Author/Editor		Avberšek-Lužnik, Ivica; Pečovnik-Balon, Breda; Adamlje, Anton; Rus, Igor; Marc, Janja
Title		Citokinski sistem OPG/RANKL/RANK pri ledvični osteodistrofiji
Translated title		OPG/RANKL/RANK cytokine system in renal osteodystrophy
Type		članek
Source		Zdrav Vestn
Vol. and No.		Letnik 76, št. 11
Publication year		2007
Volume		str. 669-75
Language		slo
Abstract		Background Renal osteodystrophy is one of the most common complications affecting patients with endstage renal disease treated with hemodialysis (HD). The action of calciotropic hormones in renal osteodystrophy is regulated by the OPG/RANKL/RANK system. Its function is modulated by interleukines, calcitriol and parathyroid hormone (PTH). The aim of our study was to confirm that this system is involved in the pathogenesis of renal osteodystrophy and supports the mechanism of PTH action on bone. Methods 106 HD patients (mean age 60 years) and 50 healthy volunteers (mean age 64 years) were enrolled in the study. In serum samples of patients and controls we determined concentrations of OPG, RANKL, tartarat resistant acid phosphatase 5b (TRAP 5b), serum Cterminal telopeptide cross-links of type I collagen (CTx), bone specific alkaline phosphatase (BALP), osteocalcin (OC) and parathyroid hormone (PTH). We compared serum measurements of HD patients and controls and assessed the correlation of OPG and RANKL with bone markers. The most frequent OPG promotor gene polymorphisms were also determined. SPSS 12.1 for Windows was used for statistical analysis. Results Median OPG concentrations were approximately three times higher in HD patients (0.804 µg/l) than in healthy volunteers (0.272 µg/l). Mean serum RANKL concentrations were 1.66- fold higher in HD patients (1.36 pmol/l) than in controls (0.82 pmol/l). Serum RANKL levels significantly differed between patients with and without calcitriol therapy (p = 0.001). After dividing HD patients into tertiles according to PTH, we observed significantly higher OPG values in the lower and RANKL in the upper tertile (p < 0.001). (Abstract truncated at 2000 characters)
Summary		Izhodišča Ledvična osteodistrofija je pogost zaplet pri bolnikih s končno ledvično odpovedjo, ki se zdravijo s hemodializo (HD). Ključni regulatorji kostnega obrata pri ledvični osteodistrofiji, kalciotropni hormoni, delujejo preko sistema OPG/RANKL/RANK. Delovanje tega sistema modulirajo interlevkini, kalcitriol in paratiroidni hormon (PTH). Namen naše raziskave je dokazati, da ima ta sistem pomembno vlogo v patogenezi ledvične osteodistrofije in predstavlja enega od mehanizmov delovanja PTH na kostno tkivo. Metode V raziskavo smo vključili 106 HD bolnikov (s povprečno starostjo 60 let) in 50 zdravih oseb (s povprečno starostjo 64 let). V serumskih vzorcih bolnikov in kontrolnih oseb smo izmerili koncentracije osteoprotegerina (OPG), liganda receptorja za aktivator jedrnega dejavnika .B (RANKL), na tartarat rezistentne kisle fosfataze 5b (TRAP 5b), prečnih povezovalcev kolagena (CTX), kostne alkalne fosfataze (BALP), osteokalcina (OC) in PTH. Primerjali smo rezultate meritev pri kontrolni skupini in bolnikih na HD. Ocenili smo povezavo med OPG in RANKL ter kazalci kostnega obrata. Analizirali smo tri najpogostejše polimorfizme v promotorski regiji OPG in ovrednotili njihov vpliv na koncentracije OPG. Za statistično analizo smo uporabili statistični program SPSS za okolje Windows. Rezultati Pri bolnikih na HD so približno 3-krat višje serumske koncentracije OPG (0,804 µg/l) kot pri zdravih osebah (0,272 µg/l), serumske koncentracije RANKL (1,36 pmol/l) pa 1,66-krat višje (0,82 pmol/l). Serumske koncentracije OPG se pri bolnikih, ki se zdravijo s kalcitriolom, ne razlikujejo značilno (p = 0,355), medtem ko so koncentracije RANKL pri bolnikih s terapijo višje (p = 0,001) kot pri tistih brez nje. Tudi pri razdelitvi bolnikov na HD v tercile PTH so značilno višje koncentracije OPG v spodnjem, RANKL pa v zgornjem tercilu (p < 0,001). (Izvleček prekinjen pri 2000 znakih)
Descriptors		KIDNEY FAILURE, CHRONIC HEMODIALYSIS RENAL OSTEODYSTROPHY CYTOKINES OSTEOBLASTS OSTEOCLASTS PARATHYROID HORMONES OSTEOCALCIN PHOSPHATES ALKALINE PHOSPHATASE POLYMORPHISM (GENETICS)