Abstract Background Acute kidney injury (AKI) is common in acute HF and associated with poor prognosis. (1-3) The cause of AKI is often unknown. Purpose The aim of this analysis was to analyse the data for patients with a severe AKI which developed during a HF admission and identify potential triggers in the preceding 7 days (e.g., infection, hypotension, contrast agents.). Methods Data between January 2022 to March 2023 was obtained from that submitted by our centre to the mandatory National HF Audit which collects data from every patient admitted with acute HF. For this analysis, baseline renal function was retrospectively collected from electronic patient records, and chronic kidney disease and AKI were subsequently defined, as per KDIGO guidelines(4), using baseline and admission measurements. Electronic patient records were reviewed for all patients who developed AKI stage 2/3 ≥48 hours after admission. Data collected during the week prior to their AKI included any radioiodine contrast exposure, temperature ≥ 38⁰C, antibiotics, CRP >100mg/L and periods of sustained hypotension. Results Of the 843 HF hospital admissions between January 2022 and March 2023, 507 (60.1%) were not associated with AKI [inpatient (IP) mortality 5.9%], 237 (28.1%) had an AKI stage 1 [IP mortality 17.3%], 51 (6.0%) had an AKI stage 2 [IP mortality 25.5%] and 48 (5.7%) had an AKI stage 3 [IP mortality 33.3%]. The age, diabetic status and ejection fraction of patients was similar across AKI stages. Of these, 64 patients developed their AKI stage 2 (n=30) or 3 (n=34) on or after their second day of HF hospital admission. 22 (34.3%) of these patients died during this admission, and 37 (57.8%) had died after a median follow-up of 217.5 days (IQR 24-331.75) (Table 1). 71.9% had evidence of an infection (defined by a temperature spike ≥38⁰C, received antibiotics, OR CRP >100mg/dL) in the week prior to developing their AKI (Table 2). 39% of patients had received a contrast agent in the preceding week, and 39% had experienced persistent hypotension in the preceding 48 hours. 25% had 2 of these potential triggers, 17.2% had 3. Six patients (9.4%) had no apparent identifiable triggers. 25% had not had renal function checked for 48h prior to AKI. Conclusion The most frequent identifiable potential trigger for severe AKI was infection in 72%, followed by contrast agent (39%) and hypotension (39%). Many patients had multiple triggers. Over-diuresis in isolation was not identified as a trigger for AKI in this cohort. Severe AKI 2/3 is a marker of extreme mortality risk and identifies patients in need of intensive monitoring. Lack of daily bloods in one quarter of patients led to a delay in AKI alert. Close observation for all acute HF patients including daily bloods and early identification and treatment of infection plus judicious and least use of contrast is needed to reduce the high mortality rates in this population.