Recently it has been shown that patients returning to hemodialysis (HD) following kidney transplant loss have poor survival, though the factors responsible for these poor outcomes remain largely unknown. In the past, we have shown that occult infection of clotted arteriovenous grafts (AVGs) leads to a chronic inflammatory state characterized by erythropoietin resistance, hypoalbuminemia, elevated C-reactive protein (CRP), and poor outcomes. It is well known that failed renal allografts induce graft intolerance syndrome, a clinical syndrome of pain, fever, and anemia, in the majority of patients. Similarly we have shown that failed renal allografts, by their nature as a nidus of chronic immunoreactivity, also induce a chronic inflammatory state. We speculate that this chronic inflammatory state, characterized by biochemical markers of poor HD outcomes, may be responsible for the excess mortality in this group. It is currently standard practice to leave failed kidney transplants in place upon return to HD and to treat symptomatic graft intolerance syndrome with immunosuppression. While this approach may reduce clinical symptoms in the short term, treatment failure and ultimately transplant nephrectomy occur in the majority of cases. There is also evidence that continued immunosuppression can even be dangerous. It should be noted that medical treatment of graft intolerance syndrome has not been shown to reduce chronic inflammation or decrease mortality. Similarly embolization of failed kidney transplants, another option for handling failed kidney transplants, has a high rate of treatment failure, has not been shown to reduce chronic inflammation, and nothing is known about the long-term safety of this approach. Therefore failed kidney transplants in patients with biochemical markers of chronic inflammation (as is the case for infected, clotted AVGs) should be removed prior to the development of clinical symptoms in order to eliminate the chronic inflammatory state.