Figure 2. Transverse colour doppler image of a normal renal allograft showing its normal position anterior to the external iliac vessels (white arrow).
Figure 2. Transverse colour doppler image of a normal renal allograft showing its normal position anterior to the external iliac vessels (white arrow).
The renal cortex is readily distinguished from the more echo-poor medullary pyramids (Fig 3). The renal sinus is normally hyperechoic in the absence of hydronephrosis, although small amounts of fluid are often seen within the renal pelvis in the immediate postoperative period [12]. Transplant volume is estimated using the formula for the volume of a prolate ellipsoid (0.5 x long x transverse x AP dimensions). Small perigraft fluid collections are common; most represent hematomas which spontaneously resolve.
Figure 3. Sagittal scan of a normal transplant. Echopoor medullary pyramids (arrows) are easily distinguished from the adjacent renal cortex.
Figures 4 & 5. CDI demonstration of normal flow within the transplant. Interlobar (small arrow) and arcuate vessels (curved arrow)
are readily visualised. (Fig 4 courtesy of ATL)
Figure 5.
The normal transplant kidney has a low resistance arterial vascular bed characterized by streamlined systolic flow and continuous forward flow in diastole on PD. Normal main renal artery flow velocity ranges between 20 and 52 cm/sec with a mean of 32 cm/sec [13]. Prior knowledge of the number and surgical anatomy of transplanted renal arteries is important as renal artery stenosis and branch renal artery thrombosis are more common among transplants with multiple vessels.
The Resistive Index (RI) is a widely used measure of resistance to arterial flow within the renal vascular bed and is calculated from the PD arterial waveform (Fig 6, Fig 7). Use of the RI eliminates the need for accurate angle-corrected measurements of blood flow in assessment of vascular resistance. An RI of less than 0.7-0.8 is considered normal [14,15], whereas an RI in excess of 0.9 is a strong indicator of transplant dysfunction.
Figure 6. Resistive Index.
Figure 7. Measurement of the Resistive Index.
| Immediate (<1 week) | Early (1-4 weeks) | Late (>1 month) | |
|---|---|---|---|
| Parenchymal | Acute Tubular Necrosis Rejection · Hyperacute · Accelerated Acute · Acute |
Acute Rejection | Acute Rejection Chronic Rejection Cyclosporine Toxicity Disease Recurrence Infection |
| Vascular | Renal Vein Thrombosis Renal Artery Thrombosis |
Renal Vein Thrombosis | Renal Artery Stenosis |
| Urologic | Ureteral Oedema | Urinary Fistulae Urinoma |
Ureteral Strictures |
| Fluid Collections | Haematoma Abcess |
Urinoma | Lymphocoele |
| Neoplastic | Skin Malignancies Lymphomas |
||
| Iatrogenic | Post Biopsy Haemorrhage Renal AV Fistula Pseudoaneurysm |
Several of these processes share the same pathologic features, namely cellular infiltration of the graft with resulting oedema, global enlargement, and vascular compromise. Consequently, they often share similar or identical sonographic and Doppler features which can cause a diagnostic dilemma for the radiologist [7]. Elevation of the RI above 0.9 or progressive elevation above a normal baseline is good evidence of renal dysfunction [7] but is often nonspecific (Table 3) [14], and must be interpreted in the context of time of onset of dysfunction, clinical status and biochemical tests.
| Parenchymal | Acute Rejection Acute Tubular Necrosis Pyelonephritis |
|---|---|
| Vascular | Renal Vein Thrombosis Hypotension |
| Urological | Ureteral Obstruction |
| Technical | Graft Compression |
While an awareness of the typical times of onset of complications and their clinical manifestations will usually facilitate a correct diagnosis [16], differentiation between ATN, Cs-A toxicity and acute rejection usually requires biopsy [15]. Ancillary invasive imaging procedures such as angiography, percutaneous nephrostomy (PN) and antegrade pyelography (AP) may also be useful in selected situations. The radiologist should always address the following questions when evaluating the failing renal graft:
Next: Parenchmal Complications
Dr C V Zwirewich
Last updated 11th August 1998