This report reviews the last mechanism, which the authors regard as most critical for the long-term survival of allografts, namely, the promotion of chronic rejection by alloantibodies. Chronic humoral rejection characteristically arises late after transplantation and causes transplant glomerulopathy, multilamination of peritubular capillary basement membranes, and C4d deposition in PTCs and glomeruli. Circulating antidonor human leukocyte antigen class II antibodies are commonly detected and may precede the development of graft injury. Prognosis is poor, especially when recognized after graft dysfunction has developed.
Improved detection and treatment are critically needed for this common cause of late graft loss.”
“Chronic rejection, the primary cause of late renal allograft loss, results from a complex interplay between immunological and non-immunological factors. During GW786034 chemical structure the past few decades, transplant research has focused almost exclusively on identifying more powerful and minimally Paclitaxel concentration toxic immunosuppressive strategies to prevent acute rejection and alloimmune response toward the graft, whereas poor attention has been paid to non-immunological factors. However, the discrepancy between remarkable improvements in the prevention
of acute rejection and failure to ameliorate long-term graft outcomes suggests that non-immunological injuries may have an important role in the progressive loss of graft function. As kidney graft resembles the remnant kidney, in which a low nephron mass initiates a self-perpetuating process of progressive renal function loss, the same Rocuronium bromide therapeutic tools able to retard progression of chronic renal disease are expected to be effective in kidney transplant patients as well. Indeed, high blood pressure (BP) levels, along with increased urinary protein excretion and hyperlipidemia, have been associated with reduced graft survival. Hence, strict BP control, renin-angiotensin system blockade to reduce proteinuria, and statins for hyperlipidemia
control should probably represent the standard of care for kidney transplant patients. Furthermore, a multimodal nephroprotective strategy that includes smoking cessation, and tight glucose control for diabetes, might eventually be crucial to improve long-term graft outcomes.”
“Despite the impressive reduction in early acute rejection rates over the past decades, chronic allograft dysfunction remains a key issue after renal transplantation. A number of factors, such as the quality of the original organ, ischemia/reperfusion injury, and/or (treated) acute rejection, will adversely affect renal structure, causing early (but often mild) tubular atrophy and interstitial fibrosis.