Heart function and structure during the first year of haemodialysis treatment: Cardiac Uraemic Fibrosis Detection in Dialysis Patients, an observational prospective study. (23rd February 2017)

• Record Type: Journal Article
• Authors: Rutherford, Elaine; Bell, Elizabeth; Mangion, Kenneth; Patel, Rajan K; McComb, Christie; Mark, Patrick B
• Is Part Of: Lancet. Volume 389(2017)Supplement 1
• Page Start: S86
• Publication Date: 2017-02-23
• Subjects: Medicine -- Periodicals; Medicine -- Periodicals; Medicine; Medicine; Electronic journals; Periodicals; 610.5
• DOI: 10.1016/S0140-6736(17)30482-8
• Languages: English
• ISSNs: 0140-6736

Abstract

Abstract: Background: Patients with end-stage renal disease undergoing haemodialysis are at high risk of sudden cardiac death. Advanced renal disease is associated with cardiac hypertrophy, which increases risk of life-threatening arrhythmias. Using a new MRI technique, T1 mapping, and the blood biomarker brain natriuretic peptide (BNP), we aimed to measure changes in function and structure of the heart muscle during the first year of haemodialysis treatment in the Cardiac Uraemic Fibrosis Detection in Dialysis Patients study. Methods: 28 adults with kidney disease on haemodialysis within Glasgow, UK, participated in this single-centre observational study. To be eligible for the study patients had to have been on haemodialysis for less than 1 year. Patients with MRI contraindications or who were expected to be on dialysis for less than 6 months were excluded. Primary outcome was volume of myocardial fibrosis (septal T1 time) on MRI at baseline and at 6 months' follow-up. Secondary outcome was change in serum BNP. Patients gave written consent, and ethics approval was given (13/WS/0301). This study is registered with the ISCTRN registry, number ISCTRN99591655. Findings: 22 patients completed both baseline and follow-up visits. There was no significant change in septal T1 time after 6 months of haemodialysis (septal T1 time baseline 1276·727 ms, follow-up 1271·837 ms). Left ventricular mass index (LVMI) was reduced at follow-up (baseline mean LVMI 78·3 g/m 2 [SD 18·2], follow-up 67·9 [19·0]; p<0·0001). Differences in septal T1 times correlated with difference in LVMI ( r =0·545, p=0·009). Median BNP did not significantly change between baseline and follow-up (2908 pg/mL [IQR 1639–5215] vs 2274·5 [1550–7055]). Change in LVMI was correlated with baseline BNP ( r =0·492, p=0·02). Correlation between change in BNP and difference in septal T1 time was not significant. Interpretation: 6 months of haemodialysis therapy was associated with significant improvement in left ventricular hypertrophy but no significant change in T1 mapping markers of cardiac fibrosis or BNP. This small study suggests that starting haemodialysis might be associated with changes in myocardial structure. These changes could potentially be linked to control of uraemia, blood pressure, or both, which commonly occur on starting renal replacement therapy. Funding: Kidney Research UK (Innovation Grant IN02/2013).