Oxidative stress is an imbalance between pro- and antioxidants that adversely influences the organism in various mechanisms and on many levels. Oxidative damage occurring concomitantly in many cellular structures may cause a deterioration of function, including apoptosis and necrosis. The damage leaves a molecular “footprint”, which can be detected by specific methodology, using certain oxidative stress biomarkers. There is an intimate relationship between oxidative stress, inflammation, and functional impairment, resulting in various diseases affecting the entire human body. In the current narrative review, we strengthen the connection between oxidative stress mechanisms and their active compounds, emphasizing kidney damage and renal transplantation. An analysis of reactive oxygen species (ROS), antioxidants, products of peroxidation, and finally signaling pathways gives a lot of promising data that potentially will modify cell responses on many levels, including gene expression. Oxidative damage, stress, and ROS are still intensively exploited research subjects. We discuss compounds mentioned earlier as biomarkers of oxidative stress and present their role documented during the last 20 years of research. The following keywords and MeSH terms were used in the search: oxidative stress, kidney, transplantation, ischemia-reperfusion injury, IRI, biomarkers, peroxidation, and treatment.

The COVID-19 pandemic, caused by severe acute respiratory syndrome coronavirus 2 virus (SARS-CoV-2), has triggered an enormous scientific response. Many studies have focused on understanding the entry of the SARS-CoV-2 virus into the host cell. The angiotensin-converting enzyme-2 (ACE2) is recognized as the host receptor used by SARS-CoV-2 to enter its target cells. Recent studies suggest that ACE2 gene polymorphisms might be candidates for genetic susceptibility to SARS-CoV-2 infection. The aim of this study is to evaluate the influence of ACE2 polymorphisms on COVID-19 disease risk and severity. In our study, we confirmed that there is a statistically significant increased risk of a more severe disease course of SARS-CoV-2 infection associated with the need for hospitalization in intensive care for patients with specific polymorphisms of the ACE2 gene. The most significant correlation was found for variant ACE2 rs2285666 (AA allele, OR = 2.12, p = 0.0189) and ACE2 rs2074192 (TT allele, OR = 2.05, p = 0.0016), and for ACE2 rs4646174 (GG allele, OR = 1.93, p = 0.0016), ACE2 rs4646156 (TT allele OR = 1.71, p = 0.008) and ACE2 rs2158083 (TT allele OR = 1.84, p = 0.0025). In conclusion, our findings identify that certain ACE2 polymorphisms impact the severity of COVID-19 disease independently of other well-known risk factors.

Ischemia-reperfusion injury (IRI) after renal transplantation is a complex biochemical process. The first component is an ischemic phase during kidney storage. The second is reperfusion, the main source of oxidative stress. This study aimed to analyze the activity of enzymes and concentrations of non-enzymatic compounds involved in the antioxidant defense mechanisms: glutathione (GSH), glutathione peroxidase (GPX), catalase (CAT), superoxide dismutase (SOD), glutathione reductase (GR), glutathione transferase (GST), thiobarbituric acid reactive substances (TBARS), malondialdehyde (MDA), measured in preservation fluid before transplantation of human kidneys (KTx) grafted from brain dead donors. The study group (N = 66) was divided according to the method of kidney storage: Group 1—hypothermic machine perfusion (HMP) in LifePort perfusion pump, n1 = 26, and Group 2—static cold storage (SCS), n2 = 40. The measurements of kidney function parameters, blood count, and adverse events were performed at constant time points during 7-day hospitalization and 3-month follow-up. Kidney perfusate in Group 2 was characterized by significantly more acidic pH (p < 0.0001), higher activity of GPX [U/mgHb] (p < 0.05) and higher concentration of MDA [μmol/L] (p < 0.05). There was a statistically significant improvement of kidney function and specific blood count alterations concerning storage method in repeated measures. There were aggregations of significant correlations (p < 0.05) between kidney function parameters after KTx and oxidative stress markers: diuresis & CAT, Na⁺ & CAT, K⁺ & GPX, urea & GR. There were aggregations of significant correlations (p < 0.05) between recipient blood count and oxidative stress markers: CAT & MON, SOD & WBC, SOD & MON. Study groups demonstrated differences concerning the method of kidney storage. A significant role of recipient’s gender, gender matching, preservation solution, and perfusate pH was not confirmed, however, basing on analyzed data, the well-established long-term beneficial impact of HMP on the outcome of transplanted kidneys might partially depend on the intensity of IRI ischemic phase and oxidative stress, reflected by the examined biomarkers.

Ischemia-reperfusion injury (IRI) occurring after renal transplantation is a complex biochemical process that can be monitored by specific biomarkers. The roles of those are not yet fully elucidated. The aim of this study was to analyze the concentrations of endothelins (ET-1, ET-2, and ET-3), interleukin-18 (IL-18), and neutrophil gelatinase-associated lipocalin (NGAL) during the reperfusion of human kidneys grafted from brain dead donors and later transplanted. The study group (n = 44) was analyzed according to the method of kidney storage: Group 1 underwent hypothermic machine perfusion (HMP) in the LifePort perfusion pump (n = 22), and Group 2 underwent static cold storage (SCS) (n = 22). The analysis of kidney function was performed daily during the first seven days after transplantation. The kidneys in Group 1 were characterized by higher absolute concentrations of ET-1, IL-18, and NGAL, as well as a lower concentration of ET-2 (p = 0.017) and ET-3. The relative increase of ET-1 (p = 0.033), ET-2, and ET-3 during reperfusion was lower in this group, while the relative decrease of NGAL was higher. Group 1 was also characterized by significant decrease of IL-18 (p = 0.026) and a tendency for better kidney function based on the higher total diuresis, higher glomerular filtration rate (GFR), higher potassium level, lower serum creatinine, and lower urea concentration during the seven-day postoperative observation period. The long-term beneficial impact of hypothermic machine perfusion on the outcome of transplanted kidneys may rely on the early modified proceedings and intensity of ischemia-reperfusion injury reflected by the dynamics of the concentrations of examined biomarkers.

Acid-base balance disorders are a crucial element of ischemia-reperfusion injury during organ transplantation. Hypoxia during organ procurement and storage cause cellular homeostasis imbalance with impact on further graft function. Acidosis in preserved kidney caused by lactate accumulation may have an important role as a common denominator of various pathways leading to cellular damage. Our trial sought to answer questions regarding a range of pH alterations in the kidney before the transplantation, their potential cause, and how this may affect further outcome of the kidney transplantation procedure. Perfusion fluid for pH analysis was obtained from perfusion pump (PP) or through kidney flushing at the end of preservation depending on the storage method. A total of 66 sample results were collated with the data from the transplant registry, hospitalization, and outpatient department. Statistical analysis was conducted linking pH results with factors related to donor, recipient, preservation, and outcome according to designed schematics. Mean perfusate pH was significantly lower in simple hypothermia (SH) vs the PP storage group (6.77 vs 7.11; P < .001). All samples of perfusate pH in the SH group were below physiological values (7.00. We concluded that kidney storage in cold ischemia is associated with organ acidosis independent of preservation method and that SH is correlated with significantly bigger acidosis than storage in PP, which is an important procedure removing an excessive amount of hydrogen ions from kidney microcirculation, decreasing cell damage.