Acute kidney injury stage 2/3 during acute heart failure admission - clinical contributors and outcomes

Abstract

Abstract Introduction Acute Heart failure (AHF) may be complicated by acute kidney injury (AKI) as a result of cardiorenal syndrome.(1) However other factors may contribute to AKI. AKI stage 2 or 3 predicts negative inpatient outcomes in the general population.(2) We have reported data in a contemporary cohort on AKI in AHF. This study looks at a larger cohort in 5 previous years to test whether those findings were consistent. Better understanding of this clinical scenario may lead to improvements in care. Aim To assess the clinical factors associated with AKI 2/3 in AHF inpatients. Methods This study used retrospective data from a single teaching hospital collected for inclusion in the UK National Heart Failure National Audit. All AHF admissions over a 5-year period, from April 2017 – April 2022 inclusive, were analysed. Renal function on admission and discharge/death were assessed. AKI stage was defined according to KDIGO guidelines based on serum creatinine levels. Electronic patient records were reviewed and the clinical course leading up to and following AKI 2/3 was reviewed. Reported mode of death was also collected. Results 3219 AHF admissions (2360 unique patients) were assessed. 257 patients died during admission (8% admission mortality, 10.9% patients). 157 (4.9%) admissions had AKI 2/3 on admission/discharge. 85 (54.1%) AKI 2/3 died during their hospital admission vs 6.1% mortality in admissions without AKI 2/3. Baseline population characteristics are summarised in Table 1. Admissions with AKI 2/3 who died were older (77.6±11.5 vs 71.5 ±15.8) and had higher rates of atrial fibrillation (48.2% vs 39.9%), diabetes (40% vs 36%), ischaemic cardiomyopathy (56.5% vs 41.7%) and LVEF <35% (38.8% vs 27.7%). The most frequent contributors to AKI 2/3 were sepsis (55, 64.7%) and congestive cardiac failure/cardiorenal syndrome (48, 56.6%). Hypotension (25, 29.4%), over-diuresis (17, 20%), radioiodine contrast (10, 11.8%) and aminoglycosides (8, 9.4%) were less common factors in development of AKI 2/3. ≥2 contributors were present in 49, 57.6%. The dominant contributor for AKI 2/3 was adjudicated to be sepsis in 33 (38.8%) of admissions, followed by cardiorenal syndrome (congestive heart failure with AKI) in 29 (34.1%), and cardiogenic shock in 7 (8.2%). AKI 2/3 contributors are summarised in Table 2. In AKI 2/3 cases who died, 35 (41.2%) involved renal specialist input; 60 (70%) involved heart failure specialist review. Conclusion AKI in AHF is associated with high inpatient mortality. Despite this, specialist renal input was uncommon. AKI 2/3 was usually multifactorial. Cardiorenal syndrome accounted for one third of cases and may not be preventable. In keeping with our findings from a smaller contemporary cohort, sepsis was the most common dominant cause of severe AKI. Prevention, early identification, and treatment of infection could reduce this risk. Awareness of the high mortality of AKI in AHF and specialist review may improve outcomes in AHF.