Figure 8a.
The spectrum of sonographic features of ATN is quite variable (Fig 8). The kidney may appear normal, but in severe cases it is typically enlarged, grossly oedematous and echo poor with loss of the normal sonographic cortical/medullary differentiation. The renal sinus echo may be compressed or obliterated due to swelling. Kidneys with severe ATN generally have elevated RIs (over 0.8) but clinically significant ATN may be seen in conjunction with a normal RI, especially within the first 24 hours after surgery [16].
Figure 8a, b. Acute tubular necrosis. Renal pyramids are clearly visualised and corticomedullary differentiation is preserved. Debris is present in the collecting system. The RI was moderately elevated, measuring 0.88.
Figure 8a.
Figure 8b.
Acute Rejection (AR): AR is a common complication occurring in 20-30% of cadaveric grafts. The occurrence of an AR episode is the single most important event determining the short (1 year) and long-term (5 year) graft survival. Among those grafts afflicted, roughly equal proportions have single and multiple episodes [6]. Fortunately, AR is successfully treated in over 80% of cases through the selective use of pulsed intravenous corticosteroids, Cs-A, and the monoclonal antibody OKT3 [6]. The first episode of AR typically occurs within six months of transplantation and often within the first 5 weeks [6]. Before the introduction of Cs-A, AR frequently presented in an advanced form with the classic clinical triad of a tender swollen graft, fever and rising creatinine. With the widespread use of Cs-A, AR is now a more indolent process commonly diagnosed by biopsy done for a rising creatinine in an asymptomatic patient.
AR is characterized pathologically by lymphocytic and polymorphonuclear cell infiltrates into the interstitial space (tubular interstitial rejection) and/or the subendothelial portion of the vessel walls (vascular rejection). Infiltrates may vary in severity and be diffuse or focal within the graft. Hemorrhage may accompany interstitial edema in severe cases. Vascular rejection may range from mild (subendothelial cellular infiltrates) to severe necrotizing arteritis with in situ vascular thrombosis, ischemia and parenchymal necrosis [6]. The more severe forms of vascular AR are associated with a higher incidence of graft loss.
The sonographic hallmarks of severe AR reflect the underlying pathology and include:
Figure 9a. Decreased cortical echogenicity and swelling of the medullary pyramids resulting in loss of cortical/medullary differentiation.
Figure 9b. Oedema within the renal sinus fat which may efface or obliterate the sinus echo complex.
Figure 9c. Oedema of the collecting system wall.
Figure 9d. Focal echo-poor areas of parenchymal infarction and perigraft fluid due to necrosis and haemorrhage.
In severe cases, PD characteristically shows reduced, absent or reversed diastolic flow with elevation of the RI (Fig 10). An early to mid diastolic notch in the PD waveform may be specific for rejection but is of low sensitivity [17]. In patients with an appropriate clinical history, these findings are typical of acute rejection and immunosuppressive therapy is started on an empirical basis.
Figure 10. Reversed diastolic flow in severe acute rejection.
More often, however, patients present with milder but clinically significant rejection episodes and have normal sonographic and doppler findings. Many studies have demonstrated that the Resistive Index lacks sufficient sensitivity and specificity to be used routinely in screening for rejection [15,18,19]. In patients with biopsy-proven rejection, over 50% of grafts have normal RIs (0.7 or less) [18]. Furthermore, a single abnormal RI measurement cannot distinguish between ATN and rejection, both of which may coexist in the early postoperative period. Consequently, most patients clinically suspected of having AR are treated empirically with corticosteroids. Sonographic assessment is reserved for those whose graft dysfunction is atypical for AR or who fail to respond. Ultrasound-guided biopsy is performed in this setting to differentiate between steroid-resistant rejection and Cs-A nephrotoxicity.
Accelerated Acute Rejection (AAR): AAR typically occurs within the first postoperative week, but is uncommon due to extensive antibody screening currently in use. The incidence of AAR is greater among patients who have rejected a previous graft. AAR is combined cellular and humoral immune response; low levels of circulating antibodies or presensitized T lymphocytes are thought to be responsible [20]. AAR can be an unusually severe form of rejection, presenting with oliguria and rapidly rising serum creatinine. The prognosis is poor with graft loss rates as high as 60% [6]. The sonographic features are identical to those seen in AR and ATN.
Chronic Rejection (CR): Chronic rejection develops months to years after engraftment and is due to antibodies directed to the graft endothelium as a consequence of repeated episodes of AR. This results in progressive vascular compromise of the graft associated with insidious decline in renal function. Sonographic findings are those of a small graft with thinned echogenic cortex and relative sparing of the medullary pyramids (Fig 11). The RI is typically normal or slightly elevated. Biopsy is often required to exclude superimposed and potentially treatable AR.
Figure 11. Chronic rejection.
The sonographic features of renal vein thrombosis include an enlarged kidney with absent venous flow on CDI or PD imaging [22]. A distended thrombus-filled main renal vein is diagnostic of this entity but absence of the finding does not exclude the disorder [23]. A prolonged "U-shaped" or plateau-like reversal of arterial flow in diastole is characteristic of RVT (Fig 12) [24,25,26], and when seen in combination with absent renal venous flow on CDI should suggest the correct diagnosis.
Figure 12a. Prolonged, plateau-like reversal of diastolic flow in a patient with renal vein obstruction. At surgery the kidney was abnormally mobile and had undergone partial torsion, kinking and obstructing the renal vein.
Figure 12b. Doppler study 12 hours after detorsion of the graft shows normal arterial and venous flow.
Figure 12c. Another example of renal vein thrombosis, in a different patient.
Figure 12d. A further example. Note the reversal of flow in diastole.
Although uncommon, Hyperacute Rejection (HAR) may still occur. This process develops when circulating antibodies directed against vascular endothelium in the graft activate the complement system within minutes to hours of surgical revascularization. Endothelial destruction, microvascular occlusion, and in situ thrombosis rapidly ensue, leading to cortical infarction. HAR becomes evident in the operating suite shortly after the renal artery is unclamped and is manifest by swelling, cyanotic congestion of the graft, and failure to produce urine (primary graft anuria). Immediate transplant nephrectomy is usually required.
Ultrasound will show a structurally normal kidney in RAS. CDI and PD findings include a high velocity jet exceeding peak flow in the iliac artery (Fig 13).
Figure 13. High grade transplant renal artery stenosis. A high velocity jet (4.95 m/s) is present proximally in the vessel (13a). Aliasing and turbulent flow are present. CD image of the same stenosis (13b) shows colour aliasing (arrows) at the site of the jet. Angiography (13c) demonstrated an 85% stenosis (arrow).
Figure 13a.
Figure 13b.
Figure 13c.
Aliasing and perivascular colour assignment may be seen in high-grade stenoses. Angle corrected flow velocities above 2 m/s and post-stenotic turbulence are sensitive (91%) [28] and reasonably specific (87%) for RAS [27]. Unfortunately, accurate angle corrected velocity measurements are not always possible, and so many investigators have turned to assessment of the flow waveform within the parenchyma. A pathologically low RI within the graft (0.6 or less) may be highly specific for stenoses over 50% [28]. Reduction in pulse amplitude and delayed systolic upstroke on PD (parvus-tardus phenomenon) may be identified within the renal parenchyma downstream from a significant stenosis (Fig 14). This waveform, characterized by an acceleration index less than 3 m/s² [2] or a systolic acceleration time over 0.07 s should be considered strong evidence of a high-grade RAS [29]. Regardless of the sonographic findings, angiography must be performed when clinical suspicion of RAS is high.
Figure 14. Note the reduction in pulse amplitude and delayed systolic upstroke of renal artery stenosis.
Next: Urologic Complications
Dr C V Zwirewich
Last updated 11th August 1998