Kidney international. Supplement
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Review
The role of renin-angiotensin-aldosterone system in the progression of chronic kidney disease.
The renin-angiotensin-aldosterone system (RAAS) is a well known regulator of blood pressure (BP) and determinant of target-organ damage. It controls fluid and electrolyte balance through coordinated effects on the heart, blood vessels, and Kidneys. Angiotensin II (AII) is the main effector of the RAAS and exerts its vasoconstrictor effect predominantly on the postglomerular arterioles, thereby increasing the glomerular hydraulic pressure and the ultrafiltration of plasma proteins, effects that may contribute to the onset and progression of chronic renal damage. ⋯ Recent evidence suggests that add-on therapy with an aldosterone antagonist may further increase renoprotection, but may also enhance the risk hyperkalemia. Maximized RAAS inhibition, combined with intensified blood pressure control (and metabolic control in diabetics) and amelioration of dyslipidemia in a multimodal approach including lifestyle modifications (Remission Clinic), may achieve remission of proteinuria and renal function stabilization in a substantial proportion of patients with proteinuric renal disease. Ongoing studies will tell whether novel drugs inhibiting the RAAS, such as the renin inhibitors or the vasopeptidase inhibitors, may offer additional benefits to those who do not respond, or only partially respond, to this multimodal regimen.
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Multicenter Study
Cardiovascular risk factors in type 2 diabetic patients: multifactorial intervention in primary care.
Cardiovascular disease is the main cause of morbidity and mortality in patients with type 2 diabetes mellitus (DM). Intervention on cardiovascular risk factors (CVRF) is essential to obtain clinical results reducing the excess of cardiovascular risk (CVR) in these patients. ⋯ The results of the study demonstrate that an integrated and multifactorial intervention in type 2 diabetic patients can achieve clinically significant reductions in CVR. However, conducted in effective conditions, it is not able to achieve optimum levels of control in spite of the initial proposal, possibly due to some degree of inertia in routine clinical practice.
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Atherosclerotic artery disease is a common condition in patients with chronic kidney disease (CKD); however, there are few published data on the prevalence of peripheral arterial disease (PAD) in nondialyzed patients with renal insufficiency. The ankle-brachial index (ABI) is a simple, noninvasive, and reliable method to assess PAD. ⋯ A high prevalence of PAD, considered as an ABI <0.9, was demonstrated in nondialyzed patients with CKD. This was related with age, male sex, and higher degree of renal insufficiency, while the presence of ABI > or =1.3 was associated with a greater degree of hyperparathyroidism. These data show the need to carry out routine ABI determinations in patients with CKD for early detection of peripheral arterial disease.
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Angiotensin II (Ang II) is a cytokine that participates in the inflammatory response. The nuclear factor kappa B (NFkappaB) is involved in the regulation of many immune and inflammatory factors. Different works have shown that both angiotensin II receptor type 1 (AT1) and type 2 (AT2) receptors are involved in the NFkappaB pathway; however, some aspects remain mysterious. AT1 antagonists increased plasma Ang II levels that could bind to AT2, so understanding the clinical importance of AT2 stimulation or inhibition is an interesting unresolved point. ⋯ Ang II, via AT1 and AT2 stimulation, leads to NFkappaB activation that was only blocked by combined therapy with both antagonists. The participation of AT2 receptors in the recruitment of inflammatory cells underscores the need of future studies that evaluate the clinical usefulness of this strategy.