著者

Mohammad Al Mamun Nahid Rumana Kumkum Pervin Muhammad Chanchal Azad Nahid Shahana Sohel Reza Choudhury M Mostafa Zaman Tanvir Chowdhury Turin

出版者

一般社団法人 日本動脈硬化学会

雑誌

Journal of Atherosclerosis and Thrombosis (ISSN:13403478)

巻号頁・発行日

pp.30445, (Released:2015-12-18)

参考文献数

46

被引用文献数

8

---

As a result of an epidemiological transition from communicable to non-communicable diseases for last few decades, cardiovascular diseases (CVD) are being considered as an important cause of mortality and morbidity in many developing countries including Bangladesh. Performing an extensive literature search, we compiled, summarized, and categorized the existing information about CVD mortality and morbidity among different clusters of Bangladeshi population. The present review reports that the burden of CVD in terms of mortality and morbidity is on the rise in Bangladesh. Despite a few non-communicable disease prevention and control programs currently running in Bangladesh, there is an urgent need for well-coordinated national intervention strategies and public health actions to minimize the CVD burden in Bangladesh. As the main challenge for CVD control in a developing country is unavailability of adequate epidemiological data related to various CVD events, the present review attempted to accumulate such data in the current context of Bangladesh. This may be of interest to all stakeholder groups working for CVD prevention and control across the country and globe.

著者

Ryosuke Fujii Asahi Hishida Takeshi Nishiyama Masahiro Nakatochi Keitaro Matsuo Hidemi Ito Yuichiro Nishida Chisato Shimanoe Yasuyuki Nakamura Tanvir Chowdhury Turin Sadao Suzuki Miki Watanabe Rie Ibusuki Toshiro Takezaki Haruo Mikami Yohko Nakamura Hiroaki Ikezaki Masayuki Murata Kiyonori Kuriki Nagato Kuriyama Daisuke Matsui Kokichi Arisawa Sakurako Katsuura-Kamano Mineko Tsukamoto Takashi Tamura Yoko Kubo Takaaki Kondo Yukihide Momozawa Michiaki Kubo Kenji Takeuchi Kenji Wakai

出版者

Japan Epidemiological Association

雑誌

Journal of Epidemiology (ISSN:09175040)

巻号頁・発行日

vol.32, no.11, pp.483-488, 2022-11-05 (Released:2022-11-05)

参考文献数

38

---

Background: Inflammation is thought to be a risk factor for kidney disease. However, whether inflammatory status is either a cause or an outcome of chronic kidney disease remains controversial. We aimed to investigate the causal relationship between high-sensitivity C-reactive protein (hs-CRP) and estimated glomerular filtration rate (eGFR) using Mendelian randomization (MR) approaches.Methods: A total of 10,521 participants of the Japan Multi-institutional Collaborative Cohort Study was analyzed in this study. We used two-sample MR approaches (the inverse-variance weighted (IVW), the weighted median (WM), and the MR-Egger method) to estimate the effect of genetically determined hs-CRP on kidney function. We selected four and three hs-CRP associated single nucleotide polymorphisms (SNPs) as two instrumental variables (IV): IVCRP and IVAsian, based on SNPs previously identified in European and Asian populations. IVCRP and IVAsian explained 3.4% and 3.9% of the variation in hs-CRP, respectively.Results: Using the IVCRP, genetically determined hs-CRP was not significantly associated with eGFR in the IVW and the WM methods (estimate per 1 unit increase in ln(hs-CRP), 0.000; 95% confidence interval [CI], −0.019 to 0.020 and −0.003; 95% CI, −0.019 to 0.014, respectively). For IVAsian, we found similar results using the IVW and the WM methods (estimate, 0.005; 95% CI, −0.020 to 0.010 and −0.004; 95% CI, −0.020 to 0.012, respectively). The MR-Egger method also showed no causal relationships between hs-CRP and eGFR (IVCRP: −0.008; 95% CI, −0.058 to 0.042; IVAsian: 0.001; 95% CI, −0.036 to 0.036).Conclusion: Our two-sample MR analyses with different IVs did not support a causal effect of hs-CRP on eGFR.

著者

Ryosuke Fujii Asahi Hishida Takeshi Nishiyama Masahiro Nakatochi Keitaro Matsuo Hidemi Ito Yuichiro Nishida Chisato Shimanoe Yasuyuki Nakamura Tanvir Chowdhury Turin Sadao Suzuki Miki Watanabe Rie Ibusuki Toshiro Takezaki Haruo Mikami Yohko Nakamura Hiroaki Ikezaki Masayuki Murata Kiyonori Kuriki Nagato Kuriyama Daisuke Matsui Kokichi Arisawa Sakurako Katsuura-Kamano Mineko Tsukamoto Takashi Tamura Yoko Kubo Takaaki Kondo Yukihide Momozawa Michiaki Kubo Kenji Takeuchi Kenji Wakai

出版者

Japan Epidemiological Association

雑誌

Journal of Epidemiology (ISSN:09175040)

巻号頁・発行日

pp.JE20200540, (Released:2021-02-20)

参考文献数

38

---

Background: Inflammation is thought to be a risk factor for kidney disease. However, discussion is controversial whether inflammatory status is either a cause or an outcome of chronic kidney disease. We aimed to investigate the causal relationship between high-sensitivity C-reactive protein (hs-CRP) and estimated glomerular filtration rate (eGFR) using mendelian randomization (MR) approaches.Methods: A total of 10,521 participants of the Japan Multi-institutional Collaborative Cohort Study was analyzed in this study. We used two-sample MR approaches (the inverse-variance weighted (IVW), the weighted median (WM), and the MR-Egger method) to estimate the effect of genetically determined hs-CRP on kidney function. We selected four and three hs-CRP associated single nucleotide polymorphisms (SNPs) as two instrumental variables (IV): IVCRP and IVAsian, based on SNPs previously identified in European and Asian populations. IVCRP and IVAsian explained 3.4% and 3.9% of the variation in hs-CRP, respectively.Results: Using the IVCRP, genetically determined hs-CRP was not significantly associated with eGFR in the IVW and the WM methods (estimate per 1 unit increase in ln(hs-CRP), 95%CI: 0.000, –0.019 to 0.020 and –0.003, –0.019 to 0.014). For IVAsian, we found similar results using the IVW and the WM methods (estimate, 95% CI: –0.005, –0.020 to 0.010 and –0.004, –0.020 to 0.012). The MR-Egger method also showed no causal relationships between hs-CRP and eGFR (IVCRP: –0.008, –0.058 to 0.042; IVAsian: 0.001, –0.036 to 0.036).Conclusions: Our two-sample MR analyses with different IVs did not support a causal effect of hs-CRP on eGFR.