title: Contrast-induced nephropathy after percutaneous coronary interventions in relation to chronic kidney disease and hemodynamic variables.
abstract: We previously found that contrast-induced nephropathy (CIN) complicating percutaneous coronary intervention adversely affects patients with chronic kidney disease (CKD). Therefore, we further investigated whether the predictors and outcome of CIN after percutaneous coronary intervention differ among patients with versus without CKD. Among 7,230 consecutive patients, CIN (>or=25% or >or=0.5 mg/dl increase in preprocedure serum creatinine 48 hours after the procedure) developed in 381 of 1,980 patients (19.2%) with baseline CKD (estimated glomerular filtration rate [eGFR] <60 ml/min/1.73 m(2)) and in 688 of 5,250 patients (13.1%) without CKD. Decreased eGFRs, periprocedural hypotension, higher contrast media volumes, lower baseline hematocrit, diabetes, pulmonary edema at presentation, intra-aortic balloon pump use, and ejection fraction <40% were the most significant predictors of CIN in patients with CKD. Apart from intra-aortic balloon pump use, predictors of CIN in patients without CKD were the same as mentioned, plus older age and type of contrast media. Regardless of baseline renal function, CIN correlated with longer in-hospital stay and higher rates of in-hospital complications and 1-year mortality compared with patients without CIN. By multivariate analysis, CIN was 1 of the most powerful predictors of 1-year mortality in patients with preexisting CKD (odds ratio 2.37, 95% confidence interval 1.63 to 3.44) or preserved eGFR (odds ratio 1.78; 95% confidence interval 1.22 to 2.60). Thus, regardless of the presence of CKD, baseline characteristics and periprocedural hemodynamic parameters predict CIN, and this complication is associated with worse in-hospital and 1-year outcomes.
authors.affiliation: Cardiovascular Research Foundation, Lenox Hill Heart and Vascular Institute, New York, New York, USA. gdangas@crf.org <gdangas@crf.org>
authors.forename: George
authors.initials: G
authors.lastname: Dangas
authors.forename: Ioannis
authors.initials: I
authors.lastname: Iakovou
authors.forename: Eugenia
authors.initials: E
authors.lastname: Nikolsky
authors.forename: Eve D
authors.initials: ED
authors.lastname: Aymong
authors.forename: Gary S
authors.initials: GS
authors.lastname: Mintz
authors.forename: Nicholas N
authors.initials: NN
authors.lastname: Kipshidze
authors.forename: Alexandra J
authors.initials: AJ
authors.lastname: Lansky
authors.forename: Issam
authors.initials: I
authors.lastname: Moussa
authors.forename: Gregg W
authors.initials: GW
authors.lastname: Stone
authors.forename: Jeffrey W
authors.initials: JW
authors.lastname: Moses
authors.forename: Martin B
authors.initials: MB
authors.lastname: Leon
authors.forename: Roxana
authors.initials: R
authors.lastname: Mehran
mesh_terms: D000368:Aged; D002908:Chronic Disease; D003287:Contrast Media / Q000009:adverse effects*; D003327:Coronary Disease / Q000628:therapy*; D005260:Female; D005500:Follow-Up Studies; D006439:Hemodynamics; D006801:Humans; D015994:Incidence; D007485:Ioxaglic Acid / Q000009:adverse effects*; D007674:Kidney Diseases / Q000139:chemically induced* / Q000150:complications / Q000453:epidemiology / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D013997:Time Factors
chemical_list: D003287:Contrast Media; D007485:Ioxaglic Acid