Keywords: Kidney transplant, Doppler ultrasound, Resistive index
|How to cite this article:|
Al-Khulaifat S. Evaluation of a Transplanted Kidney by Doppler Ultrasound. Saudi J Kidney Dis Transpl 2008;19:730-6
| Introduction|| |
Kidney transplant is the treatment of choice for patients with end-stage renal disease. It is more cost effective than hemodialysis, offers better quality of life and lower morbidity. Ultrasound is the principal imaging technique for the evaluation of a renal allograft; it is a safe imaging technique to assess the structure of the allograft and its perfusion without the need for ionizing radiation and intravenous contrast. The use of high-resolution probe (3–6 MHz), color Doppler imaging (CDI) and Pulse Doppler (PD) enables the visualization of the vasculature as well. 
| B Mode Imaging|| |
The assessment of the kidney transplant is easy due to its presence in the iliac fossa lying anterior to the iliac vessels. Evaluation of the graft includes assessment of the size and volume, parenchymal echogenecity, cortico medullary differentiation, collecting system, and the surrounding soft tissue structures.
The renal sinus is normally hyperechoic, and the medullary pyramids are distinguished by their more echolucent appearance than the renal cortex.  Small amount of fluid collection around the graft is common, mostly representing a hematoma, which generally resolves spontaneously. The estimation of a kidney transplant volume can be done using the formula of a prolate ellipsoid (length x AP width x transverse x 0.5).
| Doppler Imaging|| |
Color Doppler technology permits rapid assessment of the entire renal arterial perfusion and venous patency [Figure 1]. It also allows visualization of the main renal artery with its anterior and posterior divisions, segmental, interlobar and arcuate arteries and corresponding veins within the graft. The main renal artery shows normal Doppler waveform with flow velocity ranging between 20 and 52 cm/sec.  The resistive index (RI) is used as a measurement of resistance to arterial flow within the renal vascular bed. An RI of less than 0.7 to 0.8 is considered normal , and if the RI exceeds 0.8, it is an indicator of transplant dysfunction.
Dysfunction of the renal allograft and its complications can be classified by origin as parenchymal, vascular, urologic, infectious, neoplastic, or iatrogenic. Several of these processes share the same pathologic features, such as cellular infiltration of the graft causing edema, enlargement, and vascular compromise. They share identical Doppler and sonographic appearances which might cause a diagnostic dilemma to the radiologist.  Progressive elevation of the RI, reaching 0.9 or above indicates renal dysfunction, but is often nonspecific and must be interpreted in the context of time of onset of dysfunction, clinical status and biochemical tests [Table 1].
| Imaging of graft complications|| |
Knowing the time of onset of complications and clinical manifestations will facilitate a correct diagnosis,  particularly in the differentiation between acute tubular necrosis (ATN) and cyclosporine (Cs-A) toxicity. Diagnosis of acute rejection usually requires a biopsy.  Invasive imaging procedures like angiography, antegrade pyelography and percutaneous nephrostomy may be useful in certain situations; therefore, the radiologist should always be aware when evaluating the failing renal graft, whether the cause is renal or extrinsic. This will aid in deciding whether immediate medical or surgical treatment is needed or an allograft biopsy is required for diagnosis. According to the time of onset of complications in a renal transplant recipient, three types are identified; immediate, early and late complications.
| Immediate complications (first week)|| |
Prompt and immediate graft function is important after renal transplantation because it correlates with shorter stay in the hospital, and improved short and long-term graft survival.  The most frequent complications in this period include ATN, accelerated acute rejection, renal vein thrombosis, and renal artery thrombosis. Urgent sonography is reserved for patients with early graft dysfunction who are at low risk for ATN, and those in whom there was intraoperative bleeding. It is important to differentiate between ATN and vascular thrombosis or occlusion, because the latter requires urgent surgical intervention.
| Early complications (1–4 weeks)|| |
The causes of graft dysfunction in this period include acute rejection, urinary fistulae and ureteral obstruction. To determine whether the cause of graft dysfunction is due to parenchymal disease or a urologic complication such as presence or absence of hydronephrosis or perigraft collections, an ultrasound will be useful. However, an allograft biopsy is required to distinguish between rejection and Cs-A toxicity.
| Late complications (Over 4 weeks)|| |
The period of one to six months after renal transplantations is the most crucial time in the clinical course of a recipient as 74 % of rejection episodes, 63% of all graft losses, and 22% of deaths occur during this period. Hypertension is a common finding in the month's following transplantations and the cause might be due to Cs-A toxicity, renal artery stenosis, or recurrence of the native kidney disease.
| Parenchymal complications|| |
Acute tubular necrosis
Acute tubular necrosis is due to reversible ischemic damage to the renal tubular cells prior to engrafting and affects 20–60 % of cadaveric renal grafts in the first 48 hours after transplantation. The risk factors for ATN include cadaveric graft, hypotension in the donor, and long warm (over 30 minutes) and cold (over 24 hours) ischemic times.
Sonographic appearance of ATN is variable. The kidney may appear normal, and in severe cases it looks enlarged, edematous and echo poor with loss of cortico-medullary differentiation. The renal sinus echo may be compressed or obliterated due to swelling. Severe ATN causes elevation of the RI (above 0.8), but normal RI in conjunction with ATN can occur, especially in the first 24 hours of surgery. 
Rejection can be classified as acute rejection (AR), accelerated acute rejection (AAR) and chronic rejection (CR).
Acute rejection is a common complication occurring in 20–30 % of cadaveric grafts, and successfully treated in over 80% of cases with pulse intravenous corticosteroids, Cs-A, and the monoclonal antibody, OKT3.  The sonographic appearance [Figure 2] of AR reflects the underlying pathology and includes:
- Graft enlargement due to edema
- Decreased cortical echogenecity and swelling of the medullary pyramids resulting in loss of cortico-medullary differentiation
- Edema within the renal sinus fat, which may obliterate the sinus echo complex.
Acute rejection may show edema of the collecting system wall and focal echo poor areas of parenchymal infarction and perigraft fluid due to necrosis and hemorrhage. In severe cases, PD shows reduced, absent or reversed diastolic flow with elevation of the RI. However, patients with milder but clinically significant rejection episodes can have normal sonographic and Doppler findings. Many studies have showed that RI lacks sufficient sensitivity and specificity in patients with biopsy-proven rejection; over 50% of grafts have normal RIs less than 0.7.  Also, a single abnormal RI cannot distinguish between ATN and rejection, both of which may coexist in the early postoperative period. Sonographic assessment is reserved for patients whose graft dysfunction is atypical for AR or who fail to respond to therapy. Ultrasound-guided biopsy is performed in this setting to differentiate between steroid-resistant rejection and Cs-A nephrotoxicity.
Accelerated Acute Rejection
Accelerated acute rejection occurs typically within the first week following transplantation and can be a severe form of rejection, presenting with oliguria and rising serum creatinine levels. The prognosis is poor with graft loss rates as high as 60%.  The sonographic features are identical to those seen in AR and ATN.
Chronic rejection develops months to years after transplantation and results in progressive vascular compromise of the graft associated with insidious decline in renal function [Figure 3]. Ultrasound findings are those of a small graft with thinned echogenic cortex, the RI is normal to slightly elevated. Biopsy is often required to exclude superimposed and potentially treatable AR.
High serum levels of Cs-A have direct nephrotoxic effect and this complication may occurat any time after transplantation. The diagnosis is established when abnormal renal function occurs in the presence of high Cs-A level; ultrasound findings are nonspecific and frequently normal. 
| Vascular Complications|| |
Renal vein thrombosis or occlusion
The incidence of renal vein thrombosis (RVT) is less than 1–2 % and constitutes a surgical emergency. Patients with RVT present with oliguria or anuria and elevated serum creatinine levels. Early detection of RVT is critical in order to preserve graft function because it is prone to venous infarction and/or rupture; the treatment of choice is surgical exploration. Ultrasound findings include an enlarged kidney with absent venous flow on CDI; a thrombus filled main renal vein is diagnostic while a prolonged U-shaped or plateau-like reversal of arterial flow in diastole is characteristic of RVT. ,,
Renal artery thrombosis
It is a rare condition affecting less than 1% of grafts with the main cause being a consequence of technical problems at the site of anastomosis. Since the renal graft has no collateral arterial blood supply, irreversible injury may result if the ischemic time exceeds 1.5 hours. Patients present with anuria and hypertension; when Doppler fails to show any arterial flow within the graft, angiogram is indicated for confirmation. 
Renal artery stenosis
Renal artery stenosis (RAS) is seen in up to 12%  of renal transplant recipients. The stenosis almost always develops within one cm of the anastomosis due to neointimal hyperplasia at this site. The findings include an elevation of serum creatinine, hypertension and a bruit over the graft. The treatment of choice is percutaneous angioplasty, which is successful in over 90% of the cases. Ultrasound and CDI will show a high velocity and turbulent blood flow exceeding the peak flow in the iliac artery [Figure 4]. Angle corrected flow velocities above 2 cm/sec and post-stenotic turbulence carry a sensitivity rate of 91% and specificity of 87%.  A low RI within the graft, less than 0.6, may be highly specific for stenosis over 50%.  Reduction in pulse amplitude and delayed systolic upstroke on PD, with an acceleration index less than 3 m/sec  or a systolic acceleration time over 0.07 sec is considered strong evidence of severe RAS.  Regardless of Doppler findings, angiography is indicated when clinical suspicion of RAS is high.
| Urologic complications|| |
Renal transplants are associated with urological complications in 5–10% of cases and are associated with high mortality rates of up to 2 2%.  Allograft loss or death is more common when these complications occur within three weeks of surgery,  which in most cases are technical and usually result from inadequate blood supply to the lower pole of the kidney, or imperfect anastomosis between the ureter and the urinary bladder. 
Urinary fistula and urinoma
Fistula or leakage of urine occur in 2–5% of grafts, and account for half of the urologic complications after transplantation. Such complications occur within three weeks of surgery  mainly at the vesico-ureteral junction as a consequence of ischemia and necrosis of the distal ureter due to poor blood supply. Late leaks postoperatively are usually due to ureteral or parenchymal necrosis caused by rejection. 
Urine leaks in small amount may be undetectable by ultrasound; when leakage is large, it presents as fluid collection or urinary ascites. Urinoma appears as cystic fluid collection in the pelvis adjacent to the ureter and separated from the bladder. Diagnosis can be made by ultrasound-guided needle aspiration of the fluid, which reveals high creatinine levels. Also, needle aspiration helps to distinguish an urinoma from hematoma or a lymphocele; lymphoceles have creatinine levels similar to serum levels. The site of leak can be determined by antegrade pyelography.
Obstruction and hydronephrosis occurs in 36% of grafts; in most of them (about 90%), the site of obstruction is the uretero-vesical junction, and caused by fibrosis induced by ischemia or rejection of the ureter. Also, post-operative ureteral edema or blood clots and peri-transplant fluid collections such as lymphocele, urinomas, hematomas and abscesses, might cause obstruction to the ureter, calculi are rare constituting less than 2%.  True obstruction is seen in about 18% of the causes while in the remaining, the dilatation of the collecting system is due to ureteral edema, acute rejection and ureteral reflux which cause non-obstructive dilatation.
Lymphoceles are the most common cause of perigraft fluid collection in the transplant population; they are frequently associated with ureteral obstruction, and occur in 5–15% of patients, ,, generally within one year of transplantation. They present clinically with palpable mass, leg pain and edema; diagnosis can be made by needle aspiration while an ultrasound may show septations. The majority is asymptomatic and requires no therapy.
| Post procedure complications|| |
The rate of complications following percutaneous biopsy of transplanted kidney is about 58%. Perinephric hematomas constitute 25–30% of all such complications. Arteriovenous fistula occurs in about 18% of biopsied kidneys [Figure 5]; the features on CDI include low resistance, high velocity arterial flow within the feeding artery and high velocity arterialized venous flow in the associated draining vein. Pseudoaneurysms are rare and may occur as a consequence of renal biopsy, infection within the graft or dehiscence of arterial anastomosis.  CDI shows a high velocity jet from the feeding artery, and the classic biphasic flow pattern at the pseudoaneurysm neck.
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Department of Radiology, King Hussein Medical Center, P.O. Box 4424 Amman 11953
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]