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Complement activation is actively regulated to prevent injudicious activation, such as on peritubular endothelia and basolateral aspects of tubules. Miao et al. studied mice in which the key complement regulator, Crry, was deleted from tubular cells. This lacked functional consequence in unmanipulated animals. Yet, following ischemia-reperfusion, there was greater injury due to alternative pathway activation of C5. When the balance between complement activation and regulation is tipped towards the former, pathologic complement activation can ensue.

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Very low early rejection rates and excellent short-term kidney allograft outcomes have been the mainstay of forwarding the field of Kidney Transplantation in the last few decades. This progress is mainly achieved by using the current armamentarium of maintenance immunosuppression in different combinations and dosages of calcineurin inhibitors (CNI), corticosteroids and antiproliferative drugs. Metabolic risks and nephrotoxicity of CNIs has led to a search for strategies to minimize their use. Similarly, metabolic risks, mood abnormalities and Cushing-like side effects of steroids have forced physicians and patients alike to try to minimize their use in transplantation. Here, we review the most recent randomized controlled trials of minimization of CNI/steroids in a manner (with incident immunologic risks, state of net immunosuppression and side- effects) that may be helpful to choose the best strategy for the individual patient. New trials testing minimization strategies should include in their design, an assessment of the impact of minimization on development of donor specific antibodies and antibody-mediated rejection as well as long-term outcomes.

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