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Oxidative Imbalance and Kidney Damage: New Study Perspectives from Animal Models to Hospitalized Patients
Daniela Pellegrino1,2, Daniele La Russa2,3, Alessandro Marrone1,2
1Department of Biology, Ecology and Earth Sciences, University of Calabria, 87036 Rende, Italy.
Insights
Chronic kidney disease (CKD) involves significant renal function loss and increased cardiovascular risk. Understanding oxidative stress and inflammation mechanisms is key for personalized prevention strategies in CKD patients.
Area of Science:
- Nephrology
- Cardiovascular Medicine
- Molecular Biology
Background:
- Chronic kidney disease (CKD) is a global health issue with severe consequences, including end-stage renal disease, cardiovascular disease, and reduced quality of life.
- Key risk factors for CKD include hypertension, obesity, oxidative stress, and inflammation, necessitating a deeper understanding of their molecular mechanisms.
- A translational approach combining human and animal studies is crucial for dissecting CKD pathogenesis.
Purpose of the Study:
- To investigate the molecular mechanisms underlying kidney damage in CKD.
- To identify novel molecular pathways contributing to CKD progression.
- To explore the role of oxidative stress, inflammation, hypertension, and obesity in CKD pathogenesis for effective prevention.
Main Methods:
- Utilized spontaneously hypertensive rats and cafeteria diet-fed rats to model hypertension and obesity-induced kidney damage.
- Analyzed redox disequilibrium, oxidative damage (lipid peroxidation, antioxidant enzyme expression), and apoptotic pathways in animal models.
- Correlated global oxidative balance with inflammatory markers (C-reactive protein) and cardiovascular risk in hemodialysis patients.
Main Results:
- Hypertension and obesity induce renal alterations through redox disequilibrium, oxidative damage, and apoptosis activation in animal models.
- A strong correlation exists between a high oxidative index, elevated C-reactive protein levels, and a history of cardiovascular events in hemodialysis patients.
- These findings highlight the critical role of oxidative stress and inflammation in CKD progression and cardiovascular risk.
Conclusions:
- Redox imbalance and inflammation are central to kidney damage in CKD, influenced by factors like hypertension and obesity.
- A comprehensive, multilevel approach is essential for understanding CKD pathogenesis and developing personalized prevention strategies.
- Targeting modifiable and nonmodifiable risk factors, particularly oxidative stress and inflammation, can lead to effective CKD prevention plans.
Abstract:
Chronic kidney disease (CKD) is a major public health problem worldwide and affects both elderly and young subjects. Its main consequences include the loss of renal function, leading to end-stage renal disease, an increased risk of cardiovascular disease, a significant increase in morbidity and mortality, and a decrease in health-related quality of life. This review arose in significant part from work in the authors' laboratory, complemented by literature data, and was based on a translational approach: we studied the role of many CKD risk factors, such as hypertension, obesity, and oxidative stress/inflammation. The aim was to identify new molecular mechanisms of kidney damage to prevent it through successful behavior modifications. For this purpose, in our studies, both human and animal models were used. In the animal models, we analyzed the mechanisms of renal damage induced by hypertension (spontaneously hypertensive rats) and obesity (cafeteria diet-fed rats), showing that redox disequilibrium in plasma and tissue is extremely important in renal alteration in terms of both oxidative damage (lipid peroxidation, altered expression antioxidant enzymes) and apoptotic pathway (intrinsic/extrinsic) activation. In hemodialysis patients, we explored the correlation between the global oxidative balance and both inflammatory markers and cardiovascular risk, showing a strong correlation between the oxidative index and the blood levels of C-reactive protein and previous cardiovascular events. This multilevel approach allowed us to individually and synergistically analyze some aspects of the complex pathogenic mechanisms of CKD in order to clarify the role of the new amplified risk factors for CKD and to prepare an effective personalized prevention plan by acting on both modifiable and nonmodifiable risk factors.
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