APOL1, α-thalassemia, and BCL11A variants as a genetic risk profile for progression of chronic kidney disease in sickle cell anemia

Haematologica. 2017 Jan;102(1):e1-e6. doi: 10.3324/haematol.2016.154153. Epub 2016 Sep 22.
No abstract available

Publication types

  • Letter
  • Research Support, N.I.H., Extramural

MeSH terms

  • Adult
  • Anemia, Sickle Cell
  • Apolipoprotein L1 / genetics*
  • Carrier Proteins / genetics*
  • Female
  • Humans
  • Male
  • Nuclear Proteins / genetics*
  • Renal Insufficiency, Chronic / etiology
  • Renal Insufficiency, Chronic / genetics*
  • Repressor Proteins
  • Risk Factors
  • alpha-Thalassemia / complications
  • alpha-Thalassemia / genetics*

Substances

  • APOL1 protein, human
  • Apolipoprotein L1
  • BCL11A protein, human
  • Carrier Proteins
  • Nuclear Proteins
  • Repressor Proteins