Kiyotaka Uchiyama1, Toshio Mochizuki2,3, Yosuke Shimada4,5, Saori Nishio6, Hiroshi Kataoka2,3, Michihiro Mitobe2,3, Ken Tsuchiya7, Kazushige Hanaoka8, Yoshifumi Ubara9, Tatsuya Suwabe9, Akinari Sekine9, Kikuo Nutahara10, Kazuhiko Tsuruya11,12, Eiji Ishimura13, Shinya Nakatani14, Tadashi Sofue15, Satoshi Tanaka16, Ichiei Narita17, Shoichi Maruyama18, Shigeo Horie19,20, Satoru Muto21,22. 1. Division of Endocrinology, Metabolism and Nephrology, Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan. 2. Clinical Research Division for Polycystic Kidney Disease, Department of Nephrology, Tokyo Women's Medical University, Tokyo, Japan. 3. Department of Nephrology, Tokyo Women's Medical University, Tokyo, Japan. 4. Intelligent Systems Laboratory, SECOM CO., LTD., Mitaka, Tokyo, Japan. 5. Department of Medical Electronic Intelligence Management, Juntendo University Graduate School, Bunkyo, Tokyo, Japan. 6. Division of Rheumatology, Endocrinology and Nephrology, Hokkaido University Graduate School of Medicine, Hokkaido, Japan. 7. Department of Blood Purification, Tokyo Woman's Medical University, Tokyo, Japan. 8. Department of General Internal Medicine, Jikei University School of Medicine, Tokyo, Japan. 9. Department of Nephrology, Toranomon Hospital, Tokyo, Japan. 10. Department of Urology, Kyorin University School of Medicine, Tokyo, Japan. 11. Department of Integrated Therapy for Chronic Kidney Disease, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. 12. Department of Nephrology, Nara Medical University, Kashihara, Nara, Japan. 13. Department of Nephrology, Osaka City University Graduate School of Medicine, Osaka, Japan. 14. Department of Metabolism, Endocrinology and Molecular Medicine, Osaka City University Graduate School of Medicine, Osaka, Japan. 15. Department of Cardiorenal and Cerebrovascular Medicine, Kagawa University, Kagawa, Japan. 16. Department of Nephrology, Shizuoka General Hospital, Shizuoka, Japan. 17. Division of Clinical Nephrology and Rheumatology, Niigata University Graduate School of Medicine and Dental Science, Niigata, Japan. 18. Department of Nephrology, Nagoya University Graduate School of Medicine, Nagoya, Japan. 19. Department of Advanced Informatics for Genetic Disease, Juntendo University, Tokyo, Japan. 20. Department of Urology, Juntendo University Graduate School of Medicine, 2-1-1, Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan. 21. Department of Advanced Informatics for Genetic Disease, Juntendo University, Tokyo, Japan. s-muto@juntendo.ac.jp. 22. Department of Urology, Juntendo University Graduate School of Medicine, 2-1-1, Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan. s-muto@juntendo.ac.jp.
Abstract
BACKGROUND: Factors affecting decline in renal function and cyst growth in patients with autosomal polycystic kidney disease (ADPKD) are not fully described, particularly in Japan. METHODS: This was the first multi-facility, prospective, observational cohort study conducted in ADPKD patients at 14 centers in Japan. Patients in the J-PKD registry were assessed from December 2009 to June 2012 (follow-up until June 2017). Patients' data including estimated glomerular filtration rate (eGFR) and total kidney volume (TKV) were assessed initially and a maximum of five times annually. Contributing factors to eGFR decline and TKV growth were identified using multiple linear regression analysis. RESULTS: Of the 340 patients in the J-PKD registry, data analysis was performed for 192 patients in whom serial changes for both eGFR and TKV were obtained. eGFR slope, eGFR change, and TKV change values were as follows: - 2.7 (- 4.2 to - 1.5) (ml/min/1.73 m2/year), - 5.0 (- 9.6 to - 2.3) (%/year), and 4.78 (0.86-8.22) (%/year), respectively. Lower high-density lipoprotein (HDL) cholesterol was an independent predictor of eGFR decline, using both eGFR slope and change (P = 0.04, P = 0.02, respectively), whereas lower hemoglobin and higher uric acid were significantly associated with greater eGFR change only (P = 0.02, P = 0.002, respectively). Younger age and higher fasting blood sugar were independent predictors of greater TKV change (P = 0.01, P = 0.02, respectively). CONCLUSIONS: This real-world study in Japan identified risk factors for renal function decline in ADPKD patients. These included lower HDL cholesterol, lower hemoglobin and higher uric acid for eGFR decline, and youth and higher blood sugar levels for TKV growth.
BACKGROUND: Factors affecting decline in renal function and cyst growth in patients with autosomal polycystic kidney disease (ADPKD) are not fully described, particularly in Japan. METHODS: This was the first multi-facility, prospective, observational cohort study conducted in ADPKD patients at 14 centers in Japan. Patients in the J-PKD registry were assessed from December 2009 to June 2012 (follow-up until June 2017). Patients' data including estimated glomerular filtration rate (eGFR) and total kidney volume (TKV) were assessed initially and a maximum of five times annually. Contributing factors to eGFR decline and TKV growth were identified using multiple linear regression analysis. RESULTS: Of the 340 patients in the J-PKD registry, data analysis was performed for 192 patients in whom serial changes for both eGFR and TKV were obtained. eGFR slope, eGFR change, and TKV change values were as follows: - 2.7 (- 4.2 to - 1.5) (ml/min/1.73 m2/year), - 5.0 (- 9.6 to - 2.3) (%/year), and 4.78 (0.86-8.22) (%/year), respectively. Lower high-density lipoprotein (HDL) cholesterol was an independent predictor of eGFR decline, using both eGFR slope and change (P = 0.04, P = 0.02, respectively), whereas lower hemoglobin and higher uric acid were significantly associated with greater eGFR change only (P = 0.02, P = 0.002, respectively). Younger age and higher fasting blood sugar were independent predictors of greater TKV change (P = 0.01, P = 0.02, respectively). CONCLUSIONS: This real-world study in Japan identified risk factors for renal function decline in ADPKD patients. These included lower HDL cholesterol, lower hemoglobin and higher uric acid for eGFR decline, and youth and higher blood sugar levels for TKV growth.
Authors: Vicente E Torres; Jared J Grantham; Arlene B Chapman; Michal Mrug; Kyongtae T Bae; Bernard F King; Louis H Wetzel; Diego Martin; Mark E Lockhart; William M Bennett; Marva Moxey-Mims; Kaleab Z Abebe; Yan Lin; James E Bost Journal: Clin J Am Soc Nephrol Date: 2010-11-18 Impact factor: 8.237
Authors: Godela M Fick-Brosnahan; Mark M Belz; Kim K McFann; Ann M Johnson; Robert W Schrier Journal: Am J Kidney Dis Date: 2002-06 Impact factor: 8.860
Authors: Kristen L Nowak; Zhiying You; Berenice Gitomer; Godela Brosnahan; Vicente E Torres; Arlene B Chapman; Ronald D Perrone; Theodore I Steinman; Kaleab Z Abebe; Frederic F Rahbari-Oskoui; Alan S L Yu; Peter C Harris; Kyongtae T Bae; Marie Hogan; Dana Miskulin; Michel Chonchol Journal: J Am Soc Nephrol Date: 2017-11-08 Impact factor: 10.121
Authors: Vicente E Torres; Bernard F King; Arlene B Chapman; Marijn E Brummer; Kyongtae T Bae; James F Glockner; Kraisthith Arya; Dana Risk; Joel P Felmlee; Jared J Grantham; Lisa M Guay-Woodford; William M Bennett; Saulo Klahr; Catherine M Meyers; Xiaoling Zhang; Paul A Thompson; J Philip Miller Journal: Clin J Am Soc Nephrol Date: 2006-11-02 Impact factor: 8.237