Background: Vascular calcification (VC) is highly prevalent in dialysis (HD) patients, and its mechanism is multifactorial. Most likely that systemic or local inhibitory factor is overwhelmed by promoters of VC in these patients. VC increased arterial stiffness, and left ventricular hypertrophy. Thus, the present study aimed to investigate the association of VC and myocardial remodeling and to analyze their relationship with VC promoters (fibroblast growth factor 23-FGF23, Klotho, intact parathormon-iPTH, vitamin D) in 56 prevalent HD patients (median values: age 54 yrs, HD vintage 82 months).
Methods: Besides routine laboratory analyzes, serum levels of FGF 23, soluble Klotho, iPTH, 1,25-dihydroxyvitamin D3; pulse wave velocity (PWV); left ventricular (LV) mass by ultrasound; and VCs score by Adragao method were measured.
Results: VC was found in 60% and LV concentric or eccentric hypertrophy in 50% patients. Dialysis vintage (OR 1.025, 95%CI 1.007-1.044, p=0.006) FGF23 (OR 1.006, 95% CI 0.992-1.012, p=0.029) and serum magnesium (OR 0.000, 95%CI 0.000-0.214, p=0.04) were associated with VC. Changes in myocardial geometry was associated with male sex (beta=-0.273, 95% CI -23.967 1.513, p=0.027), iPTH (beta 0.029, 95%CI -0.059-0.001, p=0.027) and vitamin D treatment (beta 25.49, 95%CI 11.325-39.667, p=0.001). Also, patients with the more widespread VC had the highest LV remodeling categories. PWV was associated patient's age, cholesterol, diastolic blood pressure, LV mass (positively) and serum calcium (negatively), indicating potential link with atherosclerotic risk.
Conclusions: Despite to different risk factors for VC and myocardial remodeling, obtained results could indicate that risk factors intertwine in long-term treatment of HD patients and therefore careful and continuous correction of mineral metabolism disorders is undoubtedly of the utmost importance.
Uvod: Kalcifikacije krvnih sudova (VC) su prisutne kod velikog broja bolesnika lečenih dijalizom (HD), a njihov nastanak je uslovljen različitim mehanizmima. Postoji mišljenje da promoteri VC prevazilaze lokalni ili sistemski uticajinhibitora VC kod ovih bolesnika. VC povećavaju krutost krvnih sudova i izazivaju hipertrofiju leve komore (LVH). Ova studija je imala za ciljeve da ispita povezanost VC i remodelinga srčanog mišića i da analizira ulogu promotera VC (fibroblast growth factor 23-FGF23, Klotho, intakt parathormon-iPTH, vitamin D) kod 56 prevalentnih HD bolesnika (medijana: starost 54 godine, HD trajanje 82 meseca).
Metode: Pored rutinskih laboratorijskih analiza, izmereni su FGF 23, Klotho, iPTH, 1,25-dihidroksi vitamin D; brzina pulsnog talasa (PWV); LVH pomoću sonografije; a skor VC je određen Adragao metodom.
Rezultati: VC su nađene kod 60% a koncentrična i ekscentrična LVH kod 50% bolesnika. Trajanje HD (OR 1,025, p=0,006), FGF23 (OR 1,006, p=0,029) i S-magnezijum (OR 0.000, p=0,04) bili su udruženi sa VC. Promene u geometriji miokarda su bile udružene sa muškim polom (beta=-0,273, p=0,027), iPTH (beta 0,029, p=0,027) i lečenjem sa vitaminom D (beta 25,49, p=0,001). Bolesnici sa većim VC skorom imali su najviše kategorije LVH. PWV je bila udružena sa starosti bolesnika, koncentracijom holesterola, dijastolnim krvnim pritiskom i LVH (pozitivno) i S-kalcijumom (negativno).
Zaključak: Iako su različiti faktori rizika za VC i promene u geometriji miokarda, dobijeni rezultati bi mogli da ukažu na međusobno preplitanje ispitanih faktora kod bolesnika lečenih hemodijalizom. Zbog toga se savetuje pažljiva i stalna korekcija poremećaja u metabolizmu minerala.
Keywords: FGF23; Klotho; hemodialysis; myocardial remodeling; vascular calcifications.