About this Research Topic
This Research Topic is part of the Hypertension and Chronic Kidney Injury or Failure series:
Hypertension and Chronic Kidney Injury or Failure
Based on updated clinical guidelines, ~46% of adults in the U.S. or 1.13 billion people worldwide have hypertension, the leading modifiable risk factor for cardiovascular disease. Fewer than 20-40% of hypertensive patients taking medication achieve blood pressure (BP) control to recommended levels, leaving millions at increased risk of kidney, heart and vascular diseases. Hypertension-induced renal injury or hypertensive nephropathy is growing rapidly and is now the second leading cause of kidney failure worldwide. Despite improvements in anti-hypertensive therapy, the percentage of hypertensive patients who ultimately develop end stage renal disease has remained constant.
Hallmarks of hypertensive nephropathy include renal microvascular lesions and remodeling, glomerulosclerosis, and interstitial fibrosis. While intensive research has shed light on the critical roles of inflammation and oxidative stress in the development of hypertensive nephropathy, the molecular pathogenesis underlying hypertension-induced kidney injury has not been fully elucidated. The underlying disease processes responsible for those pathological changes are likely influenced by a number of different factors including, but not limited to, genetics, the variant effects of different anti-hypertensive medications, the severity of hypertension, sex/gender and aging. However, the reason that why some hypertensive patients develop kidney injury and end-stage kidney disease more rapidly than others remain unsolved. Growing evidence supports significant differences in the prevalence of hypertension-induced kidney injury and end stage kidney failure progression between males and females, yet little is known regarding cellular and molecular mechanisms mediating the sex or gender bias in hypertension-associated kidney injury. Emerging data also reveal an important role for circadian blood pressure rhythm in the high prevalence of hypertensive renal injury, yet the underlying molecular pathogenesis is still unidentified. Thus, it is vital to unravel the mechanisms underlying the hypertension-mediated renal injury, and subsequently to develop effective targeted therapeutic interventions which could prevent and hopefully could delay or even reverse the progressive renal dysfunction.
The goal of this Research Topic is to highlight recent studies and new insights on the mechanisms contributing to the progression of kidney injury in hypertension. The objective of the current Research Topic is to offer a platform to attract the most important and highly innovative papers from global research in the field of hypertension and kidney injury.
Hypertension and Chronic Kidney Injury or Failure
Based on updated clinical guidelines, ~46% of adults in the U.S. or 1.13 billion people worldwide have hypertension, the leading modifiable risk factor for cardiovascular disease. Fewer than 20-40% of hypertensive patients taking medication achieve blood pressure (BP) control to recommended levels, leaving millions at increased risk of kidney, heart and vascular diseases. Hypertension-induced renal injury or hypertensive nephropathy is growing rapidly and is now the second leading cause of kidney failure worldwide. Despite improvements in anti-hypertensive therapy, the percentage of hypertensive patients who ultimately develop end stage renal disease has remained constant.
Hallmarks of hypertensive nephropathy include renal microvascular lesions and remodeling, glomerulosclerosis, and interstitial fibrosis. While intensive research has shed light on the critical roles of inflammation and oxidative stress in the development of hypertensive nephropathy, the molecular pathogenesis underlying hypertension-induced kidney injury has not been fully elucidated. The underlying disease processes responsible for those pathological changes are likely influenced by a number of different factors including, but not limited to, genetics, the variant effects of different anti-hypertensive medications, the severity of hypertension, sex/gender and aging. However, the reason that why some hypertensive patients develop kidney injury and end-stage kidney disease more rapidly than others remain unsolved. Growing evidence supports significant differences in the prevalence of hypertension-induced kidney injury and end stage kidney failure progression between males and females, yet little is known regarding cellular and molecular mechanisms mediating the sex or gender bias in hypertension-associated kidney injury. Emerging data also reveal an important role for circadian blood pressure rhythm in the high prevalence of hypertensive renal injury, yet the underlying molecular pathogenesis is still unidentified. Thus, it is vital to unravel the mechanisms underlying the hypertension-mediated renal injury, and subsequently to develop effective targeted therapeutic interventions which could prevent and hopefully could delay or even reverse the progressive renal dysfunction.
The goal of this Research Topic is to highlight recent studies and new insights on the mechanisms contributing to the progression of kidney injury in hypertension. The objective of the current Research Topic is to offer a platform to attract the most important and highly innovative papers from global research in the field of hypertension and kidney injury.
Keywords: Inflammation, oxidative stress, renal hemodynamics, fibrosis, sex
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