Peritoneal membrane changes over time in long-term peritoneal dialysis (PD) patients lead to dialysis failure and
increased morbidity as well as mortality. Bio-incompatable PD solution, peritonitis, and uremia are hypothesized in causing
membrane damage. Fibrous organization and angiogenesis of peritoneum are crucial morphological alterations which can
diminish the efficacy of exchange and cause ultrafiltration failure. Pathophysiologic mechanisms of membrane damage have
been extensively studied to innovate therapeutic strategies. One of the potential mechanisms is a presence of local reninangiotensin-
aldosterone system (RAAS) by which injured peritoneal mesothelial cell-derived angiotensin-II (AII) causes
activations in TGF-β, VEGF expression, and epithelial-to-mesenchymal transition (EMT) which contributes to extracellular
matrix accumulation and neoangiogenesis in submesothelial tissues. Clinical evidence of RAAS blockade on human peritoneal
membrane remains under investigation and is still inconclusive but relevant data seem to demonstrate its benefit on membrane
preservation. Longitudinal effect of RAAS blockade on membrane structural, functional, and clinical relationships and
strategies to use angiotensin converting enzyme inhibitor (ACEI), angiotensin II receptor blocker (ARB), aldosterone antagonist,
and direct renin inhibitor are an interesting field to be explored.

Keywords: RAAS blockade, ACEI, ARB, Peritoneal membrane preservation