TRANSPLANT KIDNEY
| Vascular supply from end-to-side | |||||||||||
Usually parallel to incision with hilum inferiorly and posteriorly, extra-peritoneal location. Obtain longitudinal and transverse measurements. Usually hypertrophies ~ 15% in first 2 weeks and may increase by 40% in first 6 months.
Post- operative hematomas- appearance depends upon chronicity. Urine leaks or urinomas- due to anastomotic leaks or ureteric ischemia. Appear well defined, anechoic with occasional hydronephrosis. May use radionuclide imaging to confirm nature of collection. Lymphoceles- occur 4 – 8 weeks after surgery in 15%. May obstruct ureter or veins. Appear well defined and either anechoic or with fine septations.
Screen and image with color/power, looking for focal and/or diffuse hypoperfusion. Obtain spectral traces of interlobar arteries in upper, mid and lower poles with appropriate factors. Image and obtain spectral Doppler of main renal artery and vein and EIA and EIV.
Arteries- brisk upstroke, low resistance with normal RI of 0.6 to 0.8. Normal velocity main renal artery <200 cm/sec. Veins- may be monophasic with continuous flow or demonstrate some pulsatility with cardiac cycle.
ATN:
ATN:
Occurs to some extent in all cadaveric transplants. Most common cause of delayed graft function (need for dialysis in 2 weeks post transplant). Non-specific imaging features: normal or changes in echogenicity, qualitatively decreased color flow, RI may be normal or increased.
Rejection:
Hyperacute- rarely imaged since it occurs during surgery. Acute- occurs in up to 40% in first few weeks and is a poor long term prognostic indicator. Similar US and radionuclide findings. US findings non-specific.
Most common cause of late graft loss. Progressive loss renal function beginning 3 months after transplant. Patients with acute rejection are predisposed. US- Cortical thinning, mild hydronephrosis, prominent sinus fat, dystrophic calcifications, decreased color, normal or increased RI.
Hydronephrosis
Obstruction is rare, though will usually be at UV junction from stricture or intra-luminal lesion. Mild pelvocaliectasis may be 2º overhydration, decreased ureteric tone, U-V reflux.
Renal artery thrombosis
Occurs in < 1% typically within first month. Most common cause is acute rejection with retrograde thrombosis of small to large arteries. Other causes: pediatric kidneys, emboli, acquired stenosis, hypotension, vascular kink, hypercoagulable state, poor anastomosis, trauma. US: Absent arterial and venous flow in kidney and main renal artery.
Most common vascular complication in up to 10% in first year. Three possible sites:
– Donor portion, typically at end-to-side anastomosis
– Recipient portion- more uncommon, from intraoperative clamp or intrinsic atherosclerosis
– At anastomosis- more frequent in end-to-end anastomoses
US Findings of RAS
Parvus-tardus flow in intra-parenchymal vessels. Use color Doppler to locate stenosis. Peak systolic velocities > 200 cm/sec with turbulent flow. False positive diagnoses may occur with abrupt turn in the main renal artery. With chronic rejection, segmental renal artery stenoses may occur.
AVM and PSA
Both are typically the result of trauma during percutaneous biopsy. AVM- color shows focal area of mixed colors occasionally with feeding vessels. AVM produces vibrations which result in color assigned to the perivascular tissues.
PSA- may appear as a simple cyst on grey scale imaging but with typical swirling arterial flow on Doppler.
RV thrombosis
Hydronephrosis
Obstruction is rare, though will usually be at UV junction from stricture or intra-luminal lesion. Mild pelvocaliectasis may be 2º overhydration, decreased ureteric tone, U-V reflux.
Renal artery thrombosis
Occurs in < 1% typically within first month. Most common cause is acute rejection with retrograde thrombosis of small to large arteries. Other causes: pediatric kidneys, emboli, acquired stenosis, hypotension, vascular kink, hypercoagulable state, poor anastomosis, trauma. US: Absent arterial and venous flow in kidney and main renal artery.
Most common vascular complication in up to 10% in first year. Three possible sites:
– Donor portion, typically at end-to-side anastomosis
– Recipient portion- more uncommon, from intraoperative clamp or intrinsic atherosclerosis
– At anastomosis- more frequent in end-to-end anastomoses
US Findings of RAS
Parvus-tardus flow in intra-parenchymal vessels. Use color Doppler to locate stenosis. Peak systolic velocities > 200 cm/sec with turbulent flow. False positive diagnoses may occur with abrupt turn in the main renal artery. With chronic rejection, segmental renal artery stenoses may occur.
AVM and PSA
Both are typically the result of trauma during percutaneous biopsy. AVM- color shows focal area of mixed colors occasionally with feeding vessels. AVM produces vibrations which result in color assigned to the perivascular tissues.
PSA- may appear as a simple cyst on grey scale imaging but with typical swirling arterial flow on Doppler.
RV thrombosis
Occurs in up to 4% transplants. Sx: acute pain 2° swelling of kidney, oliguria in first week. Causes: surgical difficulties, hypovolemia, femoral/iliac vein thrombosis, compression by collections. US- absent venous flow, reversal of diastolic flow in artery. Kidney may be enlarged, hypoechoic.
RV stenosis
Grey Scale- normal or hypoechoic. Color Doppler- aliasing at stenotic site. Spectral Doppler- 3 to 4 times increase in velocity across the region indicates a hemodynamically significant stenosis.
RV stenosis
Grey Scale- normal or hypoechoic. Color Doppler- aliasing at stenotic site. Spectral Doppler- 3 to 4 times increase in velocity across the region indicates a hemodynamically significant stenosis.
IMPORTANT POINTS:
- Renovascular HT occures in younger patients (less than 30 y.o.)
- Usually respond well to ACE inhibitors
- Renal artery stenosis does not automatically lead to renovascular HT
- >180 cm/s is considered a sign for significant stenosis
- 2:1 is the ratio of increased blood flow bw stenotic and non stenotic segment of the renal artery that is considered to be significant
- RI difference of >10% between the kidneys is an indirect sign for stenosis
- RI is decreased in the post stenotic arterial segments (decreased blood flow -> decreased vascular resistance)
- ESP (early systolic peak) and AT (acceleration time) decrease in stenosis.
- ACC (Acceleration time) increases in stenotic segments
- ACC (Acceleration time) increases in stenotic segments
Main causes of increased flow resistance (RI values):
- Acute renal failiure
- Obstruction of the renal pelvis
- Extrarenal compresion
- Low diastolic bp
- Bradycardia
- Interstitial scarring
- Acute rejection
-Interstitial rejection: enlargement of graft due to infiltration by lymphocytes
-Vascular rejection: increased resistance due to narrowing of intrarenal arteries
- Cyclosporin A toxicity (immunosuppressant drug)
Diagnosing renal artery stenosis:
- Flow acceleration (bright colors in CDS), greater than 200 cm\s which usually results from a stenosis of more than 70%, normal values range between 50-160 cm\s.
- Post stenotic turbulance
- Rounded post stenotic systolic peaks
- Prolonged acceleration time
- RI difference of more than 0.05 between the two kidneys
Graft artery:
- Can be tortuous
- Renal blood flow depends on renal function!
- Flow acceleration of more than 2.5X the flow at a prestenotic point is a direct sign of stenosis
Graft vein thrombosis:
- Bidierctional flow in intrarenal arteries
- No flow in hilar veins
- Back and forth flow in arteries - resulting in zero net blood supply to kidny - indication for urgent surgery
AV fistulas
- Mostly caused by previous biopsy
- High risk for bleeding after biopsy
- Feeding artery -- increased diastolic flow
- Draining vein -- pulsatile accelerated flow
Graft rejection:
- Increased flow resistance - early sign, before change in creatinine by two days!
Take home message:
STENOSIS DECRESED RI
REJECTION INCREASED RI
Related links:
(main source: Teaching Manual of CDS-Thieme)
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