Influence of SLCO1B3 gene polymorphism on the pharmacokinetics of digoxin in terminal renal failure

Drug Metab Pharmacokinet. 2008;23(6):406-11. doi: 10.2133/dmpk.23.406.

Abstract

Digoxin (DX) is mainly excreted unchanged in the urine. In patients undergoing hemodialysis (HD patients), the relative contribution of hepatic elimination is increased. DX is a substrate of OATP1B3 (SLCO1B3), expressed on the sinusoidal membranes of hepatocytes in humans. Therefore, we investigated the relationship between SLCO1B3 gene polymorphisms and the value of trough concentration-to-dose ratio (C/D ratio) of DX in HD patients. We investigated two deletion polymorphisms in complete linkage disequilibrium (-28 to -11 and -7 to -4) and two SNPs in complete linkage disequilibrium (T334G and G699A). Blood was sampled 62-72 hours after the oral administration of DX. The C/D ratio of DX was lower in patients with the deletion allele than in those homozygous for the insertion allele, and was lower in patients with the 334T/669G allele than in those homozygous for the 334G/699A allele, although the differences were not statistically significant. The C/D ratio of DX was significantly higher in patients with homozygous for the insert-variant allele (median: 121.8 (ng/mL)/(mg/week/kg), range: 92.5-259.4 (ng/mL)/(mg/week/kg) than in others (median: 93.4 (ng/mL)/(mg/week/kg), range: 66.5-154.3 (ng/mL)/(mg/week/kg)). In conclusion, the insert-variant allele of the OATP1B3 gene may increase the C/D ratio of DX in HD patients.

Publication types

  • Comparative Study

MeSH terms

  • Digoxin / pharmacokinetics*
  • Digoxin / therapeutic use
  • Dose-Response Relationship, Drug
  • Female
  • Gene Frequency / drug effects
  • Genetic Variation
  • Genotype
  • Humans
  • Male
  • Mutagenesis, Insertional
  • Organic Anion Transporters, Sodium-Independent / genetics*
  • Organic Anion Transporters, Sodium-Independent / metabolism
  • Polymorphism, Genetic / genetics*
  • Renal Insufficiency / drug therapy
  • Renal Insufficiency / genetics*
  • Renal Insufficiency / metabolism
  • Solute Carrier Organic Anion Transporter Family Member 1B3

Substances

  • Organic Anion Transporters, Sodium-Independent
  • SLCO1B3 protein, human
  • Solute Carrier Organic Anion Transporter Family Member 1B3
  • Digoxin