**1. Introduction**

The renin-angiotensin system (RAS) was described in the 1980s, and since then studies have focused on its role in the hemodynamic control [1]. The RAS is classically associated with blood pressure regulation and electrolyte balance. The system main peptide angiotensin II acts through two major receptors termed type 1 and type 2. They are widely distributed in the tissues, and have different functions; hemodynamic changes such as vasoconstriction and cellular proliferation are related to type 1 receptor and vasodilation and anti-cellular proliferation to type 2 [2].

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All components of the RAS, including the receptors, are present very early in the human development (24–35 days of gestation), suggesting a role for angiotensin II in the organogenesis [3].

The RAS components are present in many tissues, and there are evidences for a tecidual angiotensin II biosynthesis with high concentrations in the kidneys (intrarenal RAS) [4, 5]. They are synthesized by different cells and interact locally with autocrine and paracrine effects. It has been suggested that the plasma RAS is important for acute regulatory mechanisms, whereas the tissue RAS may be more involved in chronic cardiovascular and renal regulation [6, 7].

Therefore, RAS maintains hemodynamic homeostasis and controls tecidual growth.

Pathologic consequences can result in overactivity of this cascade with an involvement of the RAS in several renal diseases. Regardless of the initial type of injury, all chronic renal diseases develop glomerular and vascular sclerosis, tubular atrophy and interstitial fibrosis, with progressive nephron loss and chronic renal failure. Adaptative changes in the remaining nephrons after initial injury cause more scarring and nephron loss, thus perpetuating a vicious cycle that results in the end-stage kidney. Chronic RAS activation is involved in these maladaptive mechanisms of progressive renal damage. Angiotensin II-mediated effects such as haemodynamics changes, glomerular and tubular hypertrophy and hyperplasia, infiltration of mononuclear cells and fibrogenesis were observed [8].

The system hyperactivity leads to progressive lesions presenting an important role in the pathophysiology of chronic cardiovascular and renal diseases. The RAS activation has been demonstrated in various kidney diseases, in both experimental and clinical studies [9, 10]. The system blockade, with inhibitors of angiotensin converting enzyme (ACE) of angiotensin II and angiotensin II-receptor blockers, shows large benefits in the treatment of chronic kidney diseases [11].

Thus, the classical approach of Angiotensin II as a vasoactive agent that participates in the systemic hemodynamic changes was expanded to recognize its role as a growth factor that modulates cell proliferation, synthesis and degradation of extracellular matrix.

A significant complication on renal transplantation is the chronic and progressive allograft dysfunction that develops months or years after transplantation. Recent advances with new immunosuppressive drugs did not improve the long-term allograft survival. Despite the well established knowledge of the ability of renin-angiotensin system blockade to control blood pressure and urinary protein excretion, the use of RAS inhibitors and blockers in renal transplant has been limited [12, 13].

We review our own observations and recent reports from the literature about the important role of RAS in the pathogenesis of chronic inflammatory process and local tecidual growth, in the chronic allograft dysfunction.
