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ORIGINAL ARTICLE
Year : 2020  |  Volume : 33  |  Issue : 1  |  Page : 105-109

Predictors of erythropoietin hyporesponsiveness in chronic hemodialysis patients


Department of Internal Medicine, Faculty of Medicine, Menoufia University, Shebin El-Kom, Egypt

Correspondence Address:
Ahmed M Kamal
17 El-Sayed Gomaa Street, El Bagour
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/mmj.mmj_52_19

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Objective The aim of this work was to assess different clinical and laboratory parameters to predict erythropoietin hyporesponsiveness in chronic hemodialysis patients with anemia. Background Anemia resistant to erythropoietin-stimulating agents (ESAs) is a risk factor for all-cause mortality. Determining the etiologies of hyporesponsiveness may help to overcome the resistance. Patients and methods This cross-sectional study was carried out on 97 chronic hemodialysis patients attending Menoufia University Hospital and Manshiet Sultan hemodialysis units. Patients were classified according to the presence of anemia (hemoglobin < 10 g/dl) and ESA hyporesponsiveness index more than or equal to 10 into four groups: group I comprised nonanemic and ESA-responsive patients, group II comprised nonanemic and ESA-hyporesponsive patients, group III comprised anemic and ESA-responsive patients, and group IV comprised anemic and ESA-hyporesponsive patients. We compared groups I and IV with respect to influential factors. Results The proportion of patients treated with renin-angiotensin-aldosterone system blockers (RAAS blockers) was significantly higher in group IV compared with group I (P = 0.000). Group IV patients had significantly lower dialysis adequacy (Kt/V) (P = 0.029) and significantly higher platelet to lymphocyte ratio (PLR), C-reactive protein (CRP), and intact parathormone hormone (P = 0.002, 0.000, and 0.006, respectively). There were significant positive correlations between mean ESA hyporesponsiveness index and CRP, PLR, and intact parathormone hormone and negative correlation with Kt/V. In multivariate analysis, treatment with RAAS blockers, inflammatory markers (PLR and CRP), and secondary hyperparathyroidism were independent predictors of ESA resistance. Conclusion RAAS blockers' treatment, inflammation, and secondary hyperparathyroidism could be considered as predictors of ESA hyporesponsiveness.


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