title: Relation of homocysteinemia to contrast-induced nephropathy in patients undergoing percutaneous coronary intervention.
abstract: Hyperhomocysteinemia induces oxidative stress and endothelial dysfunction, which share the proposed pathophysiologic mechanisms of contrast-induced nephropathy (CIN). However, no study has investigated the relation between hyperhomocysteinemia and CIN. The aim of the present study was to evaluate the effects of hyperhomocysteinemia on CIN in patients undergoing percutaneous coronary intervention. This was an observational cohort study that included 572 patients who underwent percutaneous coronary intervention. CIN was defined as an absolute ≥0.5 mg/dl or a relative ≥25% increase in the serum creatinine level at 48 hours after the procedure. The incidence of CIN was significantly greater in patients in the third homocysteine tertile (from lowest to highest, 4.7%, 7.3%, and 24.2%, p <0.001). Furthermore, the homocysteine levels were significantly greater in patients with CIN than in those without CIN (16.9 ± 4.9 vs 13.5 ± 4.2 μmol/L, p <0.001). In multiple logistic regression models, hyperhomocysteinemia was an independent risk factor for CIN (per the SD change in the plasma homocysteine level [4.44 μmol/L], odds ratio 1.70, 95% confidence interval 1.07 to 2.71, p = 0.025) after adjusting for major risk factors such as age, diabetes, and baseline cardiac and renal function. In subgroup analyses according to diabetes, acute coronary syndrome, or baseline estimated glomerular filtration rate, significant, graded associations were found between the homocysteine level and the incidence of CIN. In conclusion, hyperhomocysteinemia is independently associated with a greater risk of CIN in patients undergoing percutaneous coronary intervention.
authors.affiliation: Division of Nephrology, Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea.
authors.forename: Seung Jun
authors.initials: SJ
authors.lastname: Kim
authors.forename: Donghoon
authors.initials: D
authors.lastname: Choi
authors.forename: Young-Guk
authors.initials: YG
authors.lastname: Ko
authors.forename: Jung-Sun
authors.initials: JS
authors.lastname: Kim
authors.forename: Seung Hyeok
authors.initials: SH
authors.lastname: Han
authors.forename: Byung-Keuk
authors.initials: BK
authors.lastname: Kim
authors.forename: Shin-Wook
authors.initials: SW
authors.lastname: Kang
authors.forename: Myeong-Ki
authors.initials: MK
authors.lastname: Hong
authors.forename: Yangsoo
authors.initials: Y
authors.lastname: Jang
authors.forename: Kyu Hun
authors.initials: KH
authors.lastname: Choi
authors.forename: Tae-Hyun
authors.initials: TH
authors.lastname: Yoo
mesh_terms: D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D003287:Contrast Media / Q000009:adverse effects*; D017023:Coronary Angiography / Q000009:adverse effects / Q000379:methods; D005260:Female; D005500:Follow-Up Studies; D005919:Glomerular Filtration Rate / Q000187:drug effects; D006710:Homocysteine / Q000097:blood*; D006801:Humans; D020138:Hyperhomocysteinemia / Q000097:blood / Q000139:chemically induced*; D007674:Kidney Diseases / Q000097:blood / Q000139:chemically induced*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000175:diagnosis* / Q000628:therapy; D011379:Prognosis; D012189:Retrospective Studies; D013997:Time Factors; D014283:Triiodobenzoic Acids / Q000009:adverse effects
chemical_list: D003287:Contrast Media; D014283:Triiodobenzoic Acids; D006710:Homocysteine; C044834:iodixanol