Abstract: FR-PO309
Relationship between Caffeine and Autosomal Dominant Polycystic Kidney Disease Progression
Session Information
- Cystic Kidney Diseases - II
November 03, 2017 | Location: Hall H, Morial Convention Center
Abstract Time: 10:00 AM - 10:00 AM
Category: Genetic Diseases of the Kidney
- 801 Cystic Kidney Diseases
Authors
- Mckenzie, Katelyn, University of Kansas Medical Center, Kansas City, Kansas, United States
- El Ters, Mireille, Mayo Clinic, Rochester, Minnesota, United States
- Yu, Alan S.L., University of Kansas Medical Center, Kansas City, Kansas, United States
- Mahnken, Jonathan D., University of Kansas Medical Center, Kansas City, Kansas, United States
Background
Caffeine has been proposed, based on animal studies, to further progression of autosomal dominant polycystic kidney disease (ADPKD) by increasing cyst and kidney size. ADPKD patients are advised to minimize caffeine intake. We therefore investigated the effect of caffeine on kidney function in ADPKD.
Methods
Data from the Consortium for Radiologic Imaging Studies of Polycystic Kidney Disease study included 239 patients (96 males, mean age = 32.3 ± 8.9 years, 188 caffeine consumers) from 2001-2015. Caffeine intake was dichotomized (any vs. none). Linear mixed models, unadjusted and adjusted for age, sex, race, hypertension, genetics and time, were used to model the outcomes of height adjusted total kidney volume (htTKV) and iothalamate clearance (mGFR). Cox Proportional Hazard Models and Kaplan-Meier plots examined the effect of caffeine on time until ESRD/death, along with corresponding log-rank tests. Sensitivity analyses were conducted.
Results
Known risk factors (age, hypertension and genetics) were statistically significant in all adjusted models. While caffeine-by-time was statistically significant in unadjusted and adjusted models (p < 0.01) indicating faster growth in kidney volume using ln(htTKV) as an outcome, total kidney volume remained smaller from baseline (0 years) through 14 years (e.g., p = 0.60 for caffeine vs. none at 14 years). No differences in time to ESRD/death by caffeine were detected (p > 0.12).
Conclusion
We found that caffeine consumption in ADPKD was associated with statistically faster kidney growth. However, our models indicated kidney volume was smaller among caffeine consumers despite the increased rate of growth. This phenomenon persisted over all years modeled. No association with GFR over time was detected. Caffeine does not appear to be associated with larger kidney volumes.
Funding
- Other NIH Support