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<p>Severe thrombocytopenia frequently occurs in patients with sepsis in the intensive care unit (ICU) and carries a poor prognosis. The safety of prophylactic platelet transfusion in the absence of active bleeding remains debatable. As platelets possess pro-inflammatory and prothrombotic properties, we hypothesized that transfusion may contribute to renal microcirculatory injury and acute kidney injury (AKI). We evaluated whether platelet transfusion and its cumulative dose were independently associated with AKI and mortality in sepsis. We conducted a retrospective cohort study using the Medical Information Mart for Intensive Care IV (MIMIC-IV) database (2008–2019). Adults meeting Sepsis-3 criteria with platelet counts below 50 × 10^9/L and no active bleeding were eligible. Patients were classified based on whether they received platelets within 48&#xa0;h of sepsis onset. The primary endpoint was stage 2 or higher AKI (Kidney Disease: Improving Global Outcomes [KDIGO] creatinine criteria, 7-day window), and the secondary endpoint was 30-day all-cause mortality. We used propensity score matching (PSM) and multivariate logistic regression to account for confounding factors and performed multiple sensitivity analyses to evaluate robustness. Of 1,413 patients included (640 transfused, 773 not), AKI was more frequent in the transfusion group after PSM (64.9% vs. 55.3%; <i>p</i> = 0.004; adjusted odds ratio [aOR] 1.55, 95% confidence interval [CI] 1.15–2.09). A borderline dose-response trend was observed (aOR 1.03 per 1 mL/kg; <i>p</i> = 0.037), and restricted cubic splines confirmed the linearity (nonlinearity <i>p</i> = 0.72). Transfusion was not associated with 30-day mortality after adjustment (<i>p</i> = 0.877). The direction of the AKI association was consistent across all 12 sensitivity analyses (odds ratio [OR] range 1.12–1.55), including a landmark analysis that excluded patients with AKI onset before their first transfusion (aOR 1.32, <i>p</i> = 0.044) and pooled estimates from 36 multiply imputed datasets using Rubin’s rules (aOR 1.37, <i>p</i> = 0.020). When we adjusted for concurrent red blood cell transfusion, the platelet-AKI association was attenuated (aOR 1.24, <i>p</i> = 0.132), indicating that co-transfusion was a relevant confounder. Prophylactic platelet transfusion in patients with sepsis and severe thrombocytopenia was associated with a higher AKI risk across several analytic approaches. However, the attenuation after blood product adjustment and the limitations inherent to retrospective data prevent us from drawing causal conclusions. These results argue for caution with liberal transfusion and support the need for prospective investigations.</p>

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Association between platelet transfusion and acute kidney injury in septic patients with severe thrombocytopenia

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  • 发表日期：

    2026年8月5日

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  • Yusuf Karanci,
  • Fulya Ciyiltepe

摘要

Severe thrombocytopenia frequently occurs in patients with sepsis in the intensive care unit (ICU) and carries a poor prognosis. The safety of prophylactic platelet transfusion in the absence of active bleeding remains debatable. As platelets possess pro-inflammatory and prothrombotic properties, we hypothesized that transfusion may contribute to renal microcirculatory injury and acute kidney injury (AKI). We evaluated whether platelet transfusion and its cumulative dose were independently associated with AKI and mortality in sepsis. We conducted a retrospective cohort study using the Medical Information Mart for Intensive Care IV (MIMIC-IV) database (2008–2019). Adults meeting Sepsis-3 criteria with platelet counts below 50 × 10^9/L and no active bleeding were eligible. Patients were classified based on whether they received platelets within 48 h of sepsis onset. The primary endpoint was stage 2 or higher AKI (Kidney Disease: Improving Global Outcomes [KDIGO] creatinine criteria, 7-day window), and the secondary endpoint was 30-day all-cause mortality. We used propensity score matching (PSM) and multivariate logistic regression to account for confounding factors and performed multiple sensitivity analyses to evaluate robustness. Of 1,413 patients included (640 transfused, 773 not), AKI was more frequent in the transfusion group after PSM (64.9% vs. 55.3%; p = 0.004; adjusted odds ratio [aOR] 1.55, 95% confidence interval [CI] 1.15–2.09). A borderline dose-response trend was observed (aOR 1.03 per 1 mL/kg; p = 0.037), and restricted cubic splines confirmed the linearity (nonlinearity p = 0.72). Transfusion was not associated with 30-day mortality after adjustment (p = 0.877). The direction of the AKI association was consistent across all 12 sensitivity analyses (odds ratio [OR] range 1.12–1.55), including a landmark analysis that excluded patients with AKI onset before their first transfusion (aOR 1.32, p = 0.044) and pooled estimates from 36 multiply imputed datasets using Rubin’s rules (aOR 1.37, p = 0.020). When we adjusted for concurrent red blood cell transfusion, the platelet-AKI association was attenuated (aOR 1.24, p = 0.132), indicating that co-transfusion was a relevant confounder. Prophylactic platelet transfusion in patients with sepsis and severe thrombocytopenia was associated with a higher AKI risk across several analytic approaches. However, the attenuation after blood product adjustment and the limitations inherent to retrospective data prevent us from drawing causal conclusions. These results argue for caution with liberal transfusion and support the need for prospective investigations.