation, pseudoaneurysms, and thrombosis are the most common type of these complications [25]. Sonographic evaluation of such these lesions in the immediate post-

Cortical necrosis is extremely rare but severe. It can be secondary to a long cold ischemic time or rejection. Diagnosis is difficult because in the initial phase, arteries and veins remain patent. US can show a globular and heterogeneous graft with decrease in the CD sign of the cortical arteries. RI is elevated and progresses to absence of diastolic flow. Focal, patchy or diffuse zones of necrosis are better demonstrated by MRI. Biopsy is necessary to exclude

the thrombus, but they must not delay the surgical approach.

(A)

42 Current Issues and Future Direction in Kidney Transplantation

(B)

transplant period may be limited and MRI/MRA might be necessary.

*6.1.2. Vascular thrombosis — Artery / vein*

rejection [25].

sence of signal at PD.

Renal artery stenosis (RAS) is the most common VC. Stenosis can occur within a few months, most often caused by trauma to the donor's or recipient's vessel during clamping, or it may be delayed for few years, in which case atherosclerosis is usually the cause [84]. Kinking of the renal artery may cause a similar clinical condition, leading to an erroneous suspicion of RAS.

The patency of the renal artery should be performed in patients with severe hypertension refractory to medical therapy or with hypertension combined with either an audible bruit or unexplained graft dysfunction [50]. It usually occurs in the anastomosis or in the proximal donor artery, related to the surgery technique, media and intima injuries, and atherosclerosis, both from the donor or the recipient. They can occur in a short or long segment, multifocal or unifocal involvement. Flow disturbances resulting from a tight anastomosis are most readily detected in the site of the anastomosis.

**Figure 15.** Renal vein thrombosis. The enlarged, occluded vein (arrow) is seen at the hilum, with a thrombus within (\*).

(A)

(B)

There is a tardus parvus waveform and a decreased RI at spectral Doppler.

also the method of choice for therapeutic (Figure 19).

**Figure 17.** RAS. (A) Color-Doppler shows a focal stenosis near renal hilum with marked increase in PSV (4.0 m/s). (B)

Imaging in Kidney Transplantation http://dx.doi.org/10.5772/55074 45

Arteriovenous fistula (AVF) normally occurs secondary to transplant biopsy, with an incidence of 1-18% [84, 87]. Small lesions may resolve spontaneously; if not, they can be successfully treated with percutaneous embolization. They are usually asymptomatic, but can manifest with hypertension, hematuria, and graft dysfunction. Doppler US is the modality of choice for diagnosis. Focal high-velocity, low-impedance intrarenal arterial flow might suggest an arteriovenous fistula. An intense focus of high-velocity turbulent flow that is seen as a multicolored focus, persisting even with high pulse repetition frequency (or Doppler scale) at CDUS is also suspect. MRI and CT are used when US cannot define the vascular nature of the lesion. Visualization of a round abnormality in the renal parenchyma that enhances similar to the aorta at arterial-phase on MRI with an abnormal early venous drainage adjacent to the lesion is diagnostic for AVF [19]. DSA remains as the gold standard for such diagnosis and is

**Figure 16.** A reversal diastolic flow (arrow) and raising of the PSV in the interlobar artery as an indirect sign of renal vein thrombosis.

The Doppler criteria to diagnosis renal artery stenosis include: 1- high-velocity flow greater than 2 m/s measured in the renal artery (Figure 17A); 2- the ratio peak velocity in the transplant artery / peak velocity in the iliac artery close to the anastomosis higher than 2 (PVS RA/IA > 2); 3- velocity gradient between stenotic and pre-stenotic segments of more than 2:1; 4- marked distal turbulence [85, 86]. US with Doppler of the intra-renal arteries for detecting proximal artery stenosis shows a tardus parvus waveform; prolonged acceleration time, > 0.07 seconds (Figure 17B); diminished acceleration index (<3.0 m/s2 ); decreased RI (<0,56); and loss of a normal early systolic compliance peak [85]. When US is inconclusive for RAS, MRA (prefera‐ ble) and CT angiography may define the site and the degree of stenosis. The stenosis can also be confirmed by angiography, which also provides a good estimate of the vessel extent and helps in the planning of percutaneous transluminal angioplasty (Figure 18).

**Figure 17.** RAS. (A) Color-Doppler shows a focal stenosis near renal hilum with marked increase in PSV (4.0 m/s). (B) There is a tardus parvus waveform and a decreased RI at spectral Doppler.

The Doppler criteria to diagnosis renal artery stenosis include: 1- high-velocity flow greater than 2 m/s measured in the renal artery (Figure 17A); 2- the ratio peak velocity in the transplant artery / peak velocity in the iliac artery close to the anastomosis higher than 2 (PVS RA/IA > 2); 3- velocity gradient between stenotic and pre-stenotic segments of more than 2:1; 4- marked distal turbulence [85, 86]. US with Doppler of the intra-renal arteries for detecting proximal artery stenosis shows a tardus parvus waveform; prolonged acceleration time, > 0.07 seconds

**Figure 16.** A reversal diastolic flow (arrow) and raising of the PSV in the interlobar artery as an indirect sign of renal

**Figure 15.** Renal vein thrombosis. The enlarged, occluded vein (arrow) is seen at the hilum, with a thrombus within

normal early systolic compliance peak [85]. When US is inconclusive for RAS, MRA (prefera‐ ble) and CT angiography may define the site and the degree of stenosis. The stenosis can also be confirmed by angiography, which also provides a good estimate of the vessel extent and

helps in the planning of percutaneous transluminal angioplasty (Figure 18).

); decreased RI (<0,56); and loss of a

(Figure 17B); diminished acceleration index (<3.0 m/s2

(\*).

44 Current Issues and Future Direction in Kidney Transplantation

vein thrombosis.

Arteriovenous fistula (AVF) normally occurs secondary to transplant biopsy, with an incidence of 1-18% [84, 87]. Small lesions may resolve spontaneously; if not, they can be successfully treated with percutaneous embolization. They are usually asymptomatic, but can manifest with hypertension, hematuria, and graft dysfunction. Doppler US is the modality of choice for diagnosis. Focal high-velocity, low-impedance intrarenal arterial flow might suggest an arteriovenous fistula. An intense focus of high-velocity turbulent flow that is seen as a multicolored focus, persisting even with high pulse repetition frequency (or Doppler scale) at CDUS is also suspect. MRI and CT are used when US cannot define the vascular nature of the lesion. Visualization of a round abnormality in the renal parenchyma that enhances similar to the aorta at arterial-phase on MRI with an abnormal early venous drainage adjacent to the lesion is diagnostic for AVF [19]. DSA remains as the gold standard for such diagnosis and is also the method of choice for therapeutic (Figure 19).

**Figure 18.** (A): MRA reconstructed with MIP nicely demonstrates the renal artery stenosis (arrow). (B): DSA of a differ‐ ent case showing multifocal stenosis in the renal artery (arrows) and a long segmental stenosis in the polar artery (ar‐ rowhead).

other sites of pseudoaneurysms. Extrarenal arterial pseudoaneurysm following renal trans‐

**Figure 19.** arteriovenous fistula. (A) US CD shows a vascular structure with troubling flow. (B) DSA pre- treatment showing a distal communication (arrow) between arterial and venous system with early drainage (arrowhead). (C) Af‐

Imaging in Kidney Transplantation http://dx.doi.org/10.5772/55074 47

Figure 20 shows an algorithm for initial evaluation of complications after kifney transplan‐

It is a known fact that patients submitted to renal replacement therapy, whether dialysis or transplantation, are at higher risk for cancer [88]. Among neoplasias, urologic tumors are about 4 to 5 times more frequent among renal transplant recipients and their characteristics differ

**7. Other complications following renal transplantation**

(A)

(B) (C)

ter coil placement (arrow) the AV fistula is no longer seen.

**7.1. Malignancy after kidney transplantation**

plantation is extremely rare.

tation.

In general, pseudoaneurysms develop secondary to biopsy injury. Most of them resolve spontaneously within the first two months. However, if there were progressive enlargement, an unusual size (> 2 cm in diameter) or loss of renal function, intervention will be required [31]. US shows a simple or complex cyst. CD shows the to-and-fro yin and yang pattern seen in

**Figure 19.** arteriovenous fistula. (A) US CD shows a vascular structure with troubling flow. (B) DSA pre- treatment showing a distal communication (arrow) between arterial and venous system with early drainage (arrowhead). (C) Af‐ ter coil placement (arrow) the AV fistula is no longer seen.

other sites of pseudoaneurysms. Extrarenal arterial pseudoaneurysm following renal trans‐ plantation is extremely rare.

Figure 20 shows an algorithm for initial evaluation of complications after kifney transplan‐ tation.
