The majority of kidneys used for transplantation are obtained from deceased donors. These kidneys must undergo cold preservation/storage before transplantation to preserve tissue quality and allow time for recipient selection and transport. However, cold storage (CS) can result in tissue injury, kidney discardment, or long-term renal dysfunction after transplantation. We have previously determined mitochondrial superoxide and other downstream oxidants to be important signaling molecules that contribute to CS plus rewarming (RW) injury of rat renal proximal tubular cells. Thus, this study's purpose was to determine whether adding mitoquinone (MitoQ), a mitochondria-targeted antioxidant, to University of Wisconsin (UW) preservation solution could offer protection against CS injury. CS was initiated by placing renal cells or isolated rat kidneys in UW solution alone (4 h at 4°C) or UW solution containing MitoQ or its control compound, decyltriphenylphosphonium bromide (DecylTPP) (1 M in vitro; 100 M ex vivo). Oxidant production, mitochondrial function, cell viability, and alterations in renal morphology were assessed after CS exposure. CS induced a 2-to 3-fold increase in mitochondrial superoxide generation and tyrosine nitration, partial inactivation of mitochondrial complexes, and a significant increase in cell death and/or renal damage. MitoQ treatment decreased oxidant production ϳ2-fold, completely prevented mitochondrial dysfunction, and significantly improved cell viability and/or renal morphology, whereas DecylTPP treatment did not offer any protection. These findings implicate that MitoQ could potentially be of therapeutic use for reducing organ preservation damage and kidney discardment and/or possibly improving renal function after transplantation.

Comprehensive patient education improves the choice and prevalence of HoD therapies. We further find that 3 sessions of CPE may provide needed resources for the large majority of subjects for adequate decision-making.

Background Chronic kidney disease (CKD) incidence is increasing and associated mortality and morbidity are high. Educating patients is effective in delaying progression and establishing optimal renal replacement therapy (RRT). Tele-education/telemedicine (TM) can be an effective tool to provide such education, but there are no available data quantifying its effectiveness. We attempted to establish such evidence correlating the effect of education in patient choices and with the start of actual RRT. We present results from a 3-year pilot study evaluating the effectiveness of comprehensive predialysis education (CPE) through TM for CKD patients compared with a standard care group [face to face (FTF)]. The patient’s ability to choose RRT was the primary endpoint. Methods This was a randomized controlled study providing CPE over three classes at nine sites (one FTF and eight TM). Three assessment tools were utilized to compare groups: CKD knowledge, literacy and quality of life. Results A total of 47.1% of FTF and 52.2% of TM patients reported not having enough information to choose a modality. This decreased by the third visit (FTF 7.4%, TM 13.2%). Home modality choices more than doubled in both groups (FTF 25.8–67.7%, TM 22.2–50.1%). In patients that completed one visit and needed to start RRT, 47% started on a home modality or received a pre-emptive transplant (home hemodialysis 6%, peritoneal dialysis 38%, transplant 3%). Conclusions Results show almost 90% (TM 87%, FTF 95%) of the attendees could choose a modality after education. Home modality choices doubled. Patients were able to make an informed choice regardless of the modality of education.

Cold preservation is a beneficial and necessary procedure used to preserve deceased donor kidneys prior to transplantation. However, extended preservation periods result in injury that can lead to poor graft function following transplantation. Thus, this study's purpose was to evaluate the early effects of cold storage (CS) alone and to determine if MitoQ, a mitochondrial targeted antioxidant, could offer protection during this stage. We hypothesize that CS increases oxidant production and mitochondrial dysfunction, and that adding MitoQ to cold preservation solutions will attenuate injury. Renal cells and rat kidneys were exposed to CS (UW‐Viaspan solution; 4°C) with or without MitoQ (1μM; 100μM respectively) and monitored for oxidants (O2·−, NO, ONOO−), mitochondrial function (respiratory complexes, mitochondrial membrane potential), and cell viability. Our cell model results suggest that CS first causes mitochondrial membrane depolarization, followed by oxidant production, then mitochondrial dysfunction, and modest cell death. MitoQ reduced oxidant production and protected against mitochondrial complex inactivation using both cellular and isolated rat kidney models. Excitingly, we have identified a potential therapeutic reagent that could be added to existing preservation solutions to reduce CS damage and possibly improve renal function following transplantation.