Abstract
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<0.0001. On limiting the cohort to individuals under 45 years with no prior MACE this association persists, HR 1.95 (1.49, 2.55), p< 0.0001. When stratified by diabetes status using the same model the effect persisted in both groups. In low risk non-diabetics, the hazards of MACE were 2.59 times higher for AKI cases (95%CI:1.28,5.24 p<0.0001), while in low risk diabetics the hazards were 1.83 times higher for AKI cases (95%CI:1.27,2.44 p<0.0001).
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.
RAPID DESENSITIZATION WITH INTRAVENOUS INSULIN IN A PATIENT WITH DIABETIC KETOACIDOSIS AND INSULIN ALLERGY