Evaluation of the Chronic Kidney Disease Epidemiology Collaboration equation for estimating glomerular filtration rate in the Chinese population

Kong, Xianglei; Ma, Yingchun; Chen, Jianghua; Luo, Qian; Yu, Xueqing; Liu, Ying; Xu, Jinyi; Huang, Songmin; Wang, Lining; Huang, Wen; Wang, Mei; Xu, Guobin; Zhang, Luxia; Zuo, Li; Wang, Haiyan

doi:10.1093/ndt/gfs491

Cited by 161 publications

(134 citation statements)

References 24 publications

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“…Our study is also one of the first to relate varying lipid parameters to kidney disease using the novel CKD-EPI equation, which is as accurate as the MDRD Study equation at GFR<60 ml/min/1.73 m 2 but is more accurate at higher GFRs [17]. Moreover, a recent multicenter study of 977 Chinese participants, including healthy adults and CKD patients, indicated that the CKD-EPI equation performed better than the MDRD Study equation, with less bias, improved precision and greater accuracy [27]. The prevalence of CKD in our study was 3.7%, and our previous study indicated the prevalence of CKD was 9.0% in hypertensive subjects [28], which is lower than that in participants from Beijing [29], partly because of the younger age and better socioeconomic status of our present patient cohort.…”

Section: Discussionmentioning

confidence: 99%

Association of the TG/HDL-C and Non-HDL-C/HDL-C Ratios with Chronic Kidney Disease in an Adult Chinese Population

Wen

Chen

Huang

et al. 2017

Kidney Blood Press Res

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Background/Aims: Evidence indicates a role for dyslipidemia in the development of chronic kidney disease (CKD). However, the association of lipid abnormalities and their ratios with kidney disease using the new CKD Epidemiology Collaboration (CKD-EPI) equation is not well understood. Methods: This cross-sectional study included 48,054 adult subjects. CKD was defined as an estimated glomerular filtration rate <60 ml/min/1.73 m² or dipstick-positive proteinuria. Logistic regression models were used to examine the relationship between lipid variables and CKD. Results: The prevalence of CKD in this study was 3.7%. When the participants exhibited higher serum triglyceride (TG), a higher TG/high-density lipoprotein cholesterol (TG/HDL-c) ratio or a higher non-HDL-c/HDL-c ratio or HDL-c in a lower quartile, the prevalence of CKD tended to be higher. The multivariate adjusted odds ratios for CKD per 1 standard deviation increase in lipid level were 1.17 (1.10-1.23) for TG, 0.86 (0.79-0.93) for HDL-c, 1.21 (1.13-1.31) for the TG/HDL-c ratio, and 1.14 (1.06-1.22) for the non-HDL-c/HDL-c ratio. No significant association was detected between CKD and total cholesterol (TC), non-HDL-c or the low-density lipoprotein cholesterol/HDL-c (LDL-c/HDL-c) ratio. Conclusion: In this relatively healthy adult Chinese population, the CKD-EPI equation determined that the TG/HDL-c and non-HDL-c/HDL-c ratios as well as TG and HDL-c correlate with the prevalence of CKD.

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Section: Discussionmentioning

confidence: 99%

Association of the TG/HDL-C and Non-HDL-C/HDL-C Ratios with Chronic Kidney Disease in an Adult Chinese Population

Wen

Chen

Huang

et al. 2017

Kidney Blood Press Res

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“…AKI was defined and staged according to the Kidney Disease: Improving Global Outcomes criteria (24). Estimated glomerular filtration rate (eGFR) was calculated by the Chronic Kidney Disease Epidemiology Collaboration equation and is expressed as milliliters per minute per 1.73 m 2 (25). Patients were scheduled for monthly follow-ups for 6 mo and then every 3 mo until at least 1 y after renal biopsy.…”

Section: Patientsmentioning

confidence: 99%

HLA-DQA1, -DQB1, and -DRB1 Alleles Associated with Acute Tubulointerstitial Nephritis in a Chinese Population: A Single-Center Cohort Study

Jia

et al. 2018

The Journal of Immunology

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Acute tubulointerstitial nephritis (ATIN) is a common cause of acute kidney injury with various origins. HLA-DQA1, -DQB1, and -DRB1 have been associated with development of tubulointerstitial nephritis and uveitis (TINU) syndrome in case reports and small case series, but information about HLA genetic susceptibility to drug hypersensitivity–related ATIN (D-ATIN) or other types of ATIN is limited. In this article, we genotyped 154 patients with ATIN of different causes and 200 healthy controls at HLA-DQA1, -DQB1, and -DRB1 loci. We found that there was no difference between patients with D-ATIN and TINU in the carrier’s frequency of HLA-DQA1, -DQB1, or -DRB1. Patients with Sjogren’s syndrome–ATIN and IgG4-related ATIN presented a different pattern of tested HLA alleles. HLA-DQA1*0104 (p value corrected by false discovery rate method [Pc] = 4.72 × 10−22, odds ratio [OR] = 13.81), -DQB1*0503 (Pc = 1.95 × 10−14, OR = 9.51), and -DRB1*1405 (Pc = 8.06 × 10−19, OR = 12.80) were significant risk alleles for the occurrence of D-ATIN and TINU. There were no significant associations between tested HLA alleles and ATIN induced by other causes. Patients with D-ATIN/TINU carrying HLA-DQA1*0104/DQB1*0503/DRB1*1405 had higher peak serum creatinine and more severe renal tubulointerstitial inflammatory impairment. They also had significantly higher levels of tubular HLA-DR and HLA-DQ expression, which were correlated with the numbers of interstitial CD4+ T lymphocytes (r = 0.975, p < 0.001 and r = 0.832, p = 0.005, respectively) and monocytes/macrophages (r = 0.721, p = 0.004 and r = 0.615, p = 0.02, respectively). In conclusion, patients with D-ATIN or TINU have genetic susceptibility in HLA-DQA1, -DQB1, and -DRB1 alleles. HLA-DQA1*0104/DQB1*0503/DRB1*1405 serves as a significant risk haplotype for development of D-ATIN and TINU, which might facilitate renal tubulointerstitial inflammation by enhancing Ag-presenting capacity of renal tubular cells.

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“…Definition of CKD Serum creatinine (Scr) was measured by Jaffe's kinetic method and was standardized at the central laboratory to a national reference. Estimated glomerular filtration rate (eGFR) was calculated using the following estimating equation, which was developed by modifying the Modification of Diet in Renal Disease equation based on the data from Chinese CKD patients: eGFR (mL/min/1.73 m 2 ) = 175 × Scr (mg/dL) -1.234 × age (year) -0.179 (female × 0.79) [17,18]. Reduced renal function was defined as an eGFR < 60 mL/min/1.73 m 2 .…”

Section: Methodsmentioning

confidence: 99%

Fetuin-B Links Nonalcoholic Fatty Liver Disease to Chronic Kidney Disease in Obese Chinese Adults: A Cross-Sectional Study

Lin

Liu

et al. 2019

Ann Nutr Metab

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Background: There is no evidence available on the association of Fetuin-B with chronic kidney disease (CKD), and mechanisms linking nonalcoholic fatty liver disease (NAFLD) to CKD are not fully understood. We aimed to explore the independent associations and potential mechanisms of Fetuin-B and NAFLD with CKD. Methods: A cross-sectional study of 1,072 Chinese adults who underwent serum Fetuin-B test and hepatic ultrasonography scanning was conducted in Xiamen, China. CKD was defined as estimated glomerular filtration rate < 60 mL/min/1.73 m² and/or the presence of albuminuria. Results: Subjects with CKD showed significantly higher prevalence of NAFLD (69.5 vs. 57.2%, p < 0.001) and serum Fetuin-B levels (4.32 ± 1.45 vs. 4.05 ± 1.36 µg/mL, p = 0.007) than their controls. Increased serum Fetuin-B was also significantly associated with increased levels of fasting insulin and homeostasis model assessment – insulin resistance (both p values < 0.05). NAFLD and higher serum Fetuin-B were significantly associated with increased risk of CKD, and the unadjusted ORs (95% CIs) were 1.701 (1.256–2.303, p = 0.001) and 1.213 (1.053–1.399, p = 0.008, per SD increase of Fetuin-B), respectively. With adjustment for potential confounding factors, including metabolic/insulin resistance syndrome, NAFLD but not serum Fetuin-B was still significantly associated with increased risk of CKD, and the adjusted ORs (95% CIs) were 1.820 (1.327–2.496, p < 0.001) and 1.116 (0.959–1.298, p = 0.153, per SD increase of Fetuin-B), respectively. Conclusions: Fetuin-B might link NAFLD to CKD via inducing insulin resistance, and NAFLD contributes independently to the pathogenesis of CKD via multiple mechanisms besides of metabolic/insulin resistance syndrome.

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Evaluation of the Chronic Kidney Disease Epidemiology Collaboration equation for estimating glomerular filtration rate in the Chinese population

Abstract: The CKD-EPI two-level race equation and the Chinese equation performed similarly in the Chinese population, and both performed better than the MDRD Study equation and the CKD-EPI four-level race equation.

Cited by 161 publications

References 24 publications

Association of the TG/HDL-C and Non-HDL-C/HDL-C Ratios with Chronic Kidney Disease in an Adult Chinese Population

Association of the TG/HDL-C and Non-HDL-C/HDL-C Ratios with Chronic Kidney Disease in an Adult Chinese Population

HLA-DQA1, -DQB1, and -DRB1 Alleles Associated with Acute Tubulointerstitial Nephritis in a Chinese Population: A Single-Center Cohort Study

Fetuin-B Links Nonalcoholic Fatty Liver Disease to Chronic Kidney Disease in Obese Chinese Adults: A Cross-Sectional Study

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