assessment. In TEMPO 3:4, there was no requirement for follow-up after discontinuation to extend to end of study. Accordingly, the TEMPO 3:4 data may provide a less robust pool of data on noncompleters. Within the context of the demonstrated efficacy of tolvaptan in subjects with ADPKD with early- to latestage CKD, the most important factor in determining tolvaptan effect size in inhibiting eGFR decline appears to be stage of kidney disease at treatment commencement. This conclusion is consistent with earlier findings.20 Given that kidney function decline accelerates with the progression of ADPKD, the effects of tolvaptan in slowing kidney function loss are most easily discernible in later-stage patients. In clinical practice, monitoring kidney function to assess the effects of tolvaptan therapy, therefore, may be particularly useful for patients with later-stage disease. DISCLOSURES AJM reports being a Medical Advisory Board member for Otsuka; and receiving grants from Sanofi-Genzyme, PKD Australia, Queensland Health, and NHMRC for studies outside the submitted work. RDP reports grants from Otsuka and Otsuka Steering Committee Membership during the conduct of the study; grants from Department of Defense, grants from Sanofi-Genzyme, personal fees from Sanofi-Genzyme, Palladio Biosciences, and Reata, grants from Kadmon, grants from Reata, other from UpToDate, outside the submitted work. GR is a member of the Table 1. Baseline characteristics of TEMPO 3:4 and REPRISE participants by completer status Parameter TEMPO 3:4 REPRISE Completers (n [ 1157) Noncompleters (n [ 288) P value Completers (n [ 1215) Noncompleters (n [ 155) P value Male, n (%) 605 (52) 141 (49) 0.32 612 (50) 68 (44) 0.15 Age (y), mean (SD) 39.03 (6.97) 37.15 (7.47) 2000 ml, or unknown. Baseline total kidney volume was unknown for 80% of subjects. b Urine osmolality in TEMPO3:4 was collected on the day of randomization before participant exposure to tolvaptan. Urine osmolality in REPRISE was also collected on the day of randomization; however, this was at the completion of active tolvaptan run-in and therefore while participants were exposed to fully titrated tolvaptan. P-values were derived by Fisher exact test for binary characteristics. P values were derived by t-test/Wilcoxon test for continuous characteristics. CLINICAL RESEARCH AJ Mallett et al.: Adherence and Tolvaptan Effect Size in ADPKD 1038 Kidney International Reports (2021) 6, 1032–1040 Scientific Advisory Board of PKD Australia; received grants from the National Health and Medical Research Council of Australia; investigator-initiated grants from PKD Australia, Danone Nutricia (manufacturer of bottled water), Otsuka Australia, and been a member of an Advisory Board for Sanofi-Genzyme. CH reports receiving personal fees from GlaxoSmithKline, Johnson & Johnson, and Otsuka; and grants from Baxter Healthcare, Fresenius Medical Care, PKD Australia, Queensland Health, and NHMRC Australia for studies outside the submitted work. TFH reports having received research funding from AstraZeneca and GlaxoSmithKline, and having served as an advisor to AstraZeneca and Vifor Pharma. JL is an employee of Otsuka. VET reports grants and/or other fees from Acceleron Pharma Inc., Blueprint Medicines, Mironid, Otsuka Pharmaceuticals, Palladio Biosciences, Sanofi Genzyme, Regulus Therapeutics, and Vertex Pharmaceuticals, all outside the submitted work. All the other authors declared no competing interests. ACKNOWLEDGMENTS This analysis was funded by Otsuka Pharmaceutical Development & Commercialization, Inc. (Rockville, MD, USA). Editorial services in preparation of the manuscript, also funded by Otsuka, were provided by BioScience Communications, Inc (New York, NY, USA). SUPPLEMENTARY MATERIAL Supplementary File (PDF) Table S1. TEMPO 3:4 completers, annual rate of change in renal function, estimated by CKD-EPI formula (ml/min per 1.73 m2 /year). Table S2. REPRISE completers, annualized change in eGFR (ml/min per 1.73 m2 /year) from pretreatment baseline to posttreatment follow-up. Table S3. Baseline characteristics of matched subjects from TEMPO 3:4 and REPRISE. Figure S1. The age (A) and chronic kidney disease stage (B) distributions of the matched analysis population. CONSORT Statement. REFERENCES 1. Chapman AB, Devuyst O, Eckardt KU, et al. Autosomaldominant polycystic kidney disease (ADPKD): executive summary from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference. Kidney Int. 2015;88:17–27. 2. Reule S, Sexton DJ, Solid CA, et al. ESRD f Translational research approaches to study pediatric polycystic kidney disease Max Christoph Liebau1* and Djalila Mekahli2,3* Abstract Polycystic kidney diseases (PKD) are severe forms of genetic kidney disorders. The two main types of PKD are autosomal recessive and autosomal dominant PKD (ARPKD, ADPKD). While ARPKD typically is a disorder of early childhood, patients with ADPKD often remain pauci-symptomatic until adulthood even though formation of cysts in the kidney already begins in children. There is clinical and genetic overlap between both entities with very variable clinical courses. Subgroups of very early onset ADPKD may for example clinically resemble ARPKD. The basis of the