Arterial Hypertension and Renal Disease

The past decade has witnessed enormous advances in understanding the association between arterial hypertension and renal disease. This chapter aims to provide a comprehensive review about new insights generated from recent experimental and clinical studies that should shed light on the role of the kidney in causing hypertension but also the role of hypertension in causing renal disease. It will focus on pathogenic mechanisms that connect arterial hypertension with target renal damage and new markers able to identify subclinical target-renal damage. Nowadays, the most important causes of renal failure and dialysis in the world arterial are hypertension and diabetes mellitus. The kidneys have a central role in the control of sodium homeostasis through the important mechanism of regulation of blood pressure. Arterial hypertension is also a well known consequence of chronic kidney disease (CKD), and at the same time one of the main factors causing diabetic and/or non-diabetic chronic renal failure progression (Ljutić, 2003). Kidneys can be damaged by arterial hypertension by several mechanisms. Because autoregulation of glomerular pressure is impaired in CKD, elevations in systemic blood pressure are associated with increased glomerular capillary pressure. Glomerular hypertension results in increased protein filtration and endothelial damage, causing increased release of cytokines and other soluble mediators, promoting replacement of normal kidney tissue by fibrosis. An important factor contributing to progressive renal disease is activation of the renin-angiotensin system, which tends to increase blood pressure and also promotes cell proliferation, inflammation, and matrix accumulation (Dworkin, 1999). An important part of the standard of care in clinics is the evaluation of microalbuminuria in order to detect renal organ damage that may influence the occurrence of future cardiovascular events. Screening for renal organ damage is part of classification schemes and clinical assessment process and influences the therapy to prevent disease progression and delay or prevent future cardiovascular events. The presence of target organ damage defines a high-risk population that develops complications due to suboptimal disease control or accelerated development and progression of the atherosclerotic process (Lockhart, 2009). The renin-angiotensin system (RAS) is the most important mechanism for blood pressure regulation and electrolyte homeostasis. It was suggested that the major fraction of angiotensin II present in renal tissues is locally generated from angiotensinogen delivered to