*5.1.3. Calcineurin Inhibitors (CNI) nephrotoxicity*

CNI can cause renal vasoconstriction with ischemia. CNI toxicity is caused by afferent arteriolar vasoconstriction followed by a decrease in glomerular perfusion pressure and also by a tubulointerstitial injury independently from its vascular effects [51]. These physiological effects are similar between cyclosporine and tacrolimus. Monitoring the CNI serum levels is important to prevent the occurrence of nephrotoxicity and, on the other hand, to achieve the appropriate immunossupression. Moreover, nephrotoxicity of these drugs not related to their serum levels are described [52, 53].

To date, no imaging or laboratory test has been found accurate enough to discriminate the parenchymal causes of graft dysfunction and renal biopsy remains as the gold standard [22,

Imaging in Kidney Transplantation http://dx.doi.org/10.5772/55074 35

The clinical setting of most UCs is that of a decrease in graft function. Because many of the complications are treatable, it is extremely important to make an early diagnosis and separate from rejection or ATN. The first reports concerning renal transplantation showed a prevalence of UC varying from 10% to 25%, with a mortality rate ranging from 20% to 30%. Nowadays, due to advances in immunosuppressive therapy combined with careful surgical technique the incidence of UC decreased, ranging from 1% to 8% [58, 59]. The majority of the UC are seen during the first month to six months after transplant. Ureteric obstruction and urine leak are

The major causes of ureteral obstruction are ureteral ischemia, edema at the uretero-vesical anastomotic site, infection, extrinsic compression of the ureter by fluid collections, and ureteral kinking. Other relatively rare causes are stones, papillary necrosis, clots, fungi, pelvic fibrosis, and herniation of the ureter [61]. Early-onset obstruction of the ureter is secondary to kinks, clots, edema, inflammation, or a tight submucosal tunnel. Percutaneous treatment is the best treatment option. Late-onset obstruction is caused by fibrosis, ischemia, or periureteral masses or may be secondary to rejection [19]. The transplanted ureter is relatively prone to ischemia due to limited blood supply [22, 24, 50, 58]. A large majority of the ureteral strictures occur in

Sonography shows dilated renal pelvis and calyces and is useful to determine the site of ureteral obstruction (Figure 8). This is a nonspecific finding because it is also seen in cases of diminished ureteral tonus resulted from denervation of the transplant [62], mild dilated collecting system in rejection, vesico-ureteral reflux, and secondary to overdistended bladder.

When highly echogenic, weakly shadowing masses are present in the collecting system, fungus balls should be considered, whereas low-level echoes may suggest pyonephrosis or hemo‐ nephrosis [63]. Other abnormalities of the collecting system include calculi and urothelial tumors. In some cases of acute obstruction an increased RI and PI may be present, however,

At Nuclear Medicine, in patients with early partial obstruction, good perfusion and prompt uptake of the radiotracer may be seen; however, in patients with functionally significant hydronephrosis, radioactivity is retained in the collecting system. Delayed images are useful for differentiating an obstructed ureter from a dilated but unobstructed ureter, since a nonobstructed system shows clearance into the bladder. Diuretic renography and conventional

the distal third of the ureter, usually secondary to ischemia [22, 58].

again they are nonspecific findings [37, 64].

In the later condition, it's important to repeat the US with an empty bladder.

49, 50, 57].

**5.2. Urological complications**

the most common [22, 60].

*5.2.1. Obstructive uropathy*

When DGF occurs many experts prefer do not use CNI due to their possible detrimental effects in the ischemic damaged kidneys [54]. When creatinine level stabilizes without complete renal function recovery or when renal function deterioration occurs, a renal biopsy should be performed. Currently, no clinical findings are specific enough to differentiate allograft rejection from CNI nephrotoxicity. Imaging findings are also non-specific and superimposed with the other parenchymal complications. Cyclosporine toxicity may produce an enlarged kidney with increased cortical echogenicity and prominent medullary pyramids. On radio‐ nuclide images, acute cyclosporine toxicity resembles mild acute rejection, with depressed effective renal plasma flow and parenchymal retention [22, 45] Loss of the corticomedullary differentiation can be seen on MRI [55]. Findings should be correlated with cyclosporine levels. Sustained increasing in RI values (Figure 7), without a morphologic cause such as hydroneph‐ rosis, is indicative of graft dysfunction, but it´s non-specific and may be caused by acute or chronic rejection, ATN, or cyclosporine toxicity [56].

**Figure 7.** CNI toxicity. Spectral doppler evaluation with a mild elevatation of RI.

To date, no imaging or laboratory test has been found accurate enough to discriminate the parenchymal causes of graft dysfunction and renal biopsy remains as the gold standard [22, 49, 50, 57].
