Oxidative Stress in Kidney Injury and Hypertension.

Area of Science:

• Nephrology
• Cardiovascular Medicine
• Genetics

Background:

• Hypertension (HTN) is a primary driver of kidney damage, including nephrosclerosis and hypertensive nephropathy, leading to chronic kidney disease (CKD) and end-stage renal disease (ESRD).
• HTN also elevates risks for stroke and coronary heart disease.
• Oxidative stress, inflammation, and renin-angiotensin-aldosterone system (RAAS) activation are critical mediators of HTN-induced kidney injury.

Purpose of the Study:

• To review the role of NADPH oxidase (NOX) in hypertension-related kidney damage.
• To highlight the importance of managing blood pressure (BP) by targeting key pathophysiological pathways.
• To discuss the impact of genetic and environmental factors on hypertensive renal damage.

Main Methods:

• Review of existing literature on hypertension, kidney disease, oxidative stress, and RAAS.
• Analysis of animal models (e.g., spontaneously hypertensive rat) to understand HTN pathogenesis.
• Examination of the role of reactive oxygen species (ROS) and NOX isoforms in BP regulation and renal function.

Main Results:

• Overproduction of ROS, particularly via NOX enzymes, significantly contributes to HTN development and progression, impairing renal function.
• Genetic and environmental factors, including gut microbiome alterations, influence susceptibility to hypertensive renal damage.
• Targeting NOX to reduce ROS, alongside RAAS inhibition, anti-inflammatory, and antioxidant strategies, shows promise for renal and antihypertensive protection.

Conclusions:

• NOX plays a pivotal role in the pathogenesis and progression of HTN and its renal complications.
• Effective BP management requires addressing oxidative stress, inflammation, and RAAS activation.
• Emerging therapies like SGLT2 inhibitors and mineralocorticoid receptor antagonists offer potential benefits in managing HTN and CKD by mitigating these pathways.