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To meet the demand for kidney transplants (KTx), organs are frequently retrieved not only from standard criteria donors (SCD; a donor who is aged <50 years and suffered brain death from any number of causes, such as traumatic injuries or a stroke) but also from expanded criteria donors (any donor aged >60 years or donors aged >50 years with two of the following: A history of high blood pressure, a creatinine serum level ≥1.5 mg/dl or death resulting from a stroke). This comes at the cost of a higher risk of primary non‑function (the permanent hyperkalemia, hyperuremia and fluid overload that result in the need for continuous dialysis after KTx), delayed graft function (the need for dialysis session at least once during the first week after KTx), earlier graft loss and urinary complications (vesico‑ureteral reflux, obstruction of the vesico‑ureteral anastomosis, urine leakage). At present, there are no commercially available diagnostic tools for assessing kidney quality prior to KTx. Currently available predictive models based on clinical data, such as the Kidney Donor Profile Index, are insufficient. One promising option is the application of perfusion solutions for protein biomarkers of kidney quality and predictors of short‑ and long‑term outcomes. However, to date, protein markers that can be detected with ELISA, western blotting and cytotoxic assays have not been identified to be a beneficial predictors of kidney quality. These include lactate dehydrogenases, glutathione S‑transferases, fatty acid binding proteins, extracellular histones, IL‑18, neutrophil gelatinase‑associated lipocalin, MMPs and kidney injury molecule‑1. However, novel methods, including liquid chromatography‑mass spectrometry (LC‑MS) and microarrays, allow the analysis of all renal proteins suspended/dissolved in the acellular preservation solution used for kidney storage before KTx (including hypothermic machine perfusion as one of kidney storage methods) e.g. Belzer University of Wisconsin. Recent proteomic studies utilizing LC‑MS have identified complement pathway elements (C3, C1QB, C4BPA, C1S, C1R and C1RL), desmoplakin, blood coagulation pathway elements and immunoglobulin heavy variable 2‑26 to be novel predictors of kidney quality before transplantation. This was because they were found to correlate with estimated glomerular filtration rate at 3 and 12 months after kidney transplantation. However, further proteomic studies focusing on distinct markers obtained from hypothermic and normothermic machine perfusion are needed to confirm their predictive value and to improve kidney storage methods. Therefore, the present literature review from PubMed, Scopus, Embase and Web of Science was performed with the aims of summarizing the current knowledge on the most frequently studied single protein biomarkers. In addition, novel analytical methods and insights into organ injury during preservation were documented, where future directions in assessing organ quality before kidney transplantation were also discussed.

Kidney transplant (KTx) is the best method of renal insufficiency treatment. In dialyzed patients, mortality rises with the time on dialysis. There is a continuing shortage of organs for transplantation, hence a propensity to expand the donor pool with expanded-criteria donors, anti-hepatitis C virus-positive included. In the above case a transmission of hepatitis C virus (HCV) genotype to recipient is present. It has been proven that contamination with more than 1 HCV genotype did not worsen KTx outcomes. There are 2.6% anti-HCV(+) donors in Poland. Use is only possible in cases of anti-HCV(+) and anti-HCV RNA(+) recipients., Methods: Retrospective analysis covered 8675 deceased donors (1998-2012 Polish data from Poltransplant). The early (after 12 months) and late (after 60 months) graft and patient survival was assessed in KTx recipients, with documented recipient and donor data spanning at least 1 year after KTx. In comprehensive analysis, 7016 KTx recipients with known anti-HCV status were included according to anti-HCV profile of recipient and donor. The results are in absolute and percentage values and P < .05 assessed with χ 2 test., Results: Twelve-month survival: recipient (R) (95%), graft (G) (89%), total; R (95% vs 89%, P < .001), G (88 vs 79, P < .001) in HCV(-) to HCV(+/-) vs HCV(+) to HCV(+); R (95 vs 94, P = .2), G (88 vs 83, P < .001), HCV(-) to HCV(-) vs HCV(-) to HCV(+); R (93 vs 95, P = .004), G (82 vs 89, P < .001) in HCV(+/-) to HCV(+) vs HCV(-) to HCV(-); R (95 vs 89, P < .001), G (88 vs 79, P < .001) in HCV(-) to HCV(-) vs HCV(+) vs HCV (+). Sixty-month survival: R (86%), G (75%), total; R (84 vs 88, P = .01), G (63 vs 71, P = .001) in HCV(+/-) to HCV(+) vs HCV(-) to HCV(-); R (88 vs 80, P = .003) in HCV(-) to HCV(-) vs HCV(+) to HCV(+)., Conclusions: The worst anti-HCV serological profile was HCV(+) to HCV(+), although transplanting HCV(+) to HCV(+) did not worsen outcomes in that group. Worse KTx outcomes of HCV(+) over HCV(-) donors can be attributed to HCV(+) status of the recipient., (Copyright © 2018 Elsevier Inc. All rights reserved.)

The aim of the prospective study was to assess the exact kidney temperature and the effect of surface cooling of the kidney during the time of vascular anastomosis. Twenty-two renal graft recipients were incorporated into our study. We used an electronic temperature measurer provided with a needle-shaped probe pierced into the body of the kidney. The temperature was recorded every 5 min. The mean temperature of the kidney at the beginning of anastomosis (T0) was 8.87 +/- 3.97 degrees C and 17.95 +/- 5.1 degrees C at the end (Tend). The striking finding of this study was that the mean Tend delayed kidney function-negative in [ATN(-)] recipients was significantly lower than in the ATN(+) group; respectively, 14.86 +/- 3.6 degrees C and 19.71 +/- 5.07 degrees C. Therefore, we have divided all recipients according to Tend (< 15 degrees C and > 15 degrees C) in an attempt to assess the direct influence of kidney temperature on early graft function. In nine cases, a temperature below 15 degrees C was recorded and in 13 cases it exceeded 15 degrees C at the end of anastomosis. The mean cold ischemia time and anastomosis time were not different in these recipients. Delayed graft function occurred in 14 recipients; in 3 of 9 (33.3%) recipients from group Tend < 15 degrees C; and in 11 of 13 (85%) from group Tend > 15 degrees C. One case of primary non-function was observed (Tend > 15 degrees C). This study documents the value of effective cooling of the kidney during the time of vascular anastomosis. Since in most clinical reports the significance of the second warm ischemia was assessed only by the duration of the anastomosis, without measurement of the actual organ temperature, this may explain the different findings in our studies.

The current shortage of cadaveric kidneys may be alleviated to some degree by increasing our capabilities to use less than ideal donor kidneys, such as those from non-heart-beating donors. These kidneys are often exposed to no flow (ischemia) for varying lengths of time. Full utilization of these kidneys may require better methods of organ preservation that could reverse existing ischemic injury. This may conceivably require that, during preservation, energy stores (ATP) lost during warm ischemia be recharged. This would required continuous perfusion. Using a kidney slice model, we investigated the effects of simulated hypothermic machine perfusion with the UW gluconate perfusate on the capability of rabbit kidneys exposed to warm ischemia to regenerate ATP. After 30 min of warm ischemia, ATP content was low (0.2 mumol/g wet weight) but increased to 0.7-0.9 mumol/g wet weight after 24 h of simulated machine perfusion at 4 degrees C. After an additional 2 h of rewarming (37 degrees C in oxygenated Krebs Henseleit buffer), the slice ATP content increased to about 1.0 mumol/g wet weight (similar to kidneys not exposed to warm ischemia) when the antioxidants desferrioxamine and N-2-(mercaptopropionyl) glycine were included in the preservation media. Significantly less ATP was present without the antioxidants. After 60 min of warm ischemia, less ATP was regenerated after 24 h of simulated machine perfusion (about 0.4 mumol/g wet weight) than after 30 min of warm ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)