Eric Adua1, Enoch Odame Anto1, Peter Roberts1, Osei Sarfo Kantanka2, Emmanuel Aboagye3, Wei Wang1,4,5. 1. 1School of Medical and Health Sciences, Edith Cowan University, 270 Joondalup Drive, Perth, WA 6027 Australia. 2. 2Diabetes Centre, Komfo Anokye Teaching Hospital, Kumasi, Ghana. 3. 3Karolinska Institute, SE-171 77 Stockholm, Sweden. 4. 4Beijing Key Laboratory of Clinical Epidemiology, School of Public Health, Capital Medical University, Beijing, 100069 China. 5. 5School of Public Health, Taishan Medical University, Taian, 271000 Shandong China.
Abstract
BACKGROUND: On a global scale, type II diabetes mellitus (T2DM) remain a major health problem and it is the driver for chronic kidney disease (CKD). Despite this association, we still do not have sufficient biomarkers to anticipate better outcomes. N-glycosylation profiles are robust biomarkers and can be used for early monitoring of the progression of T2DM towards CKD. METHODS: In this cross-sectional study, we recruited 241 T2DM patients from January to May 2016. Demographic and anthropometric data were collected, following which fasting blood samples were collected for clinical analyses. Renal function decline was determined by estimation of glomerular filtration rate (eGFR) and N-glycosylation profiles were analysed by Ultra-performance liquid chromatography (UPLC). RESULTS: The prevalence of undiagnosed CKD was 31.53%. Compared to men, women had a statistically significantly higher HbA1c (p = 0.031), TG (p = 0.015), HDL-c (p < 0.0001), creatinine (<0.0001), urea (p < 0.028) and uric acid (p < 0.0001). T2DM patients with undiagnosed CKD had higher serum creatinine (145.75 ± 50.83 vs 88.59 ± 19.46, p < 0.0001), higher uric acid (361.10 ± 115.37 vs 294.54 ± 97.75; p < 0.0001) and higher urea (5.17 ± 2.35 vs 3.58 ± 1.19; p < 0.0001). After performing logistic regression and adjusting for age, sex and BMI, three N-glycan peaks [OR (95%CI): (GP12 (0.05(0.01-0.54), p = 0.013)); GP16 (0.61(0.43-0.87), p = 0.006)); GP22 (0.60(0.39-0.92), p = 0.018)) were associated with renal function. CONCLUSION: There was an increased prevalence of undiagnosed CKD among T2DM patients. This prevalence is the consequence of uncontrolled modifiable risk factors, which collectively may lead to end stage renal disease (ESRD). Although, the identified N-glycans could not adequately predict incident CKD, our investigation indicates the potential role of N-glycosylation in renal function and that their inclusion may improve risk stratification for CKD.
BACKGROUND: On a global scale, type II diabetes mellitus (T2DM) remain a major health problem and it is the driver for chronic kidney disease (CKD). Despite this association, we still do not have sufficient biomarkers to anticipate better outcomes. N-glycosylation profiles are robust biomarkers and can be used for early monitoring of the progression of T2DM towards CKD. METHODS: In this cross-sectional study, we recruited 241 T2DM patients from January to May 2016. Demographic and anthropometric data were collected, following which fasting blood samples were collected for clinical analyses. Renal function decline was determined by estimation of glomerular filtration rate (eGFR) and N-glycosylation profiles were analysed by Ultra-performance liquid chromatography (UPLC). RESULTS: The prevalence of undiagnosed CKD was 31.53%. Compared to men, women had a statistically significantly higher HbA1c (p = 0.031), TG (p = 0.015), HDL-c (p < 0.0001), creatinine (<0.0001), urea (p < 0.028) and uric acid (p < 0.0001). T2DM patients with undiagnosed CKD had higher serum creatinine (145.75 ± 50.83 vs 88.59 ± 19.46, p < 0.0001), higher uric acid (361.10 ± 115.37 vs 294.54 ± 97.75; p < 0.0001) and higher urea (5.17 ± 2.35 vs 3.58 ± 1.19; p < 0.0001). After performing logistic regression and adjusting for age, sex and BMI, three N-glycan peaks [OR (95%CI): (GP12 (0.05(0.01-0.54), p = 0.013)); GP16 (0.61(0.43-0.87), p = 0.006)); GP22 (0.60(0.39-0.92), p = 0.018)) were associated with renal function. CONCLUSION: There was an increased prevalence of undiagnosed CKD among T2DM patients. This prevalence is the consequence of uncontrolled modifiable risk factors, which collectively may lead to end stage renal disease (ESRD). Although, the identified N-glycans could not adequately predict incident CKD, our investigation indicates the potential role of N-glycosylation in renal function and that their inclusion may improve risk stratification for CKD.
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