Activation of renin-angiotensin-aldosteron axis (RAA) represents one of the key mechanisms of kidney damage in several primary and secondary renal diseases. Its activation is reflected by an enhanced “systemic” activity although absence of such an activity does not exclude the significant and adverse action of its particular elements on a tissue level. Angiotensin II and aldosteron are not only direct mediators of kidney damage but the also stimulate several other adverse mechanisms such as endothelial dysfunction, hypercoagulation, enhanced oxidative stress, sympathetic overactivity and inflammation. Blockade of RAA on several levels – from converting enzyme inhibition, through blocking receptors for angiotensin II and aldosteron, to interaction with receptor for prorenin appears one of the key strategies in the treatment of kidney diseases.