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Background: Leading causes of mortality and morbidity after kidney transplantation are cardiovascular diseases. One of the fundamentals of their prevention is the inhibition of platelet aggregation. Resistance to anti-platelet agents is a well-established phenomenon; however, its causes are yet to be clarified., Patients and Methods: Forty post-transplant patients, who received 75 mg clopidogrel q.d. as a prophylactic measure, were examined using optical aggregometry. Subsequently, logistic regression analysis was performed with 24 variables in order to expose possible causes of resistance., Results: Sixty percent of patients (24) were resistant to clopidogrel therapy; effective thrombocyte inhibition could only be shown in 40% of them (16). Significant correspondence between resistance and variables could not be found., Conclusion: Clopidogrel resistance is expected to occur on a large scale in patients who underwent kidney transplant surgery. Thus, a key component of preventive therapy, which stresses the importance of discovering the cause of resistance so as to decrease mortality rates, is missing., (Copyright © 2015 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved.)

Background: Cardiovascular diseases are a leading cause of mortality after kidney transplantation. According to guidelines, acetylsalicylic acid (ASA) must be given as preventive antiplatelet therapy, but resistance to this drug is also well-known., Patients and Methods: A total of 214 renal transplant patients were included in our study and took 100 mg of ASA q.d. Aggregometry was performed to determine resistance. Twenty-four variables were examined using logistic regression analysis as possible causes of resistance., Results: ASA resistance was observed in 40.18% of the patients. Resistance reduced concomitant statin therapy and significantly increased simultaneous cyclosporine therapy., Conclusion: Our study assessed the post-transplant ASA resistance in a large population. Clarification of this matter is crutial, since one of the major preventive pharmacological therapies of cardiovascular mortality is not effective in a significant number of patients., (Copyright © 2015 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved.)

Pituitary adenylate cyclase activating polypeptide (PACAP) is a multifunctional neuropeptide, showing widespread occurrence in the nervous system and also in peripheral organs. The neuroprotective effects of PACAP are well-established in different neuronal systems against noxious stimuli in vitro and in vivo. Recently, its general cytoprotective actions have been recognized, including renoprotective effects. However, the effect of endogenous PACAP in the kidneys is not known. The main aim of the present study was to investigate whether the lack of this endogenous neuropeptide influences survival of kidney cells against oxidative stress. First, we determined the presence of endogenous PACAP from mouse kidney homogenates by mass spectrometry and PACAP-like immunoreactivity by radioimmunoassay. Second, primary cultures were isolated from wild type and PACAP deficient mice and cell viability was assessed following oxidative stress induced by 0.5, 1.5 and 3mM H(2)O(2). Our mass spectrometry and radioimmunoassay results show that PACAP is endogenously present in the kidney. The main part of our study revealed that the sensitivity of cells from PACAP deficient mice was increased to oxidative stress: both after 2 or 4h of exposure, cell viability was significantly reduced compared to that from control wild type mice. This increased sensitivity of kidneys from PACAP deficient mice could be counteracted by exogenously given PACAP38. These results show, for the first time, that endogenous PACAP protects against oxidative stress in the kidney, and that PACAP may act as a stress sensor in renal cells. These findings further support the general cytoprotective nature of this neuropeptide., ((c) 2009 Elsevier Ireland Ltd. All rights reserved.)