Impact of infection on decongestion and kidney outcomes in patients with cardiorenal syndrome type 1
This was an investigator-initiated prospective cohort conducted at the Hospital Civil de Guadalajara Fray Antonio Alcalde (Guadalajara, Mexico). The study included 256 hospitalized patients meeting criteria for cardiorenal syndrome type 1 (CRS1) between 2022 and 2024. Eligible participants were identified during routine hospital rounds among patients with acute kidney injury (AKI) and acute decompensated heart failure (ADHF). Cardiology and nephrology teams confirmed the diagnosis of CRS1 using the 2008 Ronco classification; AKI was adjudicated by KDIGO serum creatinine criteria and estimated glomerular filtration rate (eGFR) was calculated using the CKD-EPI equation.
Infection was defined as a clinical suspicion of bacterial infection at any site (pulmonary, abdominal, urinary, soft tissue, or other) combined with the prescription of antibiotics. The primary outcome was successful decongestion, captured through a composite that included symptom resolution (dyspnea and peripheral edema), biomarker improvement (≥30% reduction in BNP or CA-125), and point-of-care ultrasound (POCUS) findings (absence of B-lines or VExUS < 2, and IVC status). Secondary outcomes were major adverse kidney events (MAKE) at 10 days (MAKE10) and 30 days (MAKE30), defined as death, new requirement for kidney replacement therapy (KRT), or a ≥25% decline in eGFR from baseline.
Diuretic management and other decongestive strategies were delivered at the treating teams' discretion and titrated according to clinical response. The study evaluated decongestion using a multimodal approach combining patient symptoms, biomarker trajectories (BNP/CA-125), and POCUS assessment (lung ultrasound, inferior vena cava status, and VExUS where applicable). Successful decongestion required meeting at least one of the predefined metrics described above.
Of 256 patients, 72 (28.1%) met the study definition of infection. At baseline, patients with infection showed evidence of more severe congestion: median BNP was higher in the infected group (25,264 pg/mL) compared with the non-infected group (13,405 pg/mL), a difference that reached statistical significance (p = 0.012). Oxygenation was also worse among infected patients, with lower PaO2 (median 45 mmHg) versus 65.5 mmHg in non-infected patients (p = 0.019). These findings indicate that infection in this cohort was associated with a higher burden of clinical and biomarker-detected congestion at presentation.
Total furosemide exposure over hospitalization was comparable between patients with and without infection (median 600 mg vs. 580 mg; p = 0.62). The proportion of patients who achieved successful decongestion did not differ meaningfully by infection status: 61.4% in the infected group versus 59.8% in the non-infected group (p = 0.83). In multivariable analysis, infection was not independently associated with achieving decongestion (adjusted odds ratio [aOR] 1.28, 95% CI 0.65–2.51), indicating that despite more severe baseline congestion, patients with infection were as likely to be decongested under usual care as those without infection.
Secondary kidney outcomes were evaluated as major adverse kidney events at 10 and 30 days. Infection status was not independently associated with MAKE-30 in adjusted analyses (aOR 1.26, 95% CI 0.57–2.79). The manuscript reports MAKE outcomes at both time points but does not provide additional granular subgroup event counts in the abstract; detailed MAKE10 and MAKE30 event distributions are presented in the full text tables and figures of the source article.
In this prospective cohort of hospitalized CRS1 patients, infection was common and associated with more severe baseline congestion and worse oxygenation. However, infection did not appear to compromise the ability to achieve decongestion using routine clinical care, nor was it independently associated with an increased risk of short-term MAKE. The authors conclude that attaining decongestion is feasible in patients with ADHF precipitated by infection and that infection did not confer an incremental short-term kidney risk in this cohort.
The study dataset is publicly available in a Zenodo repository (record “SX CARDIORRENAL INFECTADOS FINAL,” DOI: 10.5281/zenodo.20821008). Funding was provided by the Secretaria de Salud Jalisco and the Consejo Nacional de Ciencia, Humanidades y Tecnología (CONAHCYT); funders had no role in study design, data collection, analysis, or manuscript preparation. The authors declared no competing interests.
Note: Additional details on patient-level MAKE event counts, full multivariable model covariates, and other secondary analyses are reported in the full article and associated tables and figures. If specific granular data or subgroup results are required, consult the published tables and the shared dataset in Zenodo.