Das Renin-Angiotensin-Aldosteron-System als Zentraler Mediator der Progression der Niereninsuffizienz

The complex renin-angiotensin-aldosterone system (RAAS) plays an important role in the progression of renal insufficiency. Renin and aldosterone can contribute independently of ANG II to renal fibrosis via the induction of TGFβ synthesis. Genetic polymorphisms involving the components of RAAS, agonistic antibodies against the AT₁ receptor as well as AT₁ receptor dimers can all contribute further to deterioration in renal function. ACE inhibitors and AT₁ receptor antagonists in standard dosages incompletely inhibit intrarenal RAAS. To control blood pressure and proteinuria, ACE inhibitors or AT₁ receptor antagonists should be prescribed up to the recommended dose. Double blockade should be considered for patients with chronic renal failure and a proteinuria of more than 1 g/day. Recommendations for the additional use of aldosterone antagonists can currently not be made due to lack of data from clinical studies. Renin inhibitors are not yet licensed for the German market.