Cardiac fibrosis is prevalent in end stage renal disease (ESRD). Contraindication to late gadolinium enhancement (LGE) cardiac MRI (CMR) obstructs diagnosis, treatment selection, and potential therapeutic target identification. Currently, ventricular hypertrophy and function are used as surrogate measures of fibrosis and correlates of biomarkers. We used magnetization transfer (MT) weighted CMR to quantify fibrosis, comparing to structure, function, and blood biomarkers. We recapitulated prevalent fibrosis found previously by LGE. Results suggest hypertrophy or strains may be inappropriate fibrosis measures in ESRD. Extracellular matrix turnover markers, e.g. TIMPs, may represent more specific biomarkers of fibrosis and molecular targets for therapeutics development.