Objectives: The study was aimed to assess the early molecular and cellular features of myocardial remodeling in experimental CKD. Methods: We induced CKD by 3/4 nephrectomy (Nx) in adult male spontaneously hypertensive rats (SHR) with a 4-month follow-up. Sham Wistar rats and SHR were controls. Animals were fed standard chow (0.6% phosphate). Myocardial phosphorus (P) content was assessed by inductively coupled plasma atomic emission spectroscopy (Saint Petersburg State University, Research Park). Parameters of chronic kidney injury and myocardial remodeling, serum levels of inorganic phosphate (Pi), PTH, and FGF23 were measured. Myocardial expression of phosphate transporters PiT1, ERK1/2 (Mapk3/1), calcineurin (Ppp3ca), Tgf-beta, nestin and Lgr4 were evaluated by PCR-RT, IHC and confocal microscopy (Pavlov Institute of Physiology, Center for Collective Use). Results: Mild chronic kidney injury in Nx rats characterized with higher serum Pi and myocardial P content (Table 1). In combined SHR group Pi and P levels correlated directly with histological indices of intramyocardial arterial (IA) wall remodeling and myocardial IF. In Nx, higher cardiomyocyte diameter, myocardial interstitial and perivascular fibrosis were accompanied with upregulation in Ppp3ca (p=0.007) and Mapk1 mRNA (p=0.046), increase in phospho-ERK1/2 and PiT1 myocardium IHC-area (Table 1), nestin and Lgr4 expression in arterial wall (Figure 1b). PiT1 and pospho-ERK1/2 were co-expressed in IA media; nestin and LGR4 were expressed in IA adventitia and media, myocardial interstitium, and were co-localized occasionally (Figure 1 b). Conclusions: Mild CKD is associated with histological and molecular features of cardiomyocyte hypertrophy, myocardial fibrosis and arterial remodeling, which are probably mediated by myocardium phosphate retention involving upregulation in PiT1/MAPK, and molecules related to progenitor cells proliferation and differentiation.