We performed a retrospective review and selected the most illustrative images for each complication.
For literature review,
we have searched indexed publications using Medline as the scientific repository for current data regarding this area of interest.
A) Infarction
Infarctions in the renal transplant can be focal or diffuse and may occur as part of rejection or as a result of an associated vascular thrombosis; vasculitis may induce small segmental infarcts.
At US,
a segmental infarct appears as a hypoechoic area poorly marginated or with a well-defined echogenic wall.
At color or power Doppler US (figure 1),
segmental infarcts appear as wedge-shaped areas without arteriovenous flow within (although these findings may also be seen in severe pyelonephritis or transplant rupture).
- Renal artery (RA) occlusion (causing diffuse renal graft infarction) affects <1% of renal transplants and occurs within the first week.
It may result from hyperacute rejection,
anastomotic occlusion,
arterial kinking,
or intimal flap. DUS reveals absence of arterial signal within the renal parenchyma (distal to the site of occlusion) along with the complete absence of venous flow.
On CTA (figure 2) there’s absence of opacification of the renal artery in the arterial phase; renal artery can also appear spontaneously hyperdense (recent thrombus) on pre-contrast images.
B) Renal vein (RV) thrombosis and stenosis
RV thrombosis is rare and occurs within the first postoperative week.
Surgical problems,
hypovolemia,
venous compression (from a peritransplant fluid collection),
dysfunctional anastomosis and slow flow (as seen in rejection) are common causes of RV thrombosis.
In the presence of RV thrombosis,
the vessel has echogenic intraluminal material (figure 3) and is characterized by scarce or absent compressibility and grey-scale US reveals an enlarged kidney with reduced parenchymal and diminished/absent corticomedullary differentiation (usually in severe cases of complete/sub-occlusive thrombosis).
On DUS,
complete thrombosis results in reduced or absent venous flow and increased resistance in the arterial side,
resulting in reversed diastolic flow in the renal artery – this bidirectional flow is so specific for RV thrombosis that it is regarded as an indication for immediate surgical revision of the graft without further diagnostic confirmation.
Stenosis of the RV is rare and it may be the result of compression of the vein by a periphrenic fluid collection or perivascular fibrosis.
On US,
the parenchyma may appear normal or mildly hypoechoic.
A 3-4 fold increase in the PSV between the stenotic and pre-stenotic segments is regarded as highly suggestive of focal stenosis.
C) Renal artery stenosis
RA stenosis is the most common vascular complication (it accounts for 75% of all vascular complications) and is more frequently seen in the late post-transplant period,
although it can really accur at any time.
DUS reveals:
- RA peak systolic velocity (PSV) >250cm/s* or focal acceleration of flow that is 2.5 times higher than the pre- or post-stenotic velocity (figure 4);
*in the absence of hemodinamically significant stenosis,
the PSV of the RA in a hypertrophic,
well-functioning transplanted kidney may exceed 250-300 cm/s along the full length of the artery; in contrast,
in the presence of chronic graft dysfunction with reduced organ volume,
a focal PSV of 180-200 cm/s may be suggestive of significant RA stenosis,
particularly when the other segments of the RA exhibit markedly lower PSVs (40-50 cm/s).
- RA PSV that is >13 times higher than of an interlobular artery (sensitivity around 100%) (figure 5);
- Ratio of renal artery/iliac artery peak systolic velocities >1,8 (figure 6);
- Intraparenchymal acceleration time >0,06s (figure 7) – “tardus” fow - is the only indirect index that displays high sensitivity (93%) in the diagnosis of RA stenosis in a transplanted kidney (in contrast to native kidneys) but only when the degree of stenosis exceeds 80%; only in half of these cases (with RA stenosis exceeding 80%),
intraparenchymal resistance index <0,5 (“parvus” flow) can be seen (figure 8);
- turbulence,
reverse flow and spectral broadening can be seen in the segment immediately downstream from the stenosis.
CTA (figures 7) is used to assess the vascular anatomy and to confirm the existence of an area of reduced caliber within the RA.
The stenosis may be located before the anastomosis (due to atherosclerotic disease in the recipient vessel),
at the anastomosis (secondary to vessel perfusion injury,
faulty suture technique or reaction to suture material) or after the anastomosis because of rejection,
turbulent flow from kidney malposition or arterial twisting/ kinking/ compression – figure 8).
The majority of the stenosis affects the peri-anastomotic region (in about half of all cases) and end-to-end anastomoses have greater risk than end-to-side anastomoses.
Since RA stenosis is a major cause of graft dysfunction and/or loss,
prompt diagnosis and treatment can significantly improve graft survival.
The treatment of choice of graft arterial artery stenosis is percutaneous angioplasty with or without stent placement (figures 9,
10 and 11).
D) Pseudoaneurysms and arteriovenous fistulas are mainly seen as complications associated with renal biopsy.
On DUS:
- Arteriouvenous fistulas (figure 12) appear as localized areas of disorganized color that contains both arterial and venous flow.
They may also appear as abnormal high-velocity turbulent flow isolated to a single segmental or interlobular artery and paired vein that produces aliasing on color Doppler.
Spectral analysis of the feeding artery shows a high-velocity low-resistance waveform and the draining vein demonstrates turbulence and pulsatile acceleration.
- Pseudoaneurysms appear as cyst-like areas with anechoic/finely hyperechoic material on gray-scale but with turbulence and internal flow on color DUS.
Pseudoaneurysms with a narrow neck and no venous communication demonstrate a classic “to-and-fro” flow at their necks; those associated with arteriovenous fistulas (figures 13 and 14) exhibit a high-velocity low-resistance flow at their necks,
with minimally pulsatile high-velocity flow in the draining vein.
For large pseudoaneurisms,
assessment of the vascular anatomy may be obtained by CTA.
Although the great majority of complications after biopsy are usually small and resolve spontaneously,
a pseudomaneurysm is always at risk of rupture and therefore intervention is always warranted with selective/superselective embolization being the treatment of choice.