Diffuse Myocardial Interstitial Fibrosis and Dysfunction in Early Chronic Kidney Disease

Patients with chronic kidney disease (CKD) have a disproportionately high risk of cardiovascular (CV) morbidity and mortality from the very early stages of CKD. This excess risk is believed to be the result of myocardial disease commonly termed uremic cardiomyopathy (UC). It has been suggested that interstitial myocardial fibrosis progresses with advancing kidney disease and may be the key mediator of UC. This longitudinal study reports data on the myocardial structure and function of 30 patients with CKD with no known cardiovascular disease and healthy controls. All patients underwent cardiac magnetic resonance imaging including T1 mapping and late gadolinium enhancement (if eGFR >30ml/min/1,73m2). Over a mean follow up period of 2.7 ± 0.8 years, there was no change in left ventricular (LV) mass, volumes, ejection fraction, native myocardial T1 times or extracellular volume with CKD or in healthy controls. Global longitudinal strain (GLS 20.6 ± 2.9 vs 19.8 ± 2.9 s-1, p = 0.03) and mitral annular planar systolic excursion (MASPE 13 ± 2 vs 12 ± 2 mm, p = 0.009) decreased in CKD but were clinically insignificant. Mid-wall late gadolinium enhancement (LGE) was present in 4 patients at baseline and was unchanged at follow up. Renal function was stable in this cohort over follow up (change in eGFR was minus 3ml/min/1.73m2) with no adverse clinical CV events. In conclusion, this study demonstrates that in a cohort of patients with stable CKD, LV mass, native T1 times and ECV do not increase over a period of 2.7 years.