*5.1.1. Acute Tubular Necrosis (ATN)*

ATN is the most common cause of DGF, defined as need for dialysis in the first week following transplantation. It is related to the cold ischemic time [29] and infrequently seen in patients whose transplants are from living donors [30, 31]. ATN occurs in the first days following transplantation, even in the first hours. Renal function usually recovers within 1-2 weeks, but can last abnormal up to 3 months [19, 31].

There is no imaging specific pattern for the diagnosis of ATN [10, 32]. Images can be completely normal depending on the severity of injury [33-35]. US can reveal swollen and globular kidneys, with increasing corticomedullary differentiation (CMD) [26]. The cortex is brightly echogenic, swollen, rendering medullary pyramids very prominent and compressing fat in the renal sinus. An elevated Resistance Index (RI > 0,80) measured in the intra-renal arteries is considered to be a non-specific marker of graft dysfunction, seen on both, ATN and rejection [8, 32, 36-40]. Serial measurements of RI and Pulsatile index (PI) combined with clinical and biochemical information is useful in monitoring the patient [31, 39]. At MRI, CMD tends to be preserved [41]. Dynamic functional MRI and perfusion show slightly delayed medullary enhancement, and markedly impaired contrast excretion [42, 43]. CT demonstrates decreased graft enhancement, eventually with no contrast media excretion [19].

With radionuclide imaging (iodine-131 orthoiodohippurate and Tc-99m MAG3), the most conspicuous findings are delayed transit with delayed time to maximal activity (T-max), delayed time from maximum to one-half maximal activity (T-1/2), and a high 20 to 3 minute ratio. On sequential images, marked parenchymal retention is seen [44, 45]. (Figure 4).

to a severe vascular lesion and to cortical necrosis. Imaging does not play any role. Absence of perfusion will be seen in Doppler, angiography or scintigrams [10]. Accelerated acute rejection occurs within the first week. The imaging features are the same as of acute rejection

**Figure 4.** (A) and (B): 99mTc-DTPA renal scintigraphy. Postoperative period of 48 hours. Preserved arterial blood flow

Imaging in Kidney Transplantation http://dx.doi.org/10.5772/55074 31

Currently, the overall risk of acute rejection within 1 year after transplantation is less than 15% [46]. AR can be divided in acute-antibody mediated rejection and T-cell-mediated rejection. Acute-antibody mediated rejection is characterized by a rapid graft dysfunction due to inflammation. T-cell-mediated rejection can also present as an increasing creatinine level and

(AR). Cortical nephrocalcinosis may be seen in rejected transplants left in situ [10, 47].

(A)

(B)

and glomerular function deficit, with minor urine formation during the study.

#### *5.1.2. Rejection*

Rejection can be classified according to the period of appearance as hyperacute (occurring within minutes), acute (occurring within days to weeks), late acute (occurring after 3 months), or chronic (occurring months to years after transplantation) [46]. When hyperacute rejection happens, graft dysfunction is usually irreversible. The humoral reaction of the patient leads

also complications that can occur but in minor incidence. The most common complications of

In the early post-transplant period, delayed graft function (DGF) occurs when the decline of the serum creatinine concentration is slower than wanted. The most common medical complications (MC) related to DGF are acute tubular necrosis (ATN), drug toxicity (mainly causes by calcineurin inhibitors - CNI), and rejection. In general, imaging tools in evaluating MC following renal transplantation are non-specific [24-26]. The major role of imaging in this setting is to exclude urologic, collections, and/or vascular complications. To date, quantitative criteria for the diagnosis of acute graft dysfunction with MR renography or nuclear medicine have not been adequately standardized. Promising techniques, especially using quantitative

ATN is the most common cause of DGF, defined as need for dialysis in the first week following transplantation. It is related to the cold ischemic time [29] and infrequently seen in patients whose transplants are from living donors [30, 31]. ATN occurs in the first days following transplantation, even in the first hours. Renal function usually recovers within 1-2 weeks, but

There is no imaging specific pattern for the diagnosis of ATN [10, 32]. Images can be completely normal depending on the severity of injury [33-35]. US can reveal swollen and globular kidneys, with increasing corticomedullary differentiation (CMD) [26]. The cortex is brightly echogenic, swollen, rendering medullary pyramids very prominent and compressing fat in the renal sinus. An elevated Resistance Index (RI > 0,80) measured in the intra-renal arteries is considered to be a non-specific marker of graft dysfunction, seen on both, ATN and rejection [8, 32, 36-40]. Serial measurements of RI and Pulsatile index (PI) combined with clinical and biochemical information is useful in monitoring the patient [31, 39]. At MRI, CMD tends to be preserved [41]. Dynamic functional MRI and perfusion show slightly delayed medullary enhancement, and markedly impaired contrast excretion [42, 43]. CT demonstrates decreased

With radionuclide imaging (iodine-131 orthoiodohippurate and Tc-99m MAG3), the most conspicuous findings are delayed transit with delayed time to maximal activity (T-max), delayed time from maximum to one-half maximal activity (T-1/2), and a high 20 to 3 minute ratio. On sequential images, marked parenchymal retention is seen [44, 45]. (Figure 4).

Rejection can be classified according to the period of appearance as hyperacute (occurring within minutes), acute (occurring within days to weeks), late acute (occurring after 3 months), or chronic (occurring months to years after transplantation) [46]. When hyperacute rejection happens, graft dysfunction is usually irreversible. The humoral reaction of the patient leads

renal transplantation are discussed bellow and listed in Table 1.

and functional MRI are objects of interest in this field [14, 27, 28].

graft enhancement, eventually with no contrast media excretion [19].

**5.1. Medical complications**

30 Current Issues and Future Direction in Kidney Transplantation

*5.1.1. Acute Tubular Necrosis (ATN)*

*5.1.2. Rejection*

can last abnormal up to 3 months [19, 31].

**Figure 4.** (A) and (B): 99mTc-DTPA renal scintigraphy. Postoperative period of 48 hours. Preserved arterial blood flow and glomerular function deficit, with minor urine formation during the study.

to a severe vascular lesion and to cortical necrosis. Imaging does not play any role. Absence of perfusion will be seen in Doppler, angiography or scintigrams [10]. Accelerated acute rejection occurs within the first week. The imaging features are the same as of acute rejection (AR). Cortical nephrocalcinosis may be seen in rejected transplants left in situ [10, 47].

Currently, the overall risk of acute rejection within 1 year after transplantation is less than 15% [46]. AR can be divided in acute-antibody mediated rejection and T-cell-mediated rejection. Acute-antibody mediated rejection is characterized by a rapid graft dysfunction due to inflammation. T-cell-mediated rejection can also present as an increasing creatinine level and diminished urinary output. Fever and graft tenderness now rarely occur. As mentioned before, imaging in AR is non-specific. Imaging findings superpose with other conditions such as ATN, drug nephrotoxicity, UC, and VC. The sonographic features are similar to those described for ATN [10, 33]. They include renal enlargement, heterogeneity of renal cortex, loss, increase or decrease of CMD, hypoechogenicity of renal pyramids, cortex and sinus, thickening of renal cortex and thickening of the walls of collecting system (figure 5). Although both ATN and AR cause PI and RI rise on Doppler US, the likelihood of AR is greater with high values [31]. An elevated RI (>0,9) is highly suggestive of AR, but is not specific [32, 36-38, 48, 49]. A PI of more than 1.5 is used in some centers for helping diagnosing rejection. Radionuclide studies show decreased renal perfusion and function [45, 50]. If the isotope study is normal in early postoperative phase and becomes abnormal subsequently, acute rejection can be diagnosed. MR findings are variable and include various degrees of swelling, globular morphology with indistinct margins of the graft, decrease or loss of the CMD are common findings [10, 14, 19, 28, 31]. Perfusion abnormalities are seen in contrast enhanced scans with marked decreased cortex and medulla enhancement, prolonged arterial phase, poor wash-out and patchy nephrogram [10, 14, 24, 28] (Figure 6).

and antibodies. It presents as a progressive decline in renal function [46] and may be diffi‐ cult to diagnose by a non-invasive techniques. RI measurements are not reliable for this di‐ agnosis [24, 38, 40]. Initially, the graft is enlarged and shows increased cortical thickness, which later changes to a thin cortex and mild hydronephrosis on both US, CT, and MRI [19, 50] [28, 33]. A diminished uptake of radiopharmaceuticals and also a normal parenchymal transit with absent or minimal cortical retention is seen in scintigraphy studies. In advanced

Imaging in Kidney Transplantation http://dx.doi.org/10.5772/55074 33

stages, parenchymal retention of radiotracers is present [45].

(A)

(B)

degree and glomerular function deficit of moderate degree

**Figure 6.** (A) and (B): 99mTc-DTPA renal scintigraphy. Two week follow up. Depressed arterial blood flow of a discrete

**Figure 5.** (A) Acute rejection, longitudinal scan. The cortex is swollen, extending into the renal sinus and compressing the fat. Medullary pyramids are prominent (arrows), indicative of an increase in cortical echogenicity. (B) Spectral Dop‐ pler shows a RI > 0,90 highly suggestive of AR.

Chronic rejection (CR) occurs after at least 3 months to years after transplantation. It hap‐ pens due to an insufficient immunosuppression to control residual antigraft lymphocytes and antibodies. It presents as a progressive decline in renal function [46] and may be diffi‐ cult to diagnose by a non-invasive techniques. RI measurements are not reliable for this di‐ agnosis [24, 38, 40]. Initially, the graft is enlarged and shows increased cortical thickness, which later changes to a thin cortex and mild hydronephrosis on both US, CT, and MRI [19, 50] [28, 33]. A diminished uptake of radiopharmaceuticals and also a normal parenchymal transit with absent or minimal cortical retention is seen in scintigraphy studies. In advanced stages, parenchymal retention of radiotracers is present [45].

diminished urinary output. Fever and graft tenderness now rarely occur. As mentioned before, imaging in AR is non-specific. Imaging findings superpose with other conditions such as ATN, drug nephrotoxicity, UC, and VC. The sonographic features are similar to those described for ATN [10, 33]. They include renal enlargement, heterogeneity of renal cortex, loss, increase or decrease of CMD, hypoechogenicity of renal pyramids, cortex and sinus, thickening of renal cortex and thickening of the walls of collecting system (figure 5). Although both ATN and AR cause PI and RI rise on Doppler US, the likelihood of AR is greater with high values [31]. An elevated RI (>0,9) is highly suggestive of AR, but is not specific [32, 36-38, 48, 49]. A PI of more than 1.5 is used in some centers for helping diagnosing rejection. Radionuclide studies show decreased renal perfusion and function [45, 50]. If the isotope study is normal in early postoperative phase and becomes abnormal subsequently, acute rejection can be diagnosed. MR findings are variable and include various degrees of swelling, globular morphology with indistinct margins of the graft, decrease or loss of the CMD are common findings [10, 14, 19, 28, 31]. Perfusion abnormalities are seen in contrast enhanced scans with marked decreased cortex and medulla enhancement, prolonged arterial phase, poor wash-out and patchy

nephrogram [10, 14, 24, 28] (Figure 6).

32 Current Issues and Future Direction in Kidney Transplantation

(A)

(B)

pler shows a RI > 0,90 highly suggestive of AR.

**Figure 5.** (A) Acute rejection, longitudinal scan. The cortex is swollen, extending into the renal sinus and compressing the fat. Medullary pyramids are prominent (arrows), indicative of an increase in cortical echogenicity. (B) Spectral Dop‐

Chronic rejection (CR) occurs after at least 3 months to years after transplantation. It hap‐ pens due to an insufficient immunosuppression to control residual antigraft lymphocytes

**Figure 6.** (A) and (B): 99mTc-DTPA renal scintigraphy. Two week follow up. Depressed arterial blood flow of a discrete degree and glomerular function deficit of moderate degree
