대한신장학회

논문분류	춘계학술대회 초록집
제목	Cardiorenal-Anemia-Iron Deficiency Syndrome (CRIDS) in Hemodialysis (HD) Patients
저자	Il Young Kim, Dong Won Lee, Soo Bong Lee, Kyung Nam Lee, Ihm Soo Kwak,Eun Young Seong, Byeong Yun Yang, Harin Lee
출판정보	2013; 2013(1):
키워드	심신증후군, 철결핍성 빈혈, 혈액투석/Cardiorenal syndrome, Iron, Hemodialysis
초록	Introduction: Recently, growing awareness that HF, renal impairment, and anemia are frequent co-morbidities which can exacerbate one another in a vicious circle has led to the concept of the “cardiorenal anaemia syndrome (CRAS)”. Many researchers expected higher dose administration of ESA could improve prognosis of CRAS. However some study reported adverse effects of ESA worsening vascular diseases. However, iron therapy got cardiac function improved in some studies of patients with HF. The role of iron deficiency (ID) within the complex interplay of HF, anemia, and renal dysfunction for patient undergone HD has been less well examined, although ID is highly prevalent in this setting. Therefore we sought to assess how ID affects heart function and clinical prognosis in HD patients with anemia. Methods: We included patients with anemia defined as hemoglobin level <12 g/dl in women and <13 g/dl in men. All patients had been on HD lasting over 3 months and checked echocardiogram (echoCG) between 1. 2008-7. 2012. Demographic, clinical, laboratory, and echoCG data were reviewed from electronic records. The study population was divided into 2 subgroups according to the presence of presence of ID. ID was defined as serum ferritin<100 μg/L, or serum ferritin ≥100 μg/L and ≤300 μg/L with Tsat <20%. We compared echoCG between 2 groups. The end points were all-cause mortality and adverse cardiac event including ACS or acute pulmonary edema required hospitalization. Results: Total subjects were 243 (ID:Non ID=113:130 patients). The baseline characteristics were not different between groups. Interestingly EF and CO represented systolic heart function were not different in echoCG, but E/E’ reflected diastolic heart function was statistically different (non ID: ID, 14.3±4.73:17.0±7.65, p 0.018). ID group showed higher adverse cardiac event rate and all cause mortality. During a median follow-up of 12.3 months, the multivariateadjusted OR of ID group for adverse cardiac event was 4.11 (95% CI:1.28-13.3; p 0.018). Conclusion: In patients undergone HD with anemia, ID is common and constitutes a predictor of unfavorable cardiac and survival outcome. ID can cause diastolic heart dysfunction as well. Therefore the management of ID is becoming an important therapeutic target in patients with CKD. But the exact mechanisms are still vague. Further studies are needed to figure it out and to set the therapeutic goal for treatment ID in CKD patients.
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