Perfusion of a Kidney Graft from a Donor After Cardiac Death Based on Immediately Started Machine Perfusion: An Experimental Study on a Big Animal.

BACKGROUND: Donation after circulatory death donors are becoming a common source of organs for transplant. Despite good long-term outcomes of grafts from donation after circulatory death, this group is affected by a higher occurrence of delayed graft function and primary nonfunction. Our hypothesis is based on the assumption that washing the kidney grafts in the donor's body using a simple mechanical perfusion pump will result in faster and better perfusion of the parenchyma and more efficient cooling compared with hydrostatic perfusion alone. METHODS: A total of 7 experimental animals (pigs) were used. The animals were divided into 2 groups: group A (n = 3) and group B (n = 4). After a 30-minute ischemic period for the selected kidney (clamped renal vessels), intra-arterial perfusion was performed. In group A perfusion was performed using hydrostatic pressure; in group B mechanical controlled perfusion was performed. After perfusion, declamping of the renal vessels caused restoration of flow. For graft quality evaluation, biopsy specimens were harvested, and the cooling speed was observed. Laboratory markers or renal failure were determined. RESULTS: We found no significant differences between temperature drop and total diuresis between groups A and B. A significant difference was found between the groups in both flow parameters (flow maximum and mean flow) (P = .007, respectively P = .019). No laboratory parameters were found to be statistically significantly different. Histopathological analysis strongly supports the hypothesis of better flushing of kidney grafts using mechanical perfusion. CONCLUSIONS: Based on our results, better kidney graft quality can be expected after immediately started mechanical perfusion in situ.

Blood biomarker panel recommended for personalized prediction, prognosis, and prevention of complications associated with abdominal aortic aneurysm.

The aim of the study was to evaluate the ability of following biomarkers as diagnostic tools and risk predictors of AAA: C-reactive protein, interleukin-6, pentraxin-3, galectin-3, procollagen type III N-terminal peptide, C-terminal telopeptide of type I collagen, high-sensitive troponin I, and brain natriuretic peptide. Seventy-two patients with an AAA and 100 healthy individuals were enrolled into the study. We assessed individual biomarker performance and correlation between the AAA diameter and biomarker levels, and also, a multivariate logistic regression was used to design a possible predictive model of AAA growth and rupture risk. We identified following four parameters with the highest potential to find a useful place in AAA diagnostics: galectin-3, pentraxin-3, interleukin-6, and C-terminal telopeptide of type I. The best biomarkers in our evaluation (galectin-3 and pentraxin-3) were AAA diameter-independent. With the high AUC and AAA diameter correlation, the high-sensitive troponin I can be used as an independent prognostic biomarker of the upcoming heart complications in AAA patients. Authors recommend to add biomarkers as additional parameters to the current AAA patient management. Main addition value of biomarkers is in the assessment of the AAA with the smaller diameter. Elevated biomarkers can change the treatment decision, which would be done only based on AAA diameter size. The best way how to manage the AAA patients is to create a reliable predictive model of AAA growth and rupture risk. A created multiparameter model gives very promising results with the significantly higher efficiency compared with the use of the individual biomarkers.