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

TitleRelationship between caffeine intake and autosomal dominant polycystic kidney disease progression: A retrospective analysis using the CRISP cohort
Authors
KeywordsCaffeine
CRISP
ESRD
Linear mixed models
Polycystic kidney disease
Issue Date2018
Citation
BMC Nephrology, 2018, v. 19, n. 1, article no. 378 How to Cite?
AbstractBackground: Caffeine 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. Methods: Our 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. Results: Caffeine-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. Conclusion: We conclude that caffeine does not have a significant detrimental effect on disease progression in ADPKD.
Persistent Identifierhttp://hdl.handle.net/10722/316176
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorMcKenzie, Katelyn A.-
dc.contributor.authorEl Ters, Mirelle-
dc.contributor.authorTorres, Vicente E.-
dc.contributor.authorHarris, Peter C.-
dc.contributor.authorChapman, Arlene B.-
dc.contributor.authorMrug, Michal-
dc.contributor.authorRahbari-Oskoui, Frederic F.-
dc.contributor.authorBae, Kyongtae Ty-
dc.contributor.authorLandsittel, Douglas P.-
dc.contributor.authorBennett, William M.-
dc.contributor.authorYu, Alan S.L.-
dc.contributor.authorMahnken, Jonathan D.-
dc.date.accessioned2022-08-24T15:49:30Z-
dc.date.available2022-08-24T15:49:30Z-
dc.date.issued2018-
dc.identifier.citationBMC Nephrology, 2018, v. 19, n. 1, article no. 378-
dc.identifier.urihttp://hdl.handle.net/10722/316176-
dc.description.abstractBackground: Caffeine 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. Methods: Our 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. Results: Caffeine-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. Conclusion: We conclude that caffeine does not have a significant detrimental effect on disease progression in ADPKD.-
dc.languageeng-
dc.relation.ispartofBMC Nephrology-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectCaffeine-
dc.subjectCRISP-
dc.subjectESRD-
dc.subjectLinear mixed models-
dc.subjectPolycystic kidney disease-
dc.titleRelationship between caffeine intake and autosomal dominant polycystic kidney disease progression: A retrospective analysis using the CRISP cohort-
dc.typeArticle-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1186/s12882-018-1182-0-
dc.identifier.pmid30591038-
dc.identifier.pmcidPMC6307167-
dc.identifier.scopuseid_2-s2.0-85059226746-
dc.identifier.volume19-
dc.identifier.issue1-
dc.identifier.spagearticle no. 378-
dc.identifier.epagearticle no. 378-
dc.identifier.eissn1471-2369-
dc.identifier.isiWOS:000454573100001-

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