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Graphical Abstract, Background Automated acute kidney injury (AKI) electronic alerts (e-alerts) are rule-based warnings triggered by changes in creatinine and are intended to facilitate earlier detection in AKI. We assessed the impact of the introduction in the Tayside region of UK in April 2015 of automated AKI e-alerts with an accompanying education programme. Methods Interrupted time-series analysis using segmented regression was performed involving all adults with AKI aged ≥18 years who had a serum creatinine measured between 1 April 2013 and 31 March 2017. Analysis evaluated associations of AKI e-alert introduction on rate and severity (Stages 2–3) of AKI as well as mortality and occupied hospital bed days per patient per month in the population with AKI. Results There were 32 320 episodes of AKI during the observation period. Implementation of e-alerts had no effect on the rate of any AKI [incidence rate ratio (IRR) 0.996, 95% confidence interval (CI) 0.991 to 1.001, P = 0.086] or on the rate of severe AKI (IRR 0.995, 95% CI 0.990 to 1.000, P = 0.061). Subgroup analysis found no impact on the rate or severity of AKI in hospital or in the community. Thirty-day mortality following AKI did not improve (IRR 0.998, 95% CI 0.987 to 1.009, P = 0.688). There was a slight reduction in occupied bed days (β-coefficient −0.059, 95% CI −0.094 to −0.025, P = 0.002). Conclusions Introduction of automated AKI e-alerts was not associated with a change in the rate, severity or mortality associated with AKI, but there was a small reduction in occupied hospital bed days.

Background Improving recognition of patients at increased risk of acute kidney injury (AKI) in the community may facilitate earlier detection and implementation of proactive prevention measures that mitigate the impact of AKI. The aim of this study was to develop and externally validate a practical risk score to predict the risk of AKI in either hospital or community settings using routinely collected data. Methods Routinely collected linked datasets from Tayside, Scotland, were used to develop the risk score and datasets from Kent in the UK and Alberta in Canada were used to externally validate it. AKI was defined using the Kidney Disease: Improving Global Outcomes serum creatinine–based criteria. Multivariable logistic regression analysis was performed with occurrence of AKI within 1 year as the dependent variable. Model performance was determined by assessing discrimination (C-statistic) and calibration. Results The risk score was developed in 273 450 patients from the Tayside region of Scotland and externally validated into two populations: 218 091 individuals from Kent, UK and 1 173 607 individuals from Alberta, Canada. Four variables were independent predictors for AKI by logistic regression: older age, lower baseline estimated glomerular filtration rate, diabetes and heart failure. A risk score including these four variables had good predictive performance, with a C-statistic of 0.80 [95% confidence interval (CI) 0.80–0.81] in the development cohort and 0.71 (95% CI 0.70–0.72) in the Kent, UK external validation cohort and 0.76 (95% CI 0.75–0.76) in the Canadian validation cohort. Conclusion We have devised and externally validated a simple risk score from routinely collected data that can aid both primary and secondary care physicians in identifying patients at high risk of AKI., Graphical Abstract Graphical Abstract

Objectives to establish and quantify any observable association between the exposure to community prescriptions for quinine and acute kidney injury (AKI) events in a population of older adults. Design two observational studies using the same dataset, a retrospective longitudinal cohort study and a self-controlled case series (SCCS). Setting NHS health board in Scotland. Participants older adults (60+ years) who received quinine prescriptions in Tayside, Scotland, between January 2004 and December 2015. The first study included 12,744 individuals. The SCCS cohort included 5,907 people with quinine exposure and more than or equal to one AKI event. Main outcome measured in the first study, multivariable logistic regression was used to calculate odds ratios (ORs) for AKI comparing between episodes with and without recent quinine exposure after adjustment for demographics, comorbidities and concomitant medications. The SCCS study divided follow-up for each individual into periods ‘on’ and ‘off’ quinine, calculating incidence rate ratios (IRRs) for AKI adjusting for age. Results during the study period, 273,596 prescriptions for quinine were dispensed in Tayside. A total of 13,616 AKI events occurred during follow-up (crude incidence 12.5 per 100 person-years). In the first study, exposure to quinine before an episode of care was significantly associated with an increased probability of AKI (adjusted OR = 1.27, 95% confidence interval (CI) 1.21–1.33). In the SCCS study, exposure to quinine was associated with an increased relative incidence of AKI compared to unexposed periods (IRR = 1.20, 95% CI 1.15–1.26), with the greatest risk observed within 30 days following quinine initiation (IRR = 1.48, 95% CI 1.35–1.61). Conclusion community prescriptions for quinine in an older adult population are associated with an increased risk of AKI., Graphical Abstract Graphical Abstract

Background Patients who survive an episode of acute kidney injury (AKI) are more likely to have further episodes of AKI. AKI is associated with increased mortality, with a further increase with recurrent episodes. It is not clear whether this is due to AKI or as a result of other patient characteristics. The aim of this study was to establish whether recurrence of AKI is an independent risk factor for mortality or if excess mortality is explained by other factors. Methods This observational cohort study included adult people from the Tayside region of Scotland, with an episode of AKI between 1 January 2009 and 31 December 2009. AKI was defined using the creatinine-based Kidney Disease: Improving Global Outcomes definition. Associations between recurrent AKI and mortality were examined using a Cox proportional hazards model. Results Survival was worse in the group identified to have recurrent AKI compared with those with a single episode of AKI [hazard ratio = 1.49, 95% confidence interval (CI) 1.37–1.63; P Conclusions Recurrent AKI is associated with increased mortality. After adjusting for patient characteristics, the increase in mortality is independently associated with recurrent AKI and is not solely explained by other risk factors.

Background The application of a uniform definition for acute kidney injury (AKI) is vital to advance understanding and management of AKI. International Classification of Diseases (Tenth Revision) (ICD-10) coding is frequently used to define AKI, but its accuracy is unclear. The aim of this study was to determine whether ICD-10 coding is a reliable method of monitoring rates and outcomes of AKI in inpatients compared with biochemically defined AKI, and whether electronic alerts (e-alerts) for AKI affect ICD-10 AKI coding. Methods An observational cohort study of all 505 662 adult admissions to acute hospitals in two Scottish Health Boards [National Health Service (NHS) Tayside and NHS Fife] from January 2013 to April 2017 was performed. AKI e-alerts were implemented in NHS Tayside in April 2015. Sensitivity, specificity, positive and negative predictive values of ICD-10 coding for AKI compared with biochemically defined AKI using the Kidney Disease: Improving Global Outcomes definition and relative risk of 30-day mortality in people with ICD-10 and biochemically defined AKI before and after AKI e-alert implementation were performed. Results Sensitivity of ICD-10 coding for identifying biochemically defined AKI was very poor in both health boards for all AKI (Tayside 25.7% and Fife 35.8%) and for Stages 2 and 3 AKI (Tayside 43.8% and Fife 53.8%). Positive predictive value was poor both for all AKI (Tayside 76.1% and Fife 45.5%) and for Stages 2 and 3 AKI (Tayside 45.5% and Fife 36.8%). Measured mortality fell following implementation of AKI e-alerts in the ICD-10-coded population but not in the biochemically defined AKI population, reflecting an increase in the proportion of Stage 1 AKI in ICD-10-coded AKI. There was no evidence that the introduction of AKI e-alerts in Tayside improved ICD-10 coding of AKI. Conclusion ICD-10 coding should not be used for monitoring of rates and outcomes of AKI for either research or improvement programmes.

Background and Aims Acute kidney injury (AKI) is associated with adverse long term outcomes such as increased mortality. It is unclear however whether the increased mortality is due to cardiovascular events. The aim of this study was to examine major adverse cardiovascular events (MACE) following AKI in a population cohort in Scotland (GoDARTS) specifically examining a “low risk” younger age group without previous cardiovascular events. Method An observational cohort study of people in Tayside & Fife (Scotland, UK) recruited into GoDARTS from December 1998 to July 2017 was performed. Data were linked between the following datasets: population demography files, Scottish Morbidity Record of hospital admissions (SMR01); biochemical laboratory results, medicines dispensed by community pharmacies, the Scottish Care Initiative-Diabetes Collaboration (SCI-DC), the Scottish Renal Registry (SRR) and Scottish death registry data held by the Scottish General Records Office (GRO). AKI was defined using the creatinine based Kidney Disease Improving Global Outcomes (KDIGO) definition. MACE events were defined as hospitalisations or death due to myocardial infarction, ischaemic stroke, or coronary artery disease using International Classification of Diseases codes. Follow-up began at the time of first AKI occurrence for cases, and first recorded creatinine measurement for controls. Analyses were restricted to those who were 45 years or younger at the start of follow-up and who had no history of MACE. Survival analyses were performed using cox models adjusted for sex, age, CKD stage at baseline, Scottish index for multiple deprivation, medication use and diabetes. A forward step-wise method was used for variable selection. Analyses stratified by type 2 status were also performed. Results Data were available for 18,163 individuals in GoDARTS of which 15,884 individuals had creatinine measurements which could be used to classify whether an AKI event occurred. Of these, 6534 had at least one AKI event and 8807 never had an event. AKI was associated with more than two-fold increase in risk of MACE, independent of age, sex, type 2 diabetes, deprivation, anti-hypertensives, prior MACE and baseline renal function, HR 2.10 (1.90, 2.26), p Conclusion AKI is associated with significantly increased risk of prospective MACE with a two-fold increase when adjusted for age, prior MACE, baseline renal function, type 2 diabetes, deprivation and blood pressure. In a low-risk group (relatively younger and with no prior MACE), this risk persists. It is unclear whether AKI leads to CV events or AKI is more likely in this population but this finding highlights that cardiovascular risk reduction in patients following AKI is vital.

Background and Aims Quinine can precipitate Acute Kidney Injury (AKI) by immune-mediated reactions. Cramps, for which quinine is traditionally prescribed, may be a symptom of conditions that are risk factors for AKI. The relationship between quinine and AKI at a population level is unclear. The aim of this study was to establish and quantify any observable association between the exposure to community prescriptions for quinine and AKI events in a population of older adults. Method We performed two observational studies of older adults (60+ years) who received quinine prescriptions in Tayside, Scotland, between January 2004 and December 2015. The first study was a retrospective longitudinal cohort study with the primary outcome AKI. Creatinine measurements less than seven days apart were grouped as episodes of care. Multivariable logistic regression was used to calculate odds ratios (OR) for AKI comparing between episodes with and without recent quinine exposure after adjustment for demographics, comorbidities and concomitant medications. A self-controlled case series (SCCS) was then conducted with follow-up divided into periods “on” and “off” quinine for the same individual, calculating incidence rate ratios (IRR) for AKI adjusting for age. Results The first study included 12,744 individuals who experienced 13,616 AKI events during cohort follow-up (crude incidence 12.5 per 100 person-years). Exposure to quinine before an episode of care was significantly associated with an increased probability of AKI (adjusted OR=1.27, 95% CI 1.21-1.33). The SCCS cohort included 5,907 people with quinine exposure with ≥1 AKI event. Exposure to quinine was associated with an increased relative incidence of AKI compared to unexposed periods (IRR=1.20, 95% CI 1.15-1.26), with the greatest risk observed within 30 days of quinine initiation (IRR=1.48, 95% CI 1.35-1.61). Conclusion Exposure to quinine in patients aged 60 years and over was associated with an increased risk of AKI, the incidence of which is unlikely to simply be explained be immune-mediated reactions only. Further research is required to determine exact reasons for the increased risk of AKI.

Background Development of acute kidney injury (AKI) following the use of antibiotics such as sulphonamides, trimethoprim and aminoglycosides is a frequently described phenomenon. More recently, an association between fluoroquinolone use and AKI has been suggested. The aim of this study was to evaluate the risk of AKI as an unintended consequence of commonly prescribed antibiotics in a large community cohort using a method that fully adjusts for underlying patient characteristics, including potential unmeasured confounders. Methods A self-controlled case study was conducted and included all individuals aged 18 years and over in the Tayside region of Scotland who had a serum creatinine measured between 1 January 2004 and 31 December 2012. AKI episodes were defined using the Kidney Disease: Improving Global Outcomes definition. Data on oral community-prescribed antibiotics (penicillins, cephalosporins, fluoroquinolones, sulphonamides and trimethoprim, macrolides and nitrofurantoin) were collected for all individuals. Incidence rate ratios (IRRs) for AKI associated with antibiotic exposure versus time periods without antibiotic exposure were calculated. Results Combined use of sulphonamides, trimethoprim and nitrofurantoin rose by 47% and incidence of community-acquired AKI rose by 16% between 2008 and 2012. During the study period 12 777 individuals developed 14 900 episodes of AKI in the community, of which 68% was AKI Stage 1, 16% Stage 2 and 16% Stage 3. The IRR of AKI during any antibiotic use was 1.16 [95% confidence interval (CI) 1.10—1.23], and this was highest during sulphonamides or trimethoprim use; IRR 3.07 (95% CI 2.81–3.35). Fluoroquinolone and nitrofurantoin use was not associated with a significantly increased rate of AKI; IRR 1.13 (95% CI 0.94–1.35) and 1.16 (95% CI 0.91–1.50), respectively. Conclusions Incidence of AKI rose by 16% between 2008 and 2012. In the same period the use of sulphonamides, trimethoprim and nitrofurantoin increased by 47%. A significant increased risk of AKI was seen with the use of sulphonamides and trimethoprim, but not with fluoroquinolones or nitrofurantoin.

Background Cognitive impairment of various kinds is common in older people admitted to hospital, but previous research has usually focused on single conditions in highly-selected groups and has rarely examined associations with outcomes. This study examined prevalence and outcomes of cognitive impairment in a large unselected cohort of people aged 65+ with an emergency medical admission. Methods Between January 1, 2012, and June 30, 2013, admissions to a single general hospital acute medical unit aged 65+ underwent a structured specialist nurse assessment (n = 10,014). We defined ‘cognitive spectrum disorder’ (CSD) as any combination of delirium, known dementia, or Abbreviated Mental Test (AMT) score