Background: Immunometric assays have recently shown higher specificity in the detection of human insulin than radioimmunoassays with almost no cross-reaction with proinsulin or C peptide. The introduction of the new insulin analogues on the market, however, has raised the need to define their cross-reactivity in these assays. Several studies have been published in this regard with different results. Methods: The analogues studied were insulins lispro, aspart, glargine, detemir, and glulisine. Insulin concentrations were measured in Immulite® 2000 and Advia Centaur® XP (Siemens Healthcare Diagnostics), and Elecsys® Modular Analytics E170 (Roche). All samples were processed 15 times in the same analytical run following a random sequence. Those samples which showed statistically and clinically significant changes in insulin concentration were reprocessed using increasing concentrations of analogue, and this was done twice, using two different serum pools, one with a low concentration of insulin and one with a high concentration of insulin. Results: In the Elecsys® E170 analyser, glargine showed statistical changes (comparison of mean concentrations with p < 0.05) and clinically significant changes in measured insulin (percentage difference 986.2% > reference change value: 59.8%), and the interference increased with increasing concentrations of analogue; the differences were not significant in the case of the other analogues. In the Advia Centaur® and Immulite® 2000 only the results for glulisine did not present significance (percentage difference 44.7% < reference change value 103.5%). Increasing concentrations of aspart, glargine, and lispro showed increased interference in Immulite® 2000. Conclusions: In the Elecsys® E170 assay, relevant cross-reactivity was only detected with insulin glargine, whereas in the other analysers all analogues except glulisine showed significant interference.

Oxidative stress (OS) resulting from an imbalance between reactive oxygen species (ROS) generation and antioxidant defenses plays a pivotal role in vascular diseases such as atherosclerosis and hypertension. ROS derived from NADPH oxidase, mitochondria, and xanthine oxidase promote endothelial dysfunction by inducing lipid and protein oxidation, apoptosis, and pro-inflammatory signaling, thereby enhancing smooth muscle proliferation and atherogenesis. This review summarizes the molecular mechanisms linking OS to vascular injury and aims to systematically elucidate the role of OS in vascular diseases, with a specific focus on critiquing the current challenges in translating biomarkers to clinical practice and the emerging trends in personalized antioxidant therapy. Particular attention is given to biomarkers of oxidative stress, including those assessing antioxidant enzyme activity and oxidative damage products, which possess potential for clinical use. Therapeutic strategies targeting OS, including dietary and pharmacological antioxidants, show promise in improving vascular health, although clinical outcomes have been inconsistent and it is necessary to resolve the standardization and validation of these biomarkers, develop precise targeted therapies against specific ROS sources (e.g., NOX inhibitors, mitochondrial antioxidants), and explore personalized clinical trials based on redox stratification. Overall, OS is a central mediator in vascular pathology, and progress in biomarker validation and targeted therapies will be essential to translate current knowledge into effective prevention, diagnosis, and treatment of cardiovascular diseases. Personalized approaches based on accurate redox profiling may enhance efficacy.

Oxidative stress (OS), resulting from an imbalance between reactive oxygen species (ROS) generation and antioxidant defenses, plays a pivotal role in vascular diseases such as atherosclerosis and hypertension. ROS derived from NADPH oxidase, mitochondria, and xanthine oxidase promote endothelial dysfunction by inducing lipid and protein oxidation, apoptosis, and pro-inflammatory signaling, thereby enhancing smooth muscle proliferation and atherogenesis. This review summarizes the molecular mechanisms linking OS to vascular injury and highlights the interplay between ROS and inflammation in the progression of cardiovascular disease. Particular attention is given to biomarkers of oxidative stress, including those assessing antioxidant enzyme activity and oxidative damage products, which hold potential for clinical use. However, challenges remain regarding their standardization and variability influenced by biological and environmental factors. Therapeutic strategies targeting OS, including dietary and pharmacological antioxidants, show promise in improving vascular health, although clinical outcomes have been inconsistent. Personalized approaches based on accurate redox profiling may enhance efficacy. Overall, OS is a central mediator in vascular pathology, and progress in biomarker validation and targeted therapies will be essential to translate current knowledge into effective prevention, diagnosis, and treatment of cardiovascular diseases.

Background: Our study aims to comment on all ADPKD variants identified in our health area and explain how they are distributed geographically, to identify new variants, and relate the more frequent variants with their renal phenotype in terms of kidney survival. Materials and Methods: We identified patients suffering from ADPKD in a specialized consultation unit; genealogical trees were constructed from the proband. According to the ultrasound-defined modified Ravine–Pei criteria, relatives classified as at risk were offered participation in the genetic study. Socio-demographic, clinical, and genetic factors related to the impact of the variant on the survival of the kidney and the patient, such as age at RRT beginning and age of death, were recorded. Results: In 37 families, 33 new variants of the PKD1 gene were identified, which probably produce a truncated protein. These variants included 2 large deletions, 19 frameshifts, and 12 stop-codons, all of which had not been previously described in the databases. In 10 families, six new probably pathogenic variants in the PKD2 gene were identified. These included three substitutions; two deletions, one of which was intronic and not associated with any family; and one duplication. A total of 11 missense variants in the PKD1 gene were grouped in 14 families and classified as probably pathogenic. We found that 33 VUS were grouped into 18 families and were not described in the databases, while another 15 were without grouping, and there was only 1 in the PKD2 gene. Some of these variants were present in patients with a different pathogenic variant (described or not), and the variant was probably benign. Renal survival curves were compared to nonsense versus missense variants on the PKD1 gene to check if there were any differences. A group of 328 patients with a nonsense variant was compared with a group of 264 with a missense variant; mean renal survival for truncated variants was lower (53.1 ± 0.46 years versus non-truncated variant 59.1 ± 1.36 years; Log Rank, Breslow, and Tarone Ware, p < 0.05). Conclusions: To learn more about ADPKD, it is necessary to understand genetics. By describing new genetic variants, we are approaching creation of an accurate genetic map of the disease in our country, which could have prognostic and therapeutic implications in the future.