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Review
. 2025 Jun;21(6):677-687.
doi: 10.1080/17425255.2025.2501127. Epub 2025 May 7.

Pharmacotherapy in kidney disease: what it takes to move from general guidance to specific recommendations to stratified subgroups of patients - the tale of autosomal dominant polycystic kidney disease (ADPKD)

Annika C Tillmann  1 , Amin Rostami-Hodjegan  1   2 , Jill Barber  1 , Zubida M Al-Majdoub  1
Affiliations
Review

Pharmacotherapy in kidney disease: what it takes to move from general guidance to specific recommendations to stratified subgroups of patients - the tale of autosomal dominant polycystic kidney disease (ADPKD)

Annika C Tillmann et al. Expert Opin Drug Metab Toxicol. 2025 Jun.

Abstract

Introduction: Autosomal dominant polycystic kidney disease (ADPKD) is a hereditary condition that leads to a range of systemic manifestations. Many of them require pharmacological interventions. Most patients receive multidrug therapy.

Areas covered: The review summarizes prevalent ADPKD manifestations that might require pharmacological intervention and the most common drug therapies. It lists 2 to 3 prescribed drugs for each manifestation of ADPKD. The review identifies the drug transporters and drug-metabolizing enzymes associated with these drugs, as well as potential drug-drug interactions. To fulfill these aims, a literature search was conducted on PubMed, covering the period from 2021 to July 2024.

Expert opinion: ADPKD therapy often focuses on treating a single manifestation of the disease. However, ADPKD is a complex condition that requires multidrug treatment. While doses of renally eliminated drugs are adjusted in ADPKD patients to account for renal function decline, the condition may change the expression and function of renal and hepatic drug-metabolizing enzymes and transporters, which could result in misevaluations in drug dosing in ADPKD patients and result in under- or overdosing, as well as drug-drug interactions. PBPK modeling offers a valuable tool to predict drug-drug interactions, preventing overdosing, and support precision dosing in patients with ADPKD.

Keywords: ADPKD; acetaminophen; antihypertensives; fluoroquinolone; meropenem; opioids; tolvaptan.

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Conflict of interest statement

A. Rostami-Hodjegan is a part-time employee of Certara Inc., a provider of biosimulation solutions for pharmaceutical companies. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Figures

Figure 1.
Figure 1.
Tolvaptan uptake and metabolism as well as drug transporters inhibited by the parent drug and the metabolites. (red cross = strong-medium inhibition, pink cross = weak inhibition). This figure was created with BioRender (2025) and the software Chemsketch.
Figure 2.
Figure 2.
Uptake and metabolism of 2 antihypertensive prodrugs and the active compounds. This figure was created with BioRender (2025) and the software Chemsketch.
Figure 3.
Figure 3.
Uptake and metabolism of the 3 antibiotics in considered for ADPKD cyst infections. (red cross =inhibition). This figure was created with BioRender (2025) and the software Chemsketch.
Figure 4.
Figure 4.
Elimination and metabolism of paracetamol and tramadol in the hepatocytes. (red cross = inhibition). This figure was created with BioRender (2025) and the software Chemsketch.
See this image and copyright information in PMC

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References

    1. Liebau MC, Mekahli D, Perrone R, et al. Polycystic kidney disease drug development: a conference report. Kidney Med. 2023;5(3):100596. doi: 10.1016/j.xkme.2022.100596 - DOI - PMC - PubMed
    1. Cornec-Le Gall E, Alam A, Perrone RD.. Autosomal dominant polycystic kidney disease. Lancet. 2019;393(10174):919–935. doi: 10.1016/S0140-6736(18)32782-X - DOI - PubMed
    1. Rahbari-Oskoui F, Williams O, Chapman A.. Mechanisms and management of hypertension in autosomal dominant polycystic kidney disease. Nephrol Dial Transplant. 2014;29(12):2194–2201. doi: 10.1093/ndt/gft513 - DOI - PubMed

    2. •• Summary and critical discussion of clinical trials investigating and comparing the effectiveness of different antihypertensives.

    1. Suwabe T, Araoka H, Ubara Y, et al. Cyst infection in autosomal dominant polycystic kidney disease: causative microorganisms and susceptibility to lipid-soluble antibiotics. Eur J Clin Microbiol Infect Dis. 2015;34(7):1369–1379. doi: 10.1007/s10096-015-2361-6 - DOI - PubMed
    1. Hogan MC, Norby SM. Evaluation and management of pain in autosomal dominant polycystic kidney disease. Adv Chronic Kidney Dis. 2010;17(3):e1–e16. doi: 10.1053/j.ackd.2010.01.005 - DOI - PMC - PubMed

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