Impact of infection on decongestion and kidney outcomes in patients with cardiorenal syndrome type 1.
Infections are frequent precipitants of acute decompensated heart failure (ADHF) and may alter decongestive trajectories in patients with cardiorenal syndrome type 1 (CRS1), it may reduce diuretic efficacy and increase the risk of kidney injury. However, the impact of infection on decongestion and kidney outcomes in CRS1 remains unclear.
We conducted a prospective cohort study including 256 patients with CRS1 hospitalized at a tertiary center (2022-2024). Patients were stratified by the presence of infection, defined as clinical suspicion plus antibiotic therapy. The primary outcome was successful decongestion, assessed by symptoms, biomarkers (BNP/CA-125), and POCUS findings. Secondary outcomes included major adverse kidney events at 10 and 30 days (MAKE: death, kidney replacement therapy [KRT], or ≥25% eGFR decline).
Seventy-two patients (28.1%) had infection, presenting with higher BNP (13,405 vs. 25,264 pg/mL, p = 0.012) and lower PaO2 (45 vs. 65.5 mmHg, p = 0.019). Furosemide exposure was comparable (600 vs. 580 mg, p = 0.62). Successful decongestion occurred in 61.4% of patients with infection vs. 59.8% without infection (p = 0.83). Infection was not independently associated with decongestion (aOR 1.28, 95% CI 0.65-2.51) or MAKE-30 (aOR 1.26, 95% CI 0.57-2.79).
In CRS1, infection was associated with more severe baseline congestion but did not compromise decongestion rates or increase short-term MAKE. These findings support the notion that achieving decongestion is feasible in patients with ADHF due to infection without an incremental risk of MAKE.
We conducted a prospective cohort study including 256 patients with CRS1 hospitalized at a tertiary center (2022-2024). Patients were stratified by the presence of infection, defined as clinical suspicion plus antibiotic therapy. The primary outcome was successful decongestion, assessed by symptoms, biomarkers (BNP/CA-125), and POCUS findings. Secondary outcomes included major adverse kidney events at 10 and 30 days (MAKE: death, kidney replacement therapy [KRT], or ≥25% eGFR decline).
Seventy-two patients (28.1%) had infection, presenting with higher BNP (13,405 vs. 25,264 pg/mL, p = 0.012) and lower PaO2 (45 vs. 65.5 mmHg, p = 0.019). Furosemide exposure was comparable (600 vs. 580 mg, p = 0.62). Successful decongestion occurred in 61.4% of patients with infection vs. 59.8% without infection (p = 0.83). Infection was not independently associated with decongestion (aOR 1.28, 95% CI 0.65-2.51) or MAKE-30 (aOR 1.26, 95% CI 0.57-2.79).
In CRS1, infection was associated with more severe baseline congestion but did not compromise decongestion rates or increase short-term MAKE. These findings support the notion that achieving decongestion is feasible in patients with ADHF due to infection without an incremental risk of MAKE.
Authors
Chávez-Iñiguez Chávez-Iñiguez, Zaragoza Zaragoza, Del Toro Del Toro, Fong-Maravilla Fong-Maravilla, Navarro-Blackaller Navarro-Blackaller, Medina-González Medina-González, Gallardo-González Gallardo-González, Alcantar-Vallin Alcantar-Vallin, GĂłmez-Fregoso GĂłmez-Fregoso, Mendoza-Gaitán Mendoza-Gaitán, Arizaga-Nápoles Arizaga-Nápoles, Ivey-Miranda Ivey-Miranda, GarcĂa-GarcĂa GarcĂa-GarcĂa
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