TY - JOUR
T1 - Impact of Angiotensin Blockade on Development of Chronic Lung Allograft Dysfunction
AU - January, Spenser E.
AU - Hubbard, Julie
AU - Fester, Keith A.
AU - Dubrawka, Casey A.
AU - Vazquez Guillamet, Rodrigo
AU - Kulkarni, Hrishikesh S.
AU - Hachem, Ramsey R.
N1 - Publisher Copyright:
© The Author(s) 2023.
PY - 2023
Y1 - 2023
N2 - Background: The renin-angiotensin-aldosterone system (RAAS) is responsible for a multitude of physiological functions, including immunological effects such as promotion of TGF-β and upregulation of IL-6 and IL-8 which are also implicated in the development of chronic lung allograft dysfunction (CLAD). Blockade of the RAAS pathway in pre-clinical models has demonstrated a decrease in these cytokines and pulmonary neutrophil recruitment. Objective: This study sought to evaluate whether use of RAAS inhibitor (RAASi) in lung transplant recipients impacted CLAD-free survival. Methods: In this retrospective, single-center study, 35 lung transplant recipients who received a RAASi post-transplant were compared to 70 lung transplant recipients not exposed to a RAASi and were followed for up to 5 years post-transplant. Results: The incidence of CLAD did not differ based on RAASi treatment (34.3% in RAASi vs 38.6%, P-value.668). This was confirmed with a multivariable Cox proportional hazards model with RAASi initiation as a time-varying covariate (RAASi hazard ratio of 1.01, P-value.986). Incidence of hyperkalemia and acute kidney injury were low in the RAASi group. Conclusions: This study demonstrated no association between post-transplant RAASi use and decreased risk of CLAD development. RAASi were also well tolerated in this patient population.
AB - Background: The renin-angiotensin-aldosterone system (RAAS) is responsible for a multitude of physiological functions, including immunological effects such as promotion of TGF-β and upregulation of IL-6 and IL-8 which are also implicated in the development of chronic lung allograft dysfunction (CLAD). Blockade of the RAAS pathway in pre-clinical models has demonstrated a decrease in these cytokines and pulmonary neutrophil recruitment. Objective: This study sought to evaluate whether use of RAAS inhibitor (RAASi) in lung transplant recipients impacted CLAD-free survival. Methods: In this retrospective, single-center study, 35 lung transplant recipients who received a RAASi post-transplant were compared to 70 lung transplant recipients not exposed to a RAASi and were followed for up to 5 years post-transplant. Results: The incidence of CLAD did not differ based on RAASi treatment (34.3% in RAASi vs 38.6%, P-value.668). This was confirmed with a multivariable Cox proportional hazards model with RAASi initiation as a time-varying covariate (RAASi hazard ratio of 1.01, P-value.986). Incidence of hyperkalemia and acute kidney injury were low in the RAASi group. Conclusions: This study demonstrated no association between post-transplant RAASi use and decreased risk of CLAD development. RAASi were also well tolerated in this patient population.
KW - lung transplantation
KW - renin angiotensin aldosterone system
KW - transplant rejection
UR - http://www.scopus.com/inward/record.url?scp=85176141150&partnerID=8YFLogxK
U2 - 10.1177/08971900231213699
DO - 10.1177/08971900231213699
M3 - Article
C2 - 37923307
AN - SCOPUS:85176141150
SN - 0897-1900
JO - Journal of Pharmacy Practice
JF - Journal of Pharmacy Practice
ER -