This practice of patient recruitment may be criticized, but we think it is justified according to our low incidence of ITBL. Thus, it was possible to investigate 19 patients with ITBL. ITBL rate in CCR-5��32 patients was virtually equal to the selleck one in CCR-5 wild-type patients. No statistically significant differences regarding ITBL or retransplantation were observed. Why would CCR-5��32 mutation promote the development of ITBL? CCR-5��32 is a 32-base-pair deletion within the coding region of CCR-5, which results in a frame shift and generates a nonfunctional receptor [11]. Homozygous expression of CCR-5��32 is associated with a reduced risk of asthma and with a reduced severity of rheumatoid arthritis [17, 18], multiple sclerosis [19, 20], and primary biliary cirrhosis (PBC) [21].

In other words, the nonfunctional nature of CCR-5��32 protects the individual from autoimmune diseases where CCR-5 seems to play a central pathophysiological role. These data do not backup the theory, that immunological risk factors are dominant in the development of ITBL. Likewise, a correlation of a reduced survival rate with CCR-5��32 would not be consistent to the literature, where CCR-5��32 mutation is associated with an increased survival in renal [12], lung [13], heart [14] and islet cell transplantation [15]. In contrast to those findings, CCR-5��32 is strongly associated with an increased severity of PSC [22]. Patients suffering from PSC have been described as carrying a higher risk for ITBL, with a reported significantly increased incidence of 15.8% to 25% [1, 8, 23].

Another study reported PSC as the only independent risk factor for ITBL with an incidence of 31% compared with 9% of the control group [24]. However, the problem of differentiation between ITBL and recurrence of PSC must be addressed. Recurrence rates of 8.6% to 25% were described for PSC after OLT [25�C27]. The diagnose of recurrence of PSC is based on cholangiographic findings of intrahepatic, hilar and/or exrahepatic strictures, duct irregularities and on the histopathological picture of fibrous cholangitis and/or fibro-obliterative lesions with or without ductopenia, biliary fibrosis, or biliary cirrhosis [28]. Carfilzomib Most of these findings are neither pathognomonic for either recurrence of PSC nor ITBL [29]. All patients with ITBL in this study underwent percutaneous liver biopsy, and our pathologists ruled out PSC recurrence. There remains a diagnostic uncertainty. Since two of three studies failed to show an association between ITBL and CCR-5��32 gene polymorphism, a general recommendation for screening of OLT patients for CCR-5��32 does not seem to be justified.
Anemia is virtually universal at the time of kidney transplantation [1].