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Updated: Apr 16, 2026

Assessment of Vascular Function in Patients With Chronic Kidney Disease
Published on: June 16, 2014
[Pathophysiology of hypertension in chronic kidney disease]
Insights
Hypertension is a major cause and effect of chronic kidney disease (CKD), affecting most patients. Key factors include sodium retention, hormonal imbalances, and vascular issues contributing to high blood pressure in CKD.
Area of Science:
- Nephrology
- Cardiology
- Hypertension Research
Context:
- Hypertension is highly prevalent in chronic kidney disease (CKD) patients, present in 80-85% of cases.
- CKD significantly contributes to the development and progression of hypertension.
- Understanding the interplay between CKD and hypertension is crucial for patient management.
Purpose:
- To summarize the primary pathogenetic factors contributing to hypertension in the context of CKD.
- To provide a comprehensive overview of the mechanisms driving elevated blood pressure in CKD patients.
Summary:
- Key factors include sodium retention, overactive renin-angiotensin-aldosterone system (RAAS) and sympathetic nervous system (SNS).
- Impaired nitric oxide (NO) synthesis, oxidative stress, and endothelial dysfunction play significant roles.
- Disruptions in calcium metabolism, parathyroid hormone (PTH) secretion, vascular calcification, and increased arterial stiffness are also critical contributors.
Impact:
- Highlights the complex multifactorial nature of hypertension in CKD.
- Provides a foundation for targeted therapeutic strategies to manage blood pressure in CKD.
- Emphasizes the need for integrated approaches addressing both kidney function and cardiovascular health.
Abstract:
Hypertension is both an important cause and consequence of chronic kidney disease (CKD). It is present in 80-85% of the patients. The article summarizes the main pathogenetic factors of hypertension in CKD such as: sodium retention, increased activity the renin-angiotensin-aldosterone system and sympathetic nervous system, impaired nitric oxide synthesis and endothelium-mediated vasodilatation, oxidative stress, disorders of calcium metabolism and parathyroid hormone secretion, vascular calcification and increased arterial stiffness.
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