Variant hemoglobin phenotypes may account for differential erythropoiesis-stimulating agent dosing in African-American hemodialysis patients

Vimal K. Derebail, Patrick H. Nachman, Nigel S. Key, Heather Ansede, Ronald J. Falk, Wayne D. Rosamond, Abhijit V. Kshirsagar

Research output: Contribution to journalArticlepeer-review

10 Scopus citations

Abstract

African-American patients with end-stage renal disease have historically lower hemoglobin concentrations and higher requirements of erythropoiesis- stimulating agent (ESA). While disparities in health-care access may partially explain these findings, the role of variant hemoglobin, such as sickle trait, has not been investigated. To clarify this, we evaluated 154 African-American patients receiving in-center hemodialysis with available hemoglobin phenotyping. The primary exposure was any abnormal hemoglobin variant and the primary outcome of higher-dose ESA was defined as a dose of 6500 or more units per treatment. Logistic regression assessed the association between variant hemoglobin and higher-dose ESA. Covariates included age, gender, diabetes, iron parameters, intravenous iron dose, parathyroid hormone, albumin, phosphorus, body mass index, vascular access type, hospitalization/missed treatments, smoking status, alcohol abuse, and gastrointestinal bleeding. Of 33 patients with variant hemoglobin, 24 had HbAS and 9 had HbAC. Univariate odds of higher-dose ESA among those with hemoglobin variants were twice that of those with the normal HbAA phenotype (odds ratio 2.05). In multivariate models, the likelihood of higher-dose ESA had an odds ratio of 3.31 and the nature of this relationship did not change in Poisson regression or sensitivity analyses. Hence, our findings may explain, in part, the difference in ESA dosing between Caucasians and African-Americans with end-stage renal disease but await further study.

Original languageEnglish (US)
Pages (from-to)992-999
Number of pages8
JournalKidney international
Volume80
Issue number9
DOIs
StatePublished - Nov 1 2011

Bibliographical note

Funding Information:
We thank Len Usvyat, Stephanie McCollum RD LDN, Treva Williams RN, Zoe Davison, and Cindy Roberts RN of Carolina Dialysis and Renal Research Institute, and Patricia Atwood and Patrick Fleming of the North Carolina State Laboratory of Public Health for their assistance in compiling our data. This study was funded by UNC T-32 Renal Epidemiology Training Grant, T32-DK007750-09, NIH/NIDDK, PI: RJF, and Duke-UNC Clinical Hematology Research Career Development Program 5K12 HL087097-04, NIH/NHLBI, PI: Dr Marilyn Telen.

Keywords

  • ESRD
  • anemia
  • erythropoietin

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