Association of Acute Increases in Plasma Creatinine after Renin-Angiotensin Blockade with Subsequent Outcomes.

ACE inhibitors adult angiotensin angiotensins chronic dialysis chronic kidney disease chronic kidney failure congestive heart failure end stage kidney disease follow-up studies heart failure humans kidney failure, chronic kidney function tests mortality myocardial infarction renin renin angiotensin system renin-angiotensin system retrospective studies

Journal

Clinical journal of the American Society of Nephrology : CJASN
ISSN: 1555-905X
Titre abrégé: Clin J Am Soc Nephrol
Pays: United States
ID NLM: 101271570

Informations de publication

Date de publication:
06 09 2019
Historique:
received: 12 03 2019
accepted: 03 07 2019
pubmed: 10 8 2019
medline: 18 11 2020
entrez: 10 8 2019
Statut: ppublish

Résumé

Data from observational and interventional studies provide discordant results regarding the relationship between creatinine increase after renin-angiotensin system inhibition (RASi) and adverse outcomes. We compared health outcomes among patients with different categories of increase in creatinine upon initiation of RASi in a large population-based cohort. We performed a retrospective analysis of the Stockholm CREAtinine Measurements database, which contains complete information on diagnoses, medication dispensation claims, and laboratory test results for all Stockholm citizens accessing health care. Included were 31,951 adults initiating RASi during 2007-2011 with available pre- and postinitiation creatinine monitoring. Multivariable Cox regression was used to compare mortality, cardiovascular and ESKD events among individuals with different ranges of creatinine increases within 2 months after starting treatment. In a median follow-up of 3.5 years, acute increases in creatinine were associated with mortality (3202 events) in a graded manner: compared with creatinine increases <10%, a 10%-19% increase showed an adjusted hazard ratio (HR) of 1.15 (95% confidence interval [95% CI], 1.05 to 1.27); HR 1.22 (95% CI, 1.07 to 1.40) for 20%-29%; HR 1.55 (95% CI, 1.36 to 1.77) for ≥30%. Similar graded associations were present for heart failure (2275 events, Among real-world monitored adults, increases in creatinine (>10%) after initiation of RASi are associated with worse health outcomes. These results do not address the issue of discontinuation of RASi when plasma creatinine increases but do suggest that patients with increases in creatinine have higher subsequent risk of cardiovascular and kidney outcomes.

Sections du résumé

BACKGROUND AND OBJECTIVES
Data from observational and interventional studies provide discordant results regarding the relationship between creatinine increase after renin-angiotensin system inhibition (RASi) and adverse outcomes. We compared health outcomes among patients with different categories of increase in creatinine upon initiation of RASi in a large population-based cohort.
DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS
We performed a retrospective analysis of the Stockholm CREAtinine Measurements database, which contains complete information on diagnoses, medication dispensation claims, and laboratory test results for all Stockholm citizens accessing health care. Included were 31,951 adults initiating RASi during 2007-2011 with available pre- and postinitiation creatinine monitoring. Multivariable Cox regression was used to compare mortality, cardiovascular and ESKD events among individuals with different ranges of creatinine increases within 2 months after starting treatment.
RESULTS
In a median follow-up of 3.5 years, acute increases in creatinine were associated with mortality (3202 events) in a graded manner: compared with creatinine increases <10%, a 10%-19% increase showed an adjusted hazard ratio (HR) of 1.15 (95% confidence interval [95% CI], 1.05 to 1.27); HR 1.22 (95% CI, 1.07 to 1.40) for 20%-29%; HR 1.55 (95% CI, 1.36 to 1.77) for ≥30%. Similar graded associations were present for heart failure (2275 events,
CONCLUSIONS
Among real-world monitored adults, increases in creatinine (>10%) after initiation of RASi are associated with worse health outcomes. These results do not address the issue of discontinuation of RASi when plasma creatinine increases but do suggest that patients with increases in creatinine have higher subsequent risk of cardiovascular and kidney outcomes.

Identifiants

pubmed: 31395593
pii: 01277230-201909000-00011
doi: 10.2215/CJN.03060319
pmc: PMC6730502
doi:

Substances chimiques

Angiotensin Receptor Antagonists 0
Angiotensin-Converting Enzyme Inhibitors 0
Creatinine AYI8EX34EU

Types de publication

Comparative Study Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1336-1345

Informations de copyright

Copyright © 2019 by the American Society of Nephrology.

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Auteurs

Edouard L Fu (EL)

Departments of Clinical Epidemiology and.
Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden.

Marco Trevisan (M)

Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden.

Catherine M Clase (CM)

Department of Medicine and.
Department of Health Research Methods, Evidence, and Impact, McMaster University, Hamilton, Canada; and.

Marie Evans (M)

Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden.

Bengt Lindholm (B)

Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden.

Joris I Rotmans (JI)

Internal Medicine, Leiden University Medical Center, Leiden, The Netherlands.

Merel van Diepen (M)

Departments of Clinical Epidemiology and.

Friedo W Dekker (FW)

Departments of Clinical Epidemiology and.

Juan-Jesus Carrero (JJ)

Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden.

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