Introduction:
Acute Kidney Injury (AKI) is a known and serious complication of heart failure, typically occurring within the complex framework of cardiorenal syndrome. This is known to increase mortality, morbidity and hospitalisation durations. Hence, early detection and intervention are pivotal to prevent progression to Acute Kidney Disease (AKD) and Chronic Kidney Disease (CKD). This study identifies risk factors for AKI and its progression into AKD, aiming to facilitate early intervention.
Methods:
AKI (an increase in serum Creatinine (SCr) by more than 0.3mg/dL within 48 hours or by 1.5 times baseline SCr during hospitalisation) was defined according to the Kidney Disease: Improving Global Outcomes (KDIGO) criteria; AKD (a 50% or more increase in SCr within 3 months post-hospitalisation) was defined according to the Acute Disease Quality Initiative (ADQI). Demographic data, past medical history, drug history, laboratory test results and vital signs were recorded for 221 heart failure patients across 498 hospitalisations at the University Malaya Medical Centre (UMMC) in Malaysia from January 2020 to June 2024 . Using SPSS, univariate analysis to compare the AKI and non-AKI group was performed to identify predictors for AKI. Further analysis was performed in the AKI group to identify risk factors for the development of AKD. A binary logistic regression analysis was used to demonstrate the influence of each variable on AKI. This model was optimised via backwards stepwise regression, which was assessed via Area Under the Receiver Operating Characteristic (AUROC) Curve.
Results:
Among the patients studied, 27.3% developed AKI during hospitalisation. The median age in this cohort was 66 (interquartile range[IQR] 55-72). Males comprised 66.1% of the total patient cohort. Univariate analysis identified hypertension, CKD, length of stay in hospital (LOS), systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP), respiratory rate (RR), hypotensive episodes during hospitalisation, cumulative dose of furosemide during hospitalisation, haemoglobin level, white blood cell count (WBC), albumin level and C-reactive protein (CRP) level as significant predictors for AKI. However, subsequent multiple logistic regression indicated CKD (odds ratio[OR] 2.761, 95% confidence interval[CI] 1.557-4.898, p<0.001) as a sole predictor. Further optimisation of the regression model yields CKD (OR 2.591, CI 1.582-4.245, p<0.001), LOS (OR 1.062, CI 1.017-1.109, p=0.006), WBC (OR 1.027, CI 0.991-1.065, p=0.0147), CRP (OR 1.006, CI 1.001-1.01, p=0.012), DBP (OR 1.044, CI 0.993-1.097, p=0.091) and MAP (OR 0.939, CI 0.895-0.986, p=0.011). ROC analysis showed an area of 0.744, with a sensitivity of 70.2% and specificity of 71.1%. Notably, 55.9% of AKI patients progressed to AKD compared to 31.9% in non-AKI patients (p<0.001). Amongst AKI patients, progression into AKD involves risks factors such as diabetes mellitus (p<0.001), dyslipidemia (p=0.024) and haemoglobin (p=0.003).
Conclusions:
In this cohort, multiple risk factors correlate significantly with the incidence of AKI and AKD in heart failure patients, highlighting the need for targeted clinical intervention. Leveraging the robust predictive model for AKI, early nephrological consultation can be initiated to mitigate progression of renal damage, thereby improving patient outcomes.
I have no potential conflict of interest to disclose.
I did not use generative AI and AI-assisted technologies in the writing process.