The effect of immunosuppressive treatment on arterial stiffness and matrix Gla protein levels in renal transplant recipients

Güngör, Özlem; Kırçelli, Fatih; Carrero, Juan Jesús; Hür, Ender; Demirci, Meltem Seziş; Aşçı, Gülay; Töz, Hüseyin

doi:10.5414/cnp75491

Cited by 13 publications

(10 citation statements)

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“…In addition, matrix metalloproteinase 2 and 9, fetuin A and matrix gla protein levels have been linked to AS [15][16][17] . In this study, we confirmed our previous finding of proteinuria as a predictor of AS along with age, blood pressure and creatinine clearance 18) . In addition, we found PON1 as a novel predictor of AS in this patient populations.…”

Section: Discussionsupporting

confidence: 81%

Serum Paraoxonase 1 Activity Predicts Arterial Stiffness in Renal Transplant Recipients

Güngör

Kırçelli

Demirci

et al. 2011

JAT

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Aim: Paraoxanase 1 (PON 1) has been shown to protect against atherosclerosis by modifying lipoproteins. Its activity decreases in dialysis patients but is restored after transplantation. Whether it affects arterial stiffness is unclear. In this study we aimed to investigate the effects of PON 1 on arterial stiffness in renal transplant patients. Methods: Seventy renal transplant recipients were enrolled. Arterial stiffness was measured using a Syphmocor device. PON-1 activity was assessed from the rate of enzymatic hydrolysis of paraoxon to p-nitrophenol.

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Section: Discussionsupporting

confidence: 81%

Serum Paraoxonase 1 Activity Predicts Arterial Stiffness in Renal Transplant Recipients

Güngör

Kırçelli

Demirci

et al. 2011

JAT

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“…On the other hand, in our multivariate analysis of determinants of vitamin K status, none of the immunosuppressive drugs remained in the model after co-adjustment for creatinine clearance, suggesting that the differences in vitamin K status can be explained by differences in creatinine clearance. A recent report suggested that MGP levels were higher in patients on mTOR inhibitors [34]; unfortunately our cohort contained only two patients using this class of drugs.…”

Section: Discussionmentioning

confidence: 96%

Vitamin K Intake and Plasma Desphospho-Uncarboxylated Matrix Gla-Protein Levels in Kidney Transplant Recipients

et al. 2012

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Vitamin K is essential for activation of γ-carboxyglutamate (Gla)-proteins including the vascular calcification inhibitor matrix Gla-protein (MGP). Insufficient vitamin K intake leads to production of uncarboxylated, mostly inactive proteins and contributes to an increased cardiovascular risk. In kidney transplant recipients, cardiovascular risk is high but vitamin K intake and status have not been defined. We investigated dietary vitamin K intake, vascular vitamin K status and its determinants in kidney transplant recipients. We estimated vitamin K intake in a cohort of kidney transplant recipients (n = 60) with stable renal function (creatinine clearance 61 [42–77] (median [interquartile range]) ml/min), who were 75 [35–188] months after transplantation, using three-day food records and food frequency questionnaires. Vascular vitamin K status was assessed by measuring plasma desphospho-uncarboxylated MGP (dp-ucMGP). Total vitamin K intake was below the recommended level in 50% of patients. Lower vitamin K intake was associated with less consumption of green vegetables (33 vs 40 g/d, p = 0.06) and increased dp-ucMGP levels (621 vs 852 pmol/L, p<0.05). Accordingly, dp-ucMGP levels were elevated (>500 pmol/L) in 80% of patients. Multivariate regression identified creatinine clearance, coumarin use, body mass index, high sensitivity-CRP and sodium excretion as independent determinants of dp-ucMGP levels. In a considerable part of the kidney transplant population, vitamin K intake is too low for maximal carboxylation of vascular MGP. The high dp-ucMGP levels may result in an increased risk for arterial calcification. Whether increasing vitamin K intake may have health benefits for kidney transplant recipients should be addressed by future studies.

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“…In a recent study performed on renal transplant recipients, where arterial stiffness was measured with SphygmoCor, serum MGP level was not found to be predictor of carotid-femoral PWV [80] .…”

Section: Matrix Gla Proteinmentioning

confidence: 99%

Arterial stiffness, vascular calcification and bone metabolism in chronic kidney disease

Nemcsik

Kiss²,

Tislér³

2012

WJN

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Patients with chronic kidney disease (CKD) have an extremely poor cardiovascular outcome. Arterial stiffness, a strong independent predictor of survival in CKD, is connected to arterial media calcification. A huge number of different factors contribute to the increased arterial calcification and stiffening in CKD, a process which is in parallel with impaired bone metabolism. This coincidence was demonstrated to be part of the direct inhibition of calcification in the vessels, which is a counterbalancing effect but also leads to low bone turnover. Due to the growing evidence, the definition of "CKD mineral bone disorder" was created recently, underlining the strong connection of the two phenomena. In this review, we aim to demonstrate the mechanisms leading to increased arterial stiffness and the up-to date data of the bone-vascular axis in CKD. We overview a list of the different factors, including inhibitors of bone metabolism like osteoprotegerin, fetuin-A, pyrophosphates, matrix Gla protein, osteopontin, fibroblast growth factor 23 and bone morphogenic protein, which seem to play role in the progression of vascular calcification and we evaluate their connection to impaired arterial stiffness in the mirror of recent scientific results.

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The effect of immunosuppressive treatment on arterial stiffness and matrix Gla protein levels in renal transplant recipients

Cited by 13 publications

References 0 publications

Serum Paraoxonase 1 Activity Predicts Arterial Stiffness in Renal Transplant Recipients

Serum Paraoxonase 1 Activity Predicts Arterial Stiffness in Renal Transplant Recipients

Vitamin K Intake and Plasma Desphospho-Uncarboxylated Matrix Gla-Protein Levels in Kidney Transplant Recipients

Arterial stiffness, vascular calcification and bone metabolism in chronic kidney disease

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