Dahle, Dag Olav

Dionisi, Mauro

Hartmann, Anders

Holdaas, Hallvard

Jenssen, Trond Geir

Pasch, Andreas

Åsberg, Anders

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RENALTRANSPLANTATION. CLINICAL - 1FP830 CLINICAL CORRELATES OF SERUMCALCIFICATIONPROPENSITY IN KIDNEY TRANSPLANT RECIPIENTSDag Olav Dahle1,2, Andreas Pasch3, Anders Hartmann1,2, Hallvard Holdaas1,Trond Geir Jenssen1,4, Mauro Dionisi5 and Anders Åsberg1,61Oslo University Hospital, Department of Transplant Medicine, Oslo, Norway,2University of Oslo, Medical Faculty, Oslo, Norway, 3University Hospital Bern,Department of Clinical Chemistry, Bern, Switzerland, 4UiT The Arctic University ofNorway, Metabolic and Renal Research Group, Tromsø, Norway, 5Calcisco SA,Bern, Bern, Switzerland, 6University of Oslo, School of Pharmacy, Oslo, NorwayIntroduction and Aims: Kidney transplant recipients (KTRs) are at increased risk ofcardiovascular disease compared with the general population. In CKD, acceleratedvascular calcification contributes to arterial stiffness and mortality. A blood test forcalcification propensity was recently developed by measuring the maturation time(T50) of calciprotein particles in serum, with a lower T50 corresponding to a highercalcification propensity. The clinical correlates of T50 in KTRs are not known.Methods:We measured T50 in biobanked blood obtained 10 weeks aftertransplantation during two eras, 2000-2003 and 2009-2012. The cross-sectional clinicalcorrelates of T50 were assessed in a linear regression model with stepwise entry andbackward selection of covariates, excluding patients with missing values (1%).Results: Of 1886 eligible adult kidney or kidney-pancreas recipients during the twoeras, 1435 (76%) had T50 measured. Hospital staff shortage excluded 161 patients and290 were transferred to other hospitals before the investigation in week 10.The cohortwas primarily Caucasian with mean age 52 ± 14 years, eGFR 57 ± 19 ml/min/1.73m2,male 66%, diabetes 29.1% including 9.3% post-transplant diabetes, simultaneouspancreas transplant 6%, rejection 23%, cytomegalovirus (CMV) infection 39% and T50196 ± 72 minutes.T50 was lower in the former era (beta -26 [95% CI -32 to -20],p<0.001), diabetes (-14 [-21 to 8], p<0.001), recipients of deceased donor kidney(18 [-24 to -11], p<0.001), recipients of a first kidney (-13 [-22 to -4], p=0.01), afterrejection (-12 [-21 to -3], p=0.01), with higher dosed calcineurin inhibitors (highestquartile trough levels [tac >8.5 or csa >220 ng/mL]; -9 [-16 to -2], p=0.02) and higherprednisolone dose (≥12.5 mg; -34 [-42 to -25], p<0.001), CMV infection (-8 [-15 to -2],p=0.01) and higher phosphate (per 0.20 mmol/L; 36 [-39 to -33], p<0.001). This modelexplained 40% of the variance in T50. An association between eGFR and T50 was lostafter adjustment for phosphate, suggesting phosphate is an intermediate variable. Othervariables not independently associated with T50 included recipient age and gender,known cardiovascular disease, smoking, delayed graft function, thymoglobulininduction, diuretics, ionized calcium and log-transformed PTH.Conclusions: The clinical correlates of serum calcification propensity T50 includedmeasures of kidney graft quality and function, intensity of immunosuppression, serumphosphate and inflammatory states such as rejection and CMV infection.© The Author 2015. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.Nephrology Dialysis Transplantation 30 (Supplement 3): iii348–iii376, 2015doi:10.1093/ndt/gfv185.19

FP830CLINICAL CORRELATES OF SERUM CALCIFICATION PROPENSITY IN KIDNEY TRANSPLANT RECIPIENTS

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FP830CLINICAL CORRELATES OF SERUM CALCIFICATION PROPENSITY IN KIDNEY TRANSPLANT RECIPIENTS

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