TY - JOUR
T1 - Discontinuation of RAAS inhibition in children with advanced
AU - Van Den Belt, Sophie M.
AU - Heerspink, Hiddo J.L.
AU - Kirchner, Marietta
AU - Gracchi, Valentina
AU - Thurn-Valsassina, v.
AU - Bayazit, Aysun K.
AU - Niemirska, Anna
AU - Canpolat, Nur
AU - Bulut, Ipek Kaplan
AU - Azukaitis, Karolis
AU - Duzova, Ali
AU - Bacchetta, Justine
AU - Shroff, Rukshana
AU - Paripovic, Dusan
AU - Özçakar, Zeynep Birsin
AU - Fidan, Kibriya
AU - Erdogan, Hakan
AU - Gellermann, Jutta
AU - Wühl, Elke
AU - De Zeeuw, Dick
AU - Melk, Anette
AU - Querfeld, Uwe
AU - Schaefer, Franz
N1 - Publisher Copyright:
© 2020 by the American Society of Nephrology.
PY - 2020/5
Y1 - 2020/5
N2 - Background and objectives Although renin-angiotensin-aldosterone system inhibition (RAASi) is a cornerstone in the treatment of children with CKD, it is sometimes discontinued when kidney function declines. We studied the reasons of RAASi discontinuation and associations between RAASi discontinuation and important risk markers of CKD progression and on eGFR decline in the Cardiovascular Comorbidity in Children with CKD study. Design, setting, participants, & measurements In this study, 69 children with CKD(67% male, mean age 13.7 years, mean eGFR 27 ml/min per 1.73 m2) who discontinued RAASi during prospective follow-upwere included. Initial change in BP, albuminuria, and potassium after discontinuation were assessed (median time 6 months). Rate of eGFR decline (eGFR slope) during amedian of 1.9 years before and 1.2 years after discontinuation were estimated using linear mixed effects modeling. Results Physician-reported reasons for RAASi discontinuation were increase in serum creatinine, hyperkalemia, and symptomatic hypotension. After discontinuation of RAASi, BP and albuminuria increased, whereas potassium decreased. eGFR declinedmore rapidly after discontinuation of RAASi (-3.9ml/min per 1.73m2 per year; 95%confidence interval, -5.1 to -2.6) compared with the slope during RAASi treatment (-1.5 ml/min per 1.73 m2 per year; 95% confidence interval, -2.4 to -0.6; P=0.005). In contrast, no change in eGFR slope was observed in a matched control cohort of patients in whom RAASi was continued. Conclusions Discontinuation of RAASi in children with CKD is associated with an acceleration of kidney function decline, even in advanced CKD.
AB - Background and objectives Although renin-angiotensin-aldosterone system inhibition (RAASi) is a cornerstone in the treatment of children with CKD, it is sometimes discontinued when kidney function declines. We studied the reasons of RAASi discontinuation and associations between RAASi discontinuation and important risk markers of CKD progression and on eGFR decline in the Cardiovascular Comorbidity in Children with CKD study. Design, setting, participants, & measurements In this study, 69 children with CKD(67% male, mean age 13.7 years, mean eGFR 27 ml/min per 1.73 m2) who discontinued RAASi during prospective follow-upwere included. Initial change in BP, albuminuria, and potassium after discontinuation were assessed (median time 6 months). Rate of eGFR decline (eGFR slope) during amedian of 1.9 years before and 1.2 years after discontinuation were estimated using linear mixed effects modeling. Results Physician-reported reasons for RAASi discontinuation were increase in serum creatinine, hyperkalemia, and symptomatic hypotension. After discontinuation of RAASi, BP and albuminuria increased, whereas potassium decreased. eGFR declinedmore rapidly after discontinuation of RAASi (-3.9ml/min per 1.73m2 per year; 95%confidence interval, -5.1 to -2.6) compared with the slope during RAASi treatment (-1.5 ml/min per 1.73 m2 per year; 95% confidence interval, -2.4 to -0.6; P=0.005). In contrast, no change in eGFR slope was observed in a matched control cohort of patients in whom RAASi was continued. Conclusions Discontinuation of RAASi in children with CKD is associated with an acceleration of kidney function decline, even in advanced CKD.
UR - https://www.scopus.com/pages/publications/85084379982
U2 - 10.2215/CJN.09750819
DO - 10.2215/CJN.09750819
M3 - Article
C2 - 32253275
AN - SCOPUS:85084379982
SN - 1555-9041
VL - 15
SP - 625
EP - 632
JO - Clinical Journal of the American Society of Nephrology
JF - Clinical Journal of the American Society of Nephrology
IS - 5
ER -