RENAL ΑKLOTHO EXPRESSION IS ASSOCIATED WITH MYOCARDIAL HYPERTROPHY (EXPERIMENTAL STUDY)

Objective. The study was aimed to test a hypothesis on possible connection between αKlotho and (or) fibroblast growth factor 23 (FGF23) and myocardial hypertrophy at early stages of the renal dysfunction (RD).

Design and methods. Experimental models of chronic kidney injury were 3/4 or 5/6 nephrectomy (NE) in SHR rats. Sham-operated SHR rats were used as control. The timing of experiments was one or two months to achieve an expected fall of glomerular filtration rate (GFR) corresponding to early stages of RD. αKlotho protein in tubular epithelium was detected by immunohistochemistry. Serum concentrations of FGF23 and intact parathyroid hormone (iPTH), serum and urine levels of inorganic phosphate (Pi), Na, creatinine and protein as well as myocardial mass index (MMI) were measured.

 Results. Implemented models of RD corresponded to 1C–3C stages of human chronic kidney disease. Renal excretion of Pi significantly increased in the groups of nephrectomized animals. No significant differences were observed in serum concentrations of FGF23 and iPTH whereas the renal αKlotho expression decreases along with an increasing degree of kidney injury and MMI. The significant negative association between MMI and the renal αKlotho expression was independent of other potential confounders as confirmed by a multivariate regression analysis.

Conclusions. The obtained experimental data suggest that αKlotho can participate in mechanisms of myocardial remodeling in persistent hypertension and RD.

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