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Serum Calcification Propensity Is a Strong and Independent Determinant of Cardiac and All‐Cause Mortality in Kidney Transplant Recipients
Author(s) -
Dahle D. O.,
Åsberg A.,
Hartmann A.,
Holdaas H.,
Bachtler M.,
Jenssen T. G.,
Dionisi M.,
Pasch A.
Publication year - 2016
Publication title -
american journal of transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.89
H-Index - 188
eISSN - 1600-6143
pISSN - 1600-6135
DOI - 10.1111/ajt.13443
Subject(s) - medicine , hazard ratio , cardiology , proportional hazards model , calcification , kidney disease , immunosuppression , confidence interval , kidney transplantation , quartile , transplantation
Calcification of the vasculature is associated with cardiovascular disease and death in kidney transplant recipients. A novel functional blood test measures calcification propensity by quantifying the transformation time (T 50 ) from primary to secondary calciprotein particles. Accelerated T 50 indicates a diminished ability of serum to resist calcification. We measured T 50 in 1435 patients 10 weeks after kidney transplantation during 2000–2003 (first era) and 2009–2012 (second era). Aortic pulse wave velocity (APWV) was measured at week 10 and after 1 year in 589 patients from the second era. Accelerated T 50 was associated with diabetes, deceased donor, first transplant, rejection, stronger immunosuppression, first era, higher serum phosphate and lower albumin. T 50 was not associated with progression of APWV. During a median follow‐up of 5.1 years, 283 patients died, 70 from myocardial infarction, cardiac failure or sudden death. In Cox regression models, accelerated T 50 was strongly and independently associated with both all‐cause and cardiac mortality, low versus high T 50 quartile: hazard ratio 1.60 (95% confidence interval [CI] 1.00–2.57), p trend = 0.03, and 3.60 (95% CI 1.10–11.83), p trend = 0.02, respectively. In conclusion, calcification propensity (T 50 ) was strongly associated with all‐cause and cardiac mortality of kidney transplant recipients, potentially via a cardiac nonAPWV‐related pathway. Whether therapeutic improvement of T 50 improves outcome awaits clarification in a randomized trial.