Purpose: The increase of visceral abdominal fat (VAF) and oxidative stress (OS) are independent predictors for cardiovascular risk. This study aimed to determine the association of VAF with proinflammatory cytokines, oxidants, antioxidants, and oxidative damage to DNA in subjects with normal weight, overweight, and obesity. Patients and Methods: A cross-sectional study that included 21 men and 71 women who attended for a medical check-up was conducted. Dual-energy X-ray absorptiometry (DXA) was used to measure the VAF volume. ELISA and colorimetric techniques were used for chemical analysis. Results: Low activity of superoxide dismutase (SOD) was found in overweight and obese subjects compared to the normal weight group (p=0.005). In contrast, the activity of glutathione peroxidase (GPx) was higher in the overweight and obesity groups compared to the normal weight subjects (p=0.017). The total antioxidant capacity (TAC) was also increased in the overweight group compared to the normal weight group (p=0.04). According to the volume of VAF, the levels of tumor necrosis factor alfa and interleukin 6 showed no differences between subjects with normal and high VAF. Subjects with high VAF show higher levels of 8-isoprostans compared to normal VAF group (p=0.039). Less concentration of 8-oxoguanine-DNA-N-glycosylase-1 (hOGG1) was found in the high VAF group (p=0.032) compared to the normal VAF subjects. VAF was positively correlated with lipoperoxides (LPO) (r=0.27, p< 0.05) and 8-isoprostanes (r=0.25, p< 0.05). We also found correlations between oxidative stress markers and anthropometric ratios for intra-abdominal fat. The waist-hip ratio was positively correlated with LPO (r=0.30, p< 0.05) and TAC (r=0.24, p< 0.05). Conclusion: These findings suggest that the predominantly oxidative damage associated with VAF in overweight or obesity is lipoperoxidation and oxidative DNA damage. Alterations in endogenous antioxidant defenses may not be linked to the amount of VAF.

Early Chronic Kidney Disease (CKD) is a condition that tends to progress to End-Stage Kidney Disease (ESKD). Early diagnosis of kidney disease in the early stages can reduce complications. Alterations in renal function represent a complication of diabetes mellitus (DM). The mechanisms underlying the progression of CKD in diabetes could be associated with oxidative and inflammatory processes. This study aimed to evaluate the state of inflammation and oxidative stress (OS) on the progression of CKD in the early stages in patients with and without type 2 diabetes mellitus (T2DM). An analytical cross-sectional study was carried out in patients with CKD in early stages (1, 2, 3) with and without T2DM. The ELISA method determined the expression of pro-inflammatory cytokines IL-6 and TNF-α as well as lipoperoxides (LPO), nitric oxide (NO), and superoxide dismutase activity (SOD). Colorimetric methods determined glutathione peroxidase (GPx) and total antioxidant capacity (TAC). Patients with CKD and T2DM had significantly decreased antioxidant defenses for SOD (p < 0.01), GPx (p < 0.01), and TAC (p < 0.01) compared to patients without T2DM. Consequently, patients with T2DM had higher concentrations of oxidant markers, NO (p < 0.01), inflammation markers, IL-6 (p < 0.01), and TNF-α than patients without T2DM. CKD stages were not related to oxidative, antioxidant, and inflammatory marker outcomes in T2DM patients. Patients without T2DM presented an increase in SOD (p = 0.04) and a decrease in NO (p < 0.01) when the stage of CKD increased. In conclusion, patients with T2DM present higher levels of oxidative and inflammatory markers accompanied by a decrease in antioxidant defense. However, these oxidative status markers were associated with CKD stage progression in patients without T2DM. Thus, NO and SOD markers could help detect the early stages of CKD in patients who have not yet developed metabolic comorbidities such as T2DM.

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.

Kidney transplantation (KT) remains the optimal therapy for end-stage kidney disease (ESKD), yet long-term graft survival is limited by unremitting allograft dysfunction and non-immune treatment toxicities. Sterile inflammation primarily drives graft failure. This inflammatory process releases damage-associated molecular patterns (DAMPs). DAMPs activate pattern recognition receptors (PRRs), such as Toll-like receptors (TLRs) 2 and 4, from proximal tubule epithelial cells, endothelial compartments, and infiltrating myeloid lineages. PRR signaling and the release of pro-inflammatory cytokines (IL-1β, IL-18, TNF-α) promote pro-inflammatory M1 macrophage polarization and accelerate interstitial fibrosis and tubular atrophy (IFTA). While maintenance immunosuppression prevents adaptive rejection, it causes severe metabolic, cardiovascular, and oncologic complications, including post-transplant diabetes mellitus, hypertension, and malignancies. Sodium-glucose cotransporter 2 (SGLT2) inhibitors (dapagliflozin, empagliflozin, canagliflozin) have emerged as novel disease-modifying, immunomodulatory adjuncts that act independently of glycemic control. SGLT2 inhibition reactivates tubuloglomerular feedback to relieve intraglomerular hypertension, blunts hyperfiltration, and reduces tubular transport workload. This alleviates cortical hypoxia, curtails mitochondrial ROS production, and activates AMP-activated protein kinase (AMPK) to suppress NF-κB and NLRP3 inflammasome assembly. SGLT2 inhibitors downregulate TLR expression, drive a phenotypic shift toward reparative M2 macrophages, reduce proteinuria, and provide sustained volume decongestion without triggering compensatory activation of the renin–angiotensin–aldosterone system. By targeting both upstream bioenergetic strain and downstream fibrotic remodeling (YAP/TAZ axis), SGLT2 inhibitors complement standard immunosuppression to protect allograft architecture, reduce cardiovascular morbidity, and improve long-term transplant outcomes.

The increasing prevalence of multidrug-resistant Gram-negative bacteria has reinforced the clinical importance of last-resort antibiotics such as colistin. Their antibacterial efficacy has made them indispensable for treating life-threatening infections, yet their clinical use is constrained by substantial toxicity. Increasing evidence indicates that redox biology may influence both the antibacterial activity and host toxicity of colistin through distinct biological processes. Reactive oxygen species contribute to bacterial killing while simultaneously promoting mitochondrial dysfunction, oxidative stress, inflammation, and tubular cell death within the kidney. This mini review summarizes current knowledge on the redox mechanisms underlying the antibacterial activity and host toxicity of last-resort antibiotics, with particular emphasis on colistin-induced nephrotoxicity. We discuss experimental and clinical evidence supporting host-directed redox modulation as a strategy to mitigate renal injury, highlighting the limitations that have hindered successful clinical translation. Finally, we examine emerging opportunities, including biomarker-guided strategies and mitochondria-targeted interventions, that may facilitate the development of safer therapeutic approaches while preserving the antibacterial efficacy of colistin.

Nuestro cuerpo es un delicado y complejo sistema en el que cada órgano cumple una función entre los que destaca el riñón. Sin embargo, existen cierto medicamentos que, aunque pueden ser efectivos para tratar diversas enfermedades, pueden tener efectos negativos en nuestros riñones. Este fenómeno se conoce como nefrotoxicidad de medicamentos. En el presente artículo platicaremos acerca de las funciones del riñón y cómo estas se pueden ver afectadas por la acción de algunos fármacos.