Early stage chronic kidney disease: a paradigm for diffuse fibrosis and clinical progression

Background Early stage chronic kidney disease (CKD) is an under recognised, highly prevalent cardiovascular (CV) risk factor. Despite a clustering of conventional atherosclerotic risk factors, there is a disproportionate rate of sudden cardiac death, heart failure and stroke rather than myocardial infarction. It is hypothesised that non-atherosclerotic processes, including left ventricular (LV) hypertrophy and fibrosis account for most of the excess CV risk. Methods In total, 30 patients (mean age 57 +/- 8 years) with CKD stage 2-4 (mean GFR 58 ± 22 ml/min/1.73 m2) with no history of cardiovascular disease (mean BP 129 mmHg ± 13/70 mmHg ± 11) or diabetes were compared with age and gender matched controls. All subjects underwent cardiac MRI (1.5T Siemens Avanto) for assessment of LV volumes, myocardial deformation (SPAMM tagging) and aortic distensibility. Late gadolinium enhancement (LE) and T1-mapping using a modified look-locker inversion recovery sequence (MOLLI) before and 15 minutes post gadolinium (0.1 mmol/Kg) for myocardial extracellular volume (ECV) were performed. Global ECV was the average measure from basal and mid short axis slices excluding LGE indicative of infarcted myocardium. Results Global ECV was increased in CKD (0.30 ± 0.05 vs. 0.27 ± 0.03, p < 0.05) with associated reductions in long axis systolic deformation (strain 14.8% ± 2 vs. 17.1% ± 2, p < 0.05), early relaxation (SR e’ 0.50 ± 0.2 vs. 0.67 ± 0.2, p < 0.05) and MAPSE (13 mm ± 2 vs. 17 mm ± 3, p < 0.05). Aortic distensibility was reduced in CKD (Table 1).