Abstract
The clinical and biochemical improvement observed in kidney transplant (RT) recipients is remarkable. The correct functioning of the allograft depends on various factors such as the donor's age, the alloimmune response, the ischemia-reperfusion injury, arterial hypertension, and the interstitial fibrosis of the allograft, among others. Antihypertensive drugs are necessary for arterial hypertension patients to avoid or reduce the probability of affecting graft function in RT recipients. Oxidative stress (OS) is another complex pathophysiological process with the ability to alter posttransplant kidney function. The study's objective was to determine the effect of the administration of Enalapril, Losartan, or not antihypertensive medication on the oxidative state in RT recipients at the beginning of the study and one year of follow-up. All patients included in the study found significant overexpression of the oxidative damage marker to DNA and the antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GPx). In contrast, it was found that the determination of the total antioxidant capacity decreased significantly in the final determination at one year of follow-up in all the patients who ingested Enalapril and Losartan. We found dysregulation of the oxidative state characterized mainly by oxidative damage to DNA and a significant increase in antioxidant enzymes, which could suggest a compensatory effect against the imbalance of the oxidative state.
Highlights
Chronic allograft dysfunction (CAD) is a progressive and irreversible entity and is a cause of long-term kidney transplant failure [1–3]
Age showed a difference in the group that did not require antihypertensive medication 29 ± 3:83 years vs. those treated with Enalapril 24:38 ± 1:61 years (p ≤ 0:01)
Nuclear erythroid factor 2 (NRF2) signaling related to nuclear erythroid factor 2 (NRF2) and vitamin K play a crucial role in counteracting Oxidative stress (OS), DNA damage, senescence, and inflammation, activating NRF2 and supplementation with vitamin K which could offer an attractive therapeutic target in patients undergoing RT [29]
Summary
Chronic allograft dysfunction (CAD) is a progressive and irreversible entity and is a cause of long-term kidney transplant failure [1–3]. The mechanisms of damage that contribute to CAD involve immunological [4] and nonimmunological [3] aspects, which conditions the formation of interstitial fibrosis and tubular atrophy (IFTA) [5]. The oxidative stress (OS) characterized by the imbalance between the generation of oxidative compounds and the antioxidant defense mechanisms could be resulted in allograft damage, especially when immunosuppression in renal transplantation is based on the use of calcineurin inhibitors (CNI) inducing endothelial dysfunction, hypertension, and increased renal nephrotoxicity, characterized by renal vasoconstriction, interstitial fibrosis, and arterial hypertrophy [6–9]. When the deregulated activation of OS occurs, it can cause vascular damage favoring the progression of atherosclerosis due to oxidative damage directly to cellular components, leading to impaired cell function, aging, and activation of apoptosis [10].
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