Galectin-3 has been proposed as a novel biomarker of heart failure and cardiac fibrosis, and may also be associated with fibrosis of other organs such as the kidney. To determine this, we prospectively analyzed data from 9,148 Atherosclerosis Risk in Communities (ARIC) Study participants with measured plasma galectin-3 levels (baseline, visit 4, 1996-98) and without prevalent chronic kidney disease (CKD) or heart failure. We identified 1,983 incident CKD cases through December 31, 2013 over a median follow-up of 16 years. At baseline, galectin-3 was cross-sectionally associated with estimated glomerular filtration rate and urine albumin-to-creatinine ratio; both significant. The results were adjusted for age, sex, race-center, education, physical activity, smoking status, body mass index, systolic blood pressure, anti-hypertensive medication use, history of cardiovascular disease, diabetes, fasting blood glucose, and rs4644 (a single nucleotide polymorphism of galactin-3). There was a significant, graded, and positive association between galectin-3 and incident CKD (quartile 4 vs. 1 hazard ratio: 2.22 [95% confidence interval: 1.89, 2.60]). The association was attenuated but remained significant after adjustment for estimated glomerular filtration rate, urine albumin-to-creatinine ratio, troponin T, and N-terminal pro-brain natriuretic peptide (quartile 4 vs. 1 hazard ratio: 1.75 [95% confidence interval: 1.49, 2.06]), and was stronger among those with hypertension at baseline (significant interaction). Thus, in this community-based population, higher plasma galectin-3 levels were associated with an elevated risk of developing incident CKD, particularly among those with hypertension.
|Number of pages||8|
|State||Published - Jan 2018|
Bibliographical noteFunding Information:
The Atherosclerosis Risk in Communities study is carried out as a collaborative study supported by National Heart, Lung, and Blood Institute contracts HHSN268201100005C, HHSN268201100006C, HHSN268201100007C, HHSN268201100008C, HHSN268201100009C, HHSN268201100010C, HHSN268201100011C, and HHSN268201100012C. This research was also supported by grants R01 DK089174 and R01 HL134320. Dr. Selvin is supported by a grant from the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) (K24 DK106414). Dr. Coresh is also partially supported by the Chronic Kidney Disease Biomarkers Consortium of the NIDDK (U01 DK085689). Dr. Rebholz is supported by a mentored research scientist development grant from the NIDDK (K01 DK107782).
CMB reports being a paid consultant for Abbott and has received grant support from Abbot. RCH has received grant support from Denka Seiken and is a co-investigator on a provisional patent filed by Roche for use of biomarkers in heart failure prediction. JC has received grant support from the National Kidney Foundation and is a co-investigator on a provisional patent (“Precise estimation of glomerular filtration rate from multiple biomarkers”; filed August 15, 2014). MEG has received grant support from the National Kidney Foundation and Kidney Disease: Improving Global Outcomes (KDIGO). ES has received grant support from the Foundation for the National Institutes of Health. CMR, ES, CMB, MEG, and JC have received grant support from the National Institutes of Health. All the other authors declared no competing interests.
© 2017 International Society of Nephrology
- chronic kidney disease
ASJC Scopus subject areas