Acute kidney injury (AKI) occurs in approximately 7% of patients undergoing PCI, of whom 3% develop AKI that requires dialysis. Increased occurrence of AKI among patients undergoing PCI is associated with the presence of STEMI, preexisting baseline renal failure and cardiogenic shock. The occurrence of AKI following PCI is associated with increased in-hospital mortality.[1]
While the risk of hemodialysis is less than 3 percent in cases of uncomplicated CIN, the in-hospital mortality in the setting of hemodialysis exceeds 30 percent.
Patients with evidence of mild renal dysfunction have a 20 percent higher risk of death a one year following PCI than patients with preserved renal function.
Mild renal dysfunction following PCI may increase the risk of death up to four fold at one year following PCI compared with patients with preserved renal function.
↑Trivedi HS, Moore H, Nasr S, Aggarwal K, Agrawal A, Goel P, Hewett J (2003). "A randomized prospective trial to assess the role of saline hydration on the development of contrast nephrotoxicity". Nephron. Clinical Practice. 93 (1): C29–34. PMID12411756. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)CS1 maint: Multiple names: authors list (link)
↑Marenzi G, Assanelli E, Campodonico J, Lauri G, Marana I, De Metrio M, Moltrasio M, Grazi M, Rubino M, Veglia F, Fabbiocchi F, Bartorelli AL (2009). "Contrast volume during primary percutaneous coronary intervention and subsequent contrast-induced nephropathy and mortality". Annals of Internal Medicine. 150 (3): 170–7. PMID19189906. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)CS1 maint: Multiple names: authors list (link)
↑ Gonzales DA, Norsworthy KJ, Kern SJ, et al. A meta-analysis of N-acetylcysteine in contrast-induced nephrotoxicity: unsupervised clustering to resolve heterogeneity. BMC Med. 2007; 5: 32. Published online November 14, 2007. doi:10.1186/1741-7015-5-32
↑Ozcan EE, Guneri S, Akdeniz B, et al. Sodium bicarbonate, N-acetylcysteine, and saline for prevention of radiocontrast-induced nephropathy. A comparison of 3 regimens for protecting contrast-induced nephropathy in patients undergoing coronary procedures. A single-center prospective controlled trial. Am Heart J. 2007; 154: 539– 44.
↑Thiele H, Hildebrand L, Schirdewahn C, et al. Impact of high-dose N-acetylcysteine versus placebo on contrast-induced nephropathy and myocardial reperfusion injury in unselected patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention: the LIPSIA-N-ACC (Prospective, Single-Blind, Placebo-Controlled, Randomized Leipzig Immediate PercutaneouS Coronary Intervention Acute Myocardial Infarction N-ACC) Trial. J Am Coll Cardiol. 2010; 55: 2201– 9.
↑Webb JG, Pate GE, Humphries KH, et al. A randomized controlled trial of intravenous N-acetylcysteine for the prevention of contrast-induced nephropathy after cardiac catheterization: lack of effect. Am Heart J. 2004; 148: 422–9.
↑ACT Investigators. Acetylcysteine for prevention of renal outcomes in patients undergoing coronary and peripheral vascular angiography: main results from the randomized Acetylcysteine for Contrast-Induced Nephropathy Trial (ACT). Circulation. 2011; 124: 1250–9.
↑Levey AS, Coresh J, Greene T, Stevens LA, Zhang YL, Hendriksen S, Kusek JW, Van Lente F (2006). "Using standardized serum creatinine values in the modification of diet in renal disease study equation for estimating glomerular filtration rate". Annals of Internal Medicine. 145 (4): 247–54. PMID16908915. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)CS1 maint: Multiple names: authors list (link)