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Relationship between caffeine intake and autosomal dominant polycystic kidney disease progression: a retrospective analysis using the CRISP cohort

  • McKenzie, Katelyn A.1
  • El Ters, Mirelle2
  • Torres, Vicente E.2
  • Harris, Peter C.2
  • Chapman, Arlene B.3
  • Mrug, Michal4
  • Rahbari-Oskoui, Frederic F.5
  • Bae, Kyongtae Ty6
  • Landsittel, Douglas P.7
  • Bennett, William M.8
  • Yu, Alan S. L.9
  • Mahnken, Jonathan D.1
  • 1 University of Kansas Medical Center, Department of Biostatistics, Mail Stop 1026, 3901 Rainbow Blvd., Kansas City, KS, 66160, USA , Kansas City (United States)
  • 2 Mayo Clinic, Division of Nephrology and Hypertension, Rochester, MN, USA , Rochester (United States)
  • 3 University of Chicago School of Medicine, Section of Nephrology, Chicago, IL, USA , Chicago (United States)
  • 4 University of Alabama and the Department of Veterans Affairs Medical Center, Division of Nephrology, Birmingham, AL, USA , Birmingham (United States)
  • 5 Emory University School of Medicine, Department of Internal Medicine, Atlanta, GA, USA , Atlanta (United States)
  • 6 University of Pittsburgh School of Medicine, Department of Radiology, Pittsburgh, PA, USA , Pittsburgh (United States)
  • 7 University of Pittsburgh School of Medicine, Department of Biomedical Informatics, Pittsburgh, PA, USA , Pittsburgh (United States)
  • 8 Legacy Good Samaritan Hospital, Portland, OR, USA , Portland (United States)
  • 9 University of Kansas Medical Center, Division of Nephrology and Hypertension and the Jared Grantham Kidney Institute, Kansas City, KS, USA , Kansas City (United States)
Published Article
BMC Nephrology
Springer (Biomed Central Ltd.)
Publication Date
Dec 27, 2018
DOI: 10.1186/s12882-018-1182-0
Springer Nature


BackgroundCaffeine has been proposed, based on in vitro cultured cell studies, to accelerate progression of autosomal dominant polycystic kidney disease (ADPKD) by increasing kidney size. Since ADPKD patients are advised to minimize caffeine intake, we investigated the effect of caffeine on disease progression in the Consortium for Radiologic Imaging Studies of Polycystic Kidney Disease (CRISP), a prospective, observational cohort study.MethodsOur study included 239 patients (mean age = 32.3 ± 8.9 ys; 188 caffeine consumers) with a median follow-up time of 12.5 years. Caffeine intake reported at baseline was dichotomized (any vs. none). Linear mixed models, unadjusted and adjusted for age, race, sex, BMI, smoking, hypertension, genetics and time, were used to model height-adjusted total kidney volume (htTKV) and iothalamate clearance (mGFR). Cox proportional hazards models and Kaplan-Meier plots examined the effect of caffeine on time to ESRD or death.ResultsCaffeine-by-time was statistically significant when modeling ln(htTKV) in unadjusted and adjusted models (p < 0.01) indicating that caffeine consumers had slightly faster kidney growth (by 0.6% per year), but htTKV remained smaller from baseline throughout the study. Caffeine consumption was not associated with a difference in mGFR, or in the time to ESRD or death (p > 0.05). Moreover the results were similar when outcomes were modeled as a function of caffeine dose.ConclusionWe conclude that caffeine does not have a significant detrimental effect on disease progression in ADPKD.

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