Abstract

Objective: To assess the relationship between SCT, hemoglobin levels and anemia in CKD black patients. Method: A post-hoc analysis of data from 188 patients, enrolled in a cross-sectional study of sickle cell trait (SCT) and chronic kidney disease (CKD), was performed to assess the relationship between SCT, hemoglobin (Hb) levels and anemia defined as Hb < 12 g/dl in men and <11 g/dl in women. Student t test, Mann Whitney and Chi square test were used as appropriate for different comparisons. P < 0.05 defined the level of statistical significance. Results: SCT (HbAS) and normal hemoglobin (HbAA) were present in 39 (21%) and 149 (79%) CKD patients, respectively. Despite similar estimated GFR (eGFR) and age, HbAS patients had significantly lower Hb levels (8.8 ± 1.8 vs 10 ± 2.2 g/dl; p = 0.001) and a higher proportion of anemia (95% vs 72%, p = 0.001). In multiple linear regression analysis, eGFR, BMI, SBP and SCT emerged as independent determinants of Hb levels. The presence of SCT was associated with 1.185 g/dl decrease in Hb levels. Conclusion: In the present case series, SCT was associated with lower Hb levels suggesting its potential contribution to the pathogenesis of CKD-associated anemia.

Highlights

  • African American patients with end-stage renal disease (ESRD) have been reported to have lower hemoglobin levels at the start of dialysis compared to other racial or ethnic groups [1] [2]

  • Chronic kidney disease (CKD) black patients bearing HbAS have been reported to be resistant to ASE and require higher doses of these agents compared to other race/ethnic groups [4]

  • Clinical and biological characteristics of the whole study population and according to hemoglobin genotype are summarized in Table 1 and Table 2

Read more

Summary

Introduction

African American patients with end-stage renal disease (ESRD) have been reported to have lower hemoglobin levels at the start of dialysis compared to other racial or ethnic groups [1] [2]. Chronic kidney disease (CKD) black patients bearing HbAS have been reported to be resistant to ASE and require higher doses of these agents compared to other race/ethnic groups [4]. Bearing in mind these pathophysiological changes, one might expect HbAS to be common in patients with CKD and influential in the pathogenesis and treatment of CKD-associated anemia [8]. The identification of SCT in patients with CKD could have therapeutic and prognostic implications [8]

Methods
Results
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call