We hypothesised that LVH in CKD would be associated with: (1) deficiency of cardiac KLF15, increased expression of its transcriptional regulators (GATA4, MEF2), and increased expression of hypertrophic and pro-fibrotic markers (ANP, BNP and connective tissue growth factor (CTGF)); and (2) that ACE inhibition would reverse LVH and fibrosis in CKD and restore cardiac KLF15 levels and corresponding changes in transcriptional regulators and hypertrophic and pro-fibrotic markers. The gene discussed is KLF15; the disease is chronic kidney disease.