ArticlePharmacotherapy2014
In vivo alterations in drug metabolism and transport pathways in patients with chronic kidney diseases.
Article in Pharmacotherapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 37 citations in OpenAlex.
- Integrated Physiologically-Based Pharmacokinetic Model with a Quantitative Systems Pharmacology and Toxicology Model for Statins in Disease Population. Part 1: Model Development and Validation.The AAPS journal · 2025Article
- Clinical Pharmacokinetics of Fexofenadine: A Systematic Review.Pharmaceutics · 2024Review
- Interaction between Fexofenadine and CYP Phenotyping Probe Drugs in Geneva Cocktail.Journal of personalized medicine · 2019Article
- Effect of Chronic Kidney Disease on Nonrenal Elimination Pathways: A Systematic Assessment of CYP1A2, CYP2C8, CYP2C9, CYP2C19, and OATP.Clinical pharmacology and therapeutics · 2018Article
- Prediction of the Effect of Renal Impairment on the Pharmacokinetics of New Drugs.Clinical pharmacokinetics · 2018Article
- Microbiota-derived uremic retention solutes: perpetrators of altered nonrenal drug clearance in kidney disease.Expert review of clinical pharmacology · 2018Review
- Medication use and the risk of motor vehicle collision in West Virginia drivers 65 years of age and older: a case-crossover study.BMC research notes · 2016Article
- Consequences of renal failure on non-renal clearance of drugs.Clinical pharmacokinetics · 2014Review
- A Synopsis of Clinical Pharmacokinetic Alterations in Advanced CKD.Seminars in dialysisReview
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
Abstract
STUDY
objectiveThis study was designed to prospectively evaluate the in vivo activities of drug transporters, metabolizing enzymes, and pharmacokinetics in patients with chronic kidney diseases (CKD) caused by glomerulonephritis and nonglomerular etiologies.
designA prospective study design.
participantsEighteen adults with CKD.
settingGeneral Clinical Research Center at the University of North Carolina and University of Pittsburgh. MEASUREMENT AND MAIN
resultsBlood and urine were collected and assayed for fexofenadine (transporter function) as well as flurbiprofen and 4-hydroxyflurbiprofen (CYP2C9 function). CYP3A4 activity was assessed by the erythromycin breath test. In patients with glomerulonephritis, the apparent oral clearance of fexofenadine (representing transporter activity) was 58.8 ± 34.4 L/hour, documenting a 40% reduction compared with previous data in healthy controls. The CYP2C9 pathway (4-hydroxyflurbiprofen formation clearance) was similar in all the patients with CKD and was concordant with previous reports of patients with end-stage renal disease (ESRD) and healthy controls. For flurbiprofen, patients with glomerulonephritis had higher oral clearance than those with nonglomerular CKD, suggesting higher unbound fraction and enhanced metabolism through other (non-CYP2C9) routes. No statistically significant differences in CYP3A4 activity were observed in either group of patients or when compared with results from previous studies of patients with ESRD or healthy controls.
conclusionsThe current study suggests no statistically significant differences in the in vivo activity of CYP2C9 and CYP3A4 in patients with either glomerulonephritis or nonglomerular CKD. However, there are clinical differences in transporter function as defined by at least a 25% reduction in activity in glomerulonephritis as opposed to healthy controls. A similarity in the in vivo function between patients with glomerulonephritis and ESRD, and between patients with glomerulonephritis and nonglomerular CKD was present despite significant differences in kidney function. Further in vivo and in vitro studies are necessary to fully understand the physiologic and disease-specific nuances that contribute to alterations in drug disposition in patients with kidney diseases.
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