Medical Complications Of Kidney Transplantation align='middle'>

However, the most important position in the genesis of post-transplant neurologic complications is performed by immunosuppressive therapy, which may cause direct neurotoxicity or might favor the event of tumors and opportunistic infection. Since the introduction of new immunosuppressive protocols, the character of post-transplant neurologic complications has modified in the past few years . The prognosis of some neurologic complications in renal transplant recipients has improved considerably, because of development in diagnostic and therapeutic measures. Merkel-cell carcinoma Merkel-cell carcinoma is an unusual tumor, mostly affecting elderly Caucasians. Usually the tumor manifests as a solitary painless erythematous nodule, generally ulcerated, located on the head or neck.

In amyloidosis secondary to rheumatoid arthritis, the chance of recurrence is correlated with the exercise of the underlying main illness (Figure 7.17). Good outcomes have been reported in patients with familial Mediterranean fever (Sever et al., 2001). Recurrence is feasible, however the early administration of colchicine, 1 mg/day indefinitely, can stop the deposit of amyloid substance on the transplanted kidney.

In these cases, an increased incidence of acute rejection has been reported (Knoll et al., 2003; Pelletier et al., 2003). In reviewing the information of the USRDS , Hardinger et al. discovered that 21% of renal transplant recipients had to withdraw from MMF treatment because of gastrointestinal side-effects. The 4-year graft survival was considerably lower in sufferers who discontinued MMF than in those who continued the treatment.

Necrotizing glomerulonephritis The incidence of rapidly progressive necrotizing glomerulonephritis after kidney transplantation is uncommon, and usually leads to graft failure. Reinforcement of corticosteroid remedy and the introduction of cyclophosphamide were capable of induce restoration in a transplant affected person with necrotizing GN (Campise et al., 2003). The primary goal of immunosuppressive therapy is the prevention of rejection whereas favoring the development of an immunological adaptation. More potent and particular immunosuppressive agents have allowed a major reduction in the incidence and severity of rejection.

These infections may be progressive and result in chorioretinitis, lymphoma, liver failure, or squamous-cell most cancers. Leishmaniasis, ehrlichiosis, and other uncommon infectious illnesses may happen. A CNI-free immunosuppression based on sirolimus, mycophenolate mofetil, and steroids seemed to be efficient, but the obtainable studies have only a short follow-up (Kreis et al., 2000; Flechner et al., 2002). Thus, whether is it worthwhile and protected to avoid using calcineurin inhibitors remains to be doubtful (Meier-Kriesche and Hricik, 2006). Even discount of the dosage of calcineurin inhibitors should be done with caution. A European survey showed that doses of cyclosporine lower than 3 mg/kg per day within the first 12 months gave poorer graft survival than that obtained with doses ranging between 3 and 6 mg/kg per day . However, a randomized study showed that a 50% reduction of CsA at 1 year in renal transplant sufferers with secure graft function was secure, and improved renal operate (Pascual et al., 2003).

Kidney transplant recipients who develop donor-specific antibodies or non-HLA antibodies could develop an antibody-mediated form of rejection, additionally called humoral rejection (Figure four.2). A variety of similar methods have been proposed to prevent hyperacute rejection in ABO-incompatible kidney transplants. Graft nephrectomy may be obligatory when extreme systemic toxicity from necrotic renal tissue and consumption coagulopathy develop. Diabetes Both CsA and TAC can cause hyperglycemia, by inducing an acquired insulin sensitivity defect . Their diabetogenic effect is strongly enhanced by the concomitant administration of corticosteroids. There is settlement that tacrolimus is more diabetogenic than cyclosporine (Gourishankar et al., 2004; Martinez-Castelao et al., 2005; Wong et al., 2005), most likely because it also exerts a direct toxicity on islet cells (Tamura et al., 1995).

At endoscopic retrograde cholangiopancreatography , intraparenchymal extravasation as a outcome of necrosis may be seen (Figure thirteen.2). Prognosis The severity of pancreatitis is often assessed by contrast-enhanced computed tomography imaging (Table 13.3).

In doubtful cases, an ‘ex juvantibus’ withdrawal of sirolimus could also be instructed. Figure 7.24 Diffuse tubular damage with focal epithelial necrosis and diffuse interstitial irritation. Such morphologic features are characteristic of crystals made from oxalic acid which, on this woman affected by major oxaluria, massively precipitated destroying the graft 6 months after transplantation. At any price, it should be outlined that renal allografts as properly as native kidneys have a ‘point of no return’.