Introduction: Chronic kidney disease (CKD) has been considered an important public
health issue in all countries. Experimental and clinical studies support the general idea that the
pathophysiology of CKD is associated with the interaction of several endogenous mediators, including
components of the renin-angiotensin system (RAS) and cytokines.
Objective: This review aims to report available evidence on the interaction of RAS molecules and
cytokines in CKD.
Results: Therapeutic administration of angiotensin converting enzyme (ACE) inhibitors and/or
angiotensin type 1 (AT1) receptor antagonists can slow down the deterioration of renal function.
These medications reduce the formation (ACE inhibitor) or the receptor-mediated effects of Angiotensin
II (AT1 antagonist) and by so doing inhibit cytokine-mediated kidney tissue inflammation. In
sharp contrast, the activation of ACE2, the stimulation of Angiotensin-(1-7) synthesis and/or the
effects mediated by its G-protein coupled receptor, named Mas receptor, ameliorates experimental
renal injury by reducing renal tissue inflammation and fibrosis in many experimental models of
Conclusion: Novel compounds that activate and/or stimulate ACE2-Angiontensin-(1-7)-Mas receptor
axis may also play a role in the treatment of CKD, mainly by controlling inflammatory response
and pathways of fibrosis at kidney tissue. Clinical trials with these new pharmacological compounds
will, in due course, determine whether this promise will become a helpful treatment.