Abstract
Background: This study was to investigate the effect of long term use of Renin-Angiotensin-Aldosterone System(RAAS) blocking agents on the incidence of Contrast-Induced Nephropathy(CIN) on patients with Diabetes Mellitus(DM) and renal insufficiency underwent Percutaneous Coronary Intervention (PCI).
 Methods:A total 281 of subjects were included in this study and divided into two groups based on prior use of RAAS blocking agents (RAAS +, n = 146; RAAS -, n = 135). CIN was defined as an increase of ≥25% in creatinin over baseline value 48-72 hours after PCI.
 Result: Total incidence of CIN was 14,95%. There was no difference in the incidence of CIN between 2 study groups (p = 0,952) and relatif risk for CIN was 1,02. Left Ventricular ejection Fraction (LVEF) ≤ 40 % (OR 2,300; 95% CI 1,028 – 5,143; p = 0,043), anemia (OR 2,628; 95% CI 1,274 – 5,422; p = 0,009) and Glomerular Filtration rate (GFR) pre PCI ≤ 60 mL/menit (OR 2,782; 95% CI 1,293 – 5,987; p = 0,009) were important predictors of CIN.
 Conclusion: Long term use of RAAS blocking agents do not increase the incidence of CIN on patients with DM and renal insufficiency underwent PCI.
Highlights
Contrast-Induced Nephropathy (CIN) is one of a serious complication of Percutaneous Coronary Intervention (PCI) whose incidence varies from 2% - 25% based on population and risk factors[1,2]
Experimental data suggest that increased endothelin-1, and reactive oxygen species are vital in the development of CIN, and can be inhibited using Renin-Angiotensin-Aldosterone System (RAAS) blocking agents[13]
After PCI, RAAS (-) groups had significantly higher Glomerular Filtration rate (GFR) compare to RAAS (+) (p = 0,026), as shown on absolute change (p = 0,007)
Summary
Contrast-Induced Nephropathy (CIN) is one of a serious complication of Percutaneous Coronary Intervention (PCI) whose incidence varies from 2% - 25% based on population and risk factors[1,2]. Some study concluded that it was effective in the prevention of CIN2,6, but other studies concluded that it was a risk factor[1,7,8,9]. The reason behind these conflicting results is the pathomechanism of CIN that remain unclear. It has been speculated that RAAS blocking agents may decrease the vascular tone of efferent arteriole used to maintain glomerular hydrostatic pressure. Experimental data suggest that increased endothelin-1, and reactive oxygen species are vital in the development of CIN, and can be inhibited using RAAS blocking agents[13]
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