AKI development is an independent predictor of mortality in infective endocarditis.

INTRODUCTION: Infective endocarditis presents a 25% mortality. Acute kidney injury (AKI) develops in up to 70% of the cases. The aim of this study is to evaluate the predictive value of AKI in mortality due to endocarditis and to assess its associated factors. METHODS: Unicentric and retrospective study including all patients with in-hospital diagnosis of endocarditis between 2015 and 2021. Epidemiological data and comorbidities were collected at baseline. During admission, renal function parameters, infection-related variables and mortality were collected. Using adjusted multivariate models, LRA predictive value was determined. RESULTS: One hundred and thirty-four patients (63% males, age 72±15 years) were included. Of them 94 (70%) developed AKI (50% AKIN-1, 29% AKIN-2 and 21% AKIN-3). Factors associated to AKI were age (p=0.03), hypertension (p=0.005), previous chronic kidney disease (p=0.001), heart failure (p=0.006), peripheral vascular disease (p=0.022) and glomerular filtration rate (GFR) at baseline (p<0.001). GFR at baseline was the only factor independently associated to AKI (OR 0.94, p=0.001). In-hospital deaths were registered in 46 (34%) patients. Of them, 45 (98%) patients had developed AKI. AKI was independently associated to mortality through diverse multivariate models. GFR loss (OR 1.054, p<0.001) and GFR at baseline (0.963, p=0.012) also predicted mortality during admission. CONCLUSIONS: AKI development and its severity (GFR loss and AKIN severity) impacts in in-hospital mortality due to infective endocarditis.

Infectious consequences of the AKI-to-CKD transition.

Background: Acute kidney injury (AKI) is associated with short- and long-term complications but the consequences of the AKI-to-CKD transition are still poorly understood. We aimed to evaluate the association between the AKI-to-CKD transition and the long-term risk of infection. Methods: This retrospective study included patients admitted in a tertiary hospital with community-acquired AKI in 2013 and 2014 who had their estimated glomerular filtration rate (eGFR) assessed at 3 months (±2 weeks) after serum creatinine peaked in the AKI episode. Key exclusion criteria were baseline CKD or confounding factors (active neoplasia, primary immunodeficiency, human immunodeficiency virus, immunosuppressive drugs). The association between the AKI-to-CKD transition (defined as an eGFR <60 ml/min/1.73 m2 at 3 months) and long-term infections (defined using clinical features, blood/urine analysis, cultures and imaging) was assessed during a follow-up of 9 months (range 2-56). Results: Among the 1731 patients admitted with AKI, 367 (21%) were included in the present analysis (64% male, 71 ± 15 years). Three months after AKI, 159 (43%) developed AKI-to-CKD transition. Baseline and post-AKI eGFR were independent predictors of AKI-to-CKD transition [hazard ratio (HR) 0.97, P = .044 and HR 0.96, P < .001, respectively].During follow-up, 153 (42%) patients developed an infection. Factors associated with infection were older age, cognitive impairment, lower post-AKI eGFR, eGFR loss from baseline to 3 months and AKI-to-CKD transition. Adjusted Cox regression showed that baseline eGFR, 3-month eGFR, eGFR loss and AKI-to-CKD transition were independent predictors of the long-term risk of infection. Conclusions: The AKI-to-CKD transition independently predicts the long-term risk of infection following an episode of AKI.