Graft dysfunction

Infection with SENV-D and -H adversely affected the outcome of antiviral therapy for HCV (572), whereas in another study SENV did not influence the clinical or histological features of HCV at all. (577) SENV infection is not associated with increased evidence of liver disease or the risk of HCC. (576, 579) Likewise, this virus does not play any role in graft dysfunction after liver transplantation, although SENV was found in 35% of unselected liver transplant recipients. It is possible that SENV is a causative agent of posttransfusion-associated hepatitis, especially since specific DNA could be detected in liver tissue. 

Bartlett, A.S., Ramadas, R., Furness, S., Gane, E., McCall, J.L. The natural history of acute histologic rejection without biochemical graft dysfunction in orthotopic liver transplantation A systematic review. Liver Transplant. 2002 8 1147—1153... 

Kohli HS, Sud K, Jha V, Gupta KL, Minz M, Joshi K, Sakhuja V. Cyclosporin-induced haemolytic-uraemic syndrome presenting as primary graft dysfunction. Nephrol Dial Transplant 1998 13(ll) 2940-2. 

The effect of ketoconazole in ciclosporin-treated kidney transplant recipients has been the subject of a prospective randomized study (37). In 51 ketoconazole-treated patients and 49 controls there was a similar frequency of acute rejection episodes. However, in the control group, rejection episodes were more recurrent, with a poorer response to treatment. Acute ciclosporin nephrotoxicity was more common in the ketoconazole group, but this was encountered more at induction and rapidly reversed on further reduction of the dose of ciclosporin. Chronic graft dysfunction was significantly less in... 

Leflunomide has been used as an immunosuppressive agent in kidney and liver transplant recipients to spare cal-cineurin inhibitors and glucocorticoids and to slow progression of chronic kidney graft dysfunction (28,37) (Table 1). 

Francois H, Durrbach A, Amor M, Djeffal R, Kriaa F, Paradis V, et al. The long-term effect of switching from cyclosporin A to mycophenolate mofetil m chronic renal graft dysfunction compared with conventional management. Nephrol Dial Transplant 2003 18 1909-16. 

Hyperacute rejection rarely occurs in patients receiving a liver transplant. The liver s special status for transplantation is not fully understood, but the local release of cytokines may alter the immunologic reaction taking place in the liver. Early graft dysfunction is treated with supportive care and retransplantation if possible. 

Transient kidney graft dysfunction and acute tubular necrosis... 

Minamiguchi, S., Sakurai, T., Fujita, S., Okuno, T., Haga, H., Mino, M., Kanehira, K., Matsushiro, H., Nakashima, Y, Inomata, Y., Tanaka, K., and Yamabe, H. (1999). Living related liver transplantation Histopathologic analysis of graft dysfunction in 304 patients. Human Pathol. 30, 1479-1487. 

VI. Treatment of Transient Graft Dysfunction following Lung Transplantation ... 

FIGURE 9 The effects of 80-ppm nitric oxide (NO) inhalation in six patients with transient graft dysfunction after lung transplantation. Pulmonary artery pressure (PAp), pulmonary vascular resistance index (PVRI), and intrapulmonary shunt fraction (Qs/Qt) decreased significantly, while arterial oxygen pressure (PaOi increased. [Adapted and reproduced with permission from Adatia et al. (77).]... 

Adatia, I., Lillehei, C., Arnold, J. FI., et al. (1994). Inhaled nitric oxide in the treatment of postoperative graft dysfunction after lung transplantation. Ann. Thorac. Surg. 57, 1311-1318. 

Treille S, Quoidbach A, Demol H, Vereerstiaeten P, Abramowicz D. Kidney graft dysfunction after drug interaction between clarithromycin and cyclosporin. Nephrol Dial Transplant (1996) 11,1192-3,... 

Fig. 1. Various ways chemokines might accelerate transplant rejection. Release of chemokines from the transplanted organ and/or cells infiltrating the graft may result in shifting the TH-l/TH-2 cytokine balance and cell activation that lead to further chemokine release and continued cell reemitment. Collectively these changes lead to tissue damage, graft arteriosclerosis, and eventually graft dysfunction.

Severe hypertension with or without allograft dysfunction is the most frequent clinical symptom. Hypertension is a common feature in transplant recipients (up to 80%). Therefore, as for native kidneys, RAS is specifically suspected when hypertension develops suddenly, rapidly becomes more severe and resistant to medical therapy, and is associated with graft dysfunction without any other cause or when associated with an audible bruit over the graft (Palleschi et al. 1980 Rijksen et al. 1982). It may account for around l%-5% of post-transplant hypertension. However, at present, early RAS are often detected systematically with color flow US, despite no blood pressure or renal function change. 

---