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.
| Original language | English |
|---|---|
| Pages (from-to) | 1086-1091 |
| Number of pages | 6 |
| Journal | American Journal of Cardiology |
| Volume | 108 |
| Issue number | 8 |
| DOIs | |
| Publication status | Published - 2011 Oct 15 |
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All Science Journal Classification (ASJC) codes
- Cardiology and Cardiovascular Medicine
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Relation of homocysteinemia to contrast-induced nephropathy in patients undergoing percutaneous coronary intervention. / Kim, Seung Jun; Choi, Donghoon; Ko, Young Guk; Kim, Jung Sun; Han, Seung Hyeok; Kim, Byung Keuk; Kang, Shin Wook; Hong, Myeong Ki; Jang, Yangsoo; Choi, Kyu Hun; Yoo, Tae Hyun.
In: American Journal of Cardiology, Vol. 108, No. 8, 15.10.2011, p. 1086-1091.Research output: Contribution to journal › Article
TY - JOUR
T1 - Relation of homocysteinemia to contrast-induced nephropathy in patients undergoing percutaneous coronary intervention
AU - Kim, Seung Jun
AU - Choi, Donghoon
AU - Ko, Young Guk
AU - Kim, Jung Sun
AU - Han, Seung Hyeok
AU - Kim, Byung Keuk
AU - Kang, Shin Wook
AU - Hong, Myeong Ki
AU - Jang, Yangsoo
AU - Choi, Kyu Hun
AU - Yoo, Tae Hyun
PY - 2011/10/15
Y1 - 2011/10/15
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=80053999688&partnerID=8YFLogxK
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U2 - 10.1016/j.amjcard.2011.06.010
DO - 10.1016/j.amjcard.2011.06.010
M3 - Article
C2 - 21791335
AN - SCOPUS:80053999688
VL - 108
SP - 1086
EP - 1091
JO - American Journal of Cardiology
JF - American Journal of Cardiology
SN - 0002-9149
IS - 8
ER -