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Evidence of enhanced systemic inflammation in stable kidney transplant recipients with low Framingham risk scores
Author(s) -
Mansell Holly,
Rosaasen Nicola,
Dean Jonathan,
Shoker Ahmed
Publication year - 2013
Publication title -
clinical transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 76
eISSN - 1399-0012
pISSN - 0902-0063
DOI - 10.1111/ctr.12159
Subject(s) - medicine , inflammation , cohort , framingham heart study , framingham risk score , population , chemokine , cardiology , gastroenterology , disease , environmental health
Background While the Framingham risk score ( FRS ) predicts cardiovascular risk in the general population, it underestimates cardiovascular events in renal transplant recipients ( RTR ). Inflammation is common in RTR , and it is also a hallmark of vascular injury contributing to cardiovascular events. Objective To explore the relationship between inflammatory chemokines ( CCL family) and FRS in a stable RTR . Methods The modified FRS (2009) was used to calculate the 10‐yr probability of CVE in 150 RTR . A cross‐sectional study measured plasma levels of 14 CCL s by Luminex technique in 53% (79/150) of the cohort and 28 controls. Results 43.3% of RTR was classified as low, 16% moderate, and 40.7% high FRS . FRS correlated with eGFR and all CCLs with R of <0.2(p = n.s). Compared with controls, CCL 1,4,8,15, and 27 were equally increased in both the high and low FRS groups (p < 0.04 and 0.03, respectively). The percentage of patients with low FRS and CCL 8,15, and 27 values above the 95% cutoff control levels was 46.1%, 76.9%, and 53.8%, respectively. Conclusions Over one half of stable RTR , including those with low FRS , have increased inflammatory chemokine levels. Inflammation is not accounted for in the FRS , and this may explain the poor performance of FRS in transplant patients.