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Acute kidney injury: an acceptable risk of treatment with renin-angiotensin system blockade in primary care?

Bedford M, Farmer CK, Irving J, Stevens PE - Can J Kidney Health Dis (2015)

Bottom Line: However, prescription of RAS blockade in the absence of indication appeared to be associated with greater risk of AKI.Use of RAS antagonists increased the risk of AKI, independent of common confounding variables.After correction for confounders the risk fell away and became non-significant for moderate and severe AKI.

View Article: PubMed Central - PubMed

Affiliation: Kent Kidney Research Group, East Kent Hospitals University NHS Foundation Trust, Kent and Canterbury Hospital, Ethelbert Road, CT1 3NG Canterbury, Kent.

ABSTRACT

Background: Use of renin-angiotensin system (RAS) blockade has become increasingly widespread driven by evidence-based guidance. There is concern about the role of these agents in the genesis of avoidable acute kidney injury (AKI).

Objectives: To investigate the association between AKI and use of RAS blockade.

Design: Multilevel hierarchical analysis of a large cohort of patients registered with UK general practitioners.

Setting: Primary care practices in East and West Kent, United Kingdom.

Patients: 244,715 patients from 27 practices.

Measurements: Demographic, clinical, biochemical and prescription data.

Methods: Analyses of data acquired between 02/3/2004 and 17/04/2012 using multilevel logistic regression to determine the relationship between AKI and use of RAS blockade; further analysed by indication for treatment with RAS blockade.

Results: Sufficient serum creatinine data were available to define AKI in 63,735 patients with 208,275 blood test instances. In 95,569 instances the patient was prescribed a RAS antagonist of which 5.4% fulfilled criteria for AKI. The unadjusted odds ratio (OR) for AKI in those prescribed RAS blockade was 1.93 (1.81-2.06, 95%CI) falling to 1.11 (1.02-1.20, 95%CI) when adjusted for age, gender, co-morbidity, GFR category, proteinuria, systolic blood pressure and diuretic therapy. In patients with an evidence-based indication there was no difference in absolute risk of AKI. However, prescription of RAS blockade in the absence of indication appeared to be associated with greater risk of AKI. When analysis was repeated with AKIN2/AKIN3 as the outcome, although risk of AKI remained significant when unadjusted (OR 1.73, 95%CI 1.42-2.11, p<0.001), after full adjustment there was no increased risk (OR 0.83, 95%CI 0.63-1.09) in those taking RAS antagonists. However, when analysed by indication AKIN2/AKIN3 was significantly more likely in those prescribed RAS antagonists without indication (OR 2.04, 95%CI 1.41-2.94, p<0.001).

Limitations: Observational database study. No information concerning hospitalisation. Prescribing assumptions and potential inaccurate coding. Potential survival bias; patients surviving longer will contribute more data.

Conclusions: Use of RAS antagonists increased the risk of AKI, independent of common confounding variables. After correction for confounders the risk fell away and became non-significant for moderate and severe AKI. However, where there was no evidence-based indication for RAS antagonists the risk of AKI, whether mild, moderate or severe, remained greater.

No MeSH data available.


Related in: MedlinePlus

Study cohort and acute kidney injury (AKI) subdivided by RAS antagonist prescription and proteinuria testing.
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Fig1: Study cohort and acute kidney injury (AKI) subdivided by RAS antagonist prescription and proteinuria testing.

Mentions: There were 345,986 “blood test instances” from 121,933 patients in a practice population of 244,715. In 137,276 (39.7%) of the “blood test instances” no prior creatinine data were available and the presence or absence of AKI could not be assessed. The baseline characteristics of these subjects showed them to be significantly younger, with very little co-morbidity compared to those with baseline GFR data (Table 1). Only 5 percent had CKD and 21 percent hypertension, unsurprisingly they were prescribed significantly fewer medications and only 13 percent had an evidence-based indication for RAS blockade. 435 “blood test instances” from 83 patients were removed as the patient’s baseline GFR was <15 ml/min/1.73 m2. This left outcome data for 208,275 “blood test instances” from 63,722 patients. Table 1 demonstrates the population demographics of these 63,722 patients at baseline. In 112,706 of these instances the patient was not taking a RAS antagonist, 3.1% (3,440) of these instances fulfilled criteria for AKI. In 95,569 blood test instances the patient was taking a RAS antagonist, 5.4% (5,194) of these instances fulfilled criteria for AKI (Figure 1). Of the 63,722 patients: 27,970 (44%) also had proteinuria testing. Of these 22,552 (35%) had “normal to mildly elevated”, 4,473 (7%) had “Moderately elevated” and 945 (1.5%) had “Severely elevated” levels of proteinuria.Table 1


Acute kidney injury: an acceptable risk of treatment with renin-angiotensin system blockade in primary care?

Bedford M, Farmer CK, Irving J, Stevens PE - Can J Kidney Health Dis (2015)

Study cohort and acute kidney injury (AKI) subdivided by RAS antagonist prescription and proteinuria testing.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4414427&req=5

Fig1: Study cohort and acute kidney injury (AKI) subdivided by RAS antagonist prescription and proteinuria testing.
Mentions: There were 345,986 “blood test instances” from 121,933 patients in a practice population of 244,715. In 137,276 (39.7%) of the “blood test instances” no prior creatinine data were available and the presence or absence of AKI could not be assessed. The baseline characteristics of these subjects showed them to be significantly younger, with very little co-morbidity compared to those with baseline GFR data (Table 1). Only 5 percent had CKD and 21 percent hypertension, unsurprisingly they were prescribed significantly fewer medications and only 13 percent had an evidence-based indication for RAS blockade. 435 “blood test instances” from 83 patients were removed as the patient’s baseline GFR was <15 ml/min/1.73 m2. This left outcome data for 208,275 “blood test instances” from 63,722 patients. Table 1 demonstrates the population demographics of these 63,722 patients at baseline. In 112,706 of these instances the patient was not taking a RAS antagonist, 3.1% (3,440) of these instances fulfilled criteria for AKI. In 95,569 blood test instances the patient was taking a RAS antagonist, 5.4% (5,194) of these instances fulfilled criteria for AKI (Figure 1). Of the 63,722 patients: 27,970 (44%) also had proteinuria testing. Of these 22,552 (35%) had “normal to mildly elevated”, 4,473 (7%) had “Moderately elevated” and 945 (1.5%) had “Severely elevated” levels of proteinuria.Table 1

Bottom Line: However, prescription of RAS blockade in the absence of indication appeared to be associated with greater risk of AKI.Use of RAS antagonists increased the risk of AKI, independent of common confounding variables.After correction for confounders the risk fell away and became non-significant for moderate and severe AKI.

View Article: PubMed Central - PubMed

Affiliation: Kent Kidney Research Group, East Kent Hospitals University NHS Foundation Trust, Kent and Canterbury Hospital, Ethelbert Road, CT1 3NG Canterbury, Kent.

ABSTRACT

Background: Use of renin-angiotensin system (RAS) blockade has become increasingly widespread driven by evidence-based guidance. There is concern about the role of these agents in the genesis of avoidable acute kidney injury (AKI).

Objectives: To investigate the association between AKI and use of RAS blockade.

Design: Multilevel hierarchical analysis of a large cohort of patients registered with UK general practitioners.

Setting: Primary care practices in East and West Kent, United Kingdom.

Patients: 244,715 patients from 27 practices.

Measurements: Demographic, clinical, biochemical and prescription data.

Methods: Analyses of data acquired between 02/3/2004 and 17/04/2012 using multilevel logistic regression to determine the relationship between AKI and use of RAS blockade; further analysed by indication for treatment with RAS blockade.

Results: Sufficient serum creatinine data were available to define AKI in 63,735 patients with 208,275 blood test instances. In 95,569 instances the patient was prescribed a RAS antagonist of which 5.4% fulfilled criteria for AKI. The unadjusted odds ratio (OR) for AKI in those prescribed RAS blockade was 1.93 (1.81-2.06, 95%CI) falling to 1.11 (1.02-1.20, 95%CI) when adjusted for age, gender, co-morbidity, GFR category, proteinuria, systolic blood pressure and diuretic therapy. In patients with an evidence-based indication there was no difference in absolute risk of AKI. However, prescription of RAS blockade in the absence of indication appeared to be associated with greater risk of AKI. When analysis was repeated with AKIN2/AKIN3 as the outcome, although risk of AKI remained significant when unadjusted (OR 1.73, 95%CI 1.42-2.11, p<0.001), after full adjustment there was no increased risk (OR 0.83, 95%CI 0.63-1.09) in those taking RAS antagonists. However, when analysed by indication AKIN2/AKIN3 was significantly more likely in those prescribed RAS antagonists without indication (OR 2.04, 95%CI 1.41-2.94, p<0.001).

Limitations: Observational database study. No information concerning hospitalisation. Prescribing assumptions and potential inaccurate coding. Potential survival bias; patients surviving longer will contribute more data.

Conclusions: Use of RAS antagonists increased the risk of AKI, independent of common confounding variables. After correction for confounders the risk fell away and became non-significant for moderate and severe AKI. However, where there was no evidence-based indication for RAS antagonists the risk of AKI, whether mild, moderate or severe, remained greater.

No MeSH data available.


Related in: MedlinePlus