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Critical care medicine

August 3, 2026 · via Europe PMC

H3.1 Nucleosomes to Predict Renal Replacement Therapy and Mortality in Sepsis-A Secondary Analysis of the SISPCT Randomized Control Trial.

Neumann C, Bloos F, Hla TTW, +7 more, SepNet Critical Care Trials Group.

Randomized Controlled TrialOpen access

AI summary — for doctors, generated from the abstract only

Higher admission H3.1 nucleosome levels were associated with mortality and kidney injury requiring renal replacement therapy in sepsis.

What was studied

Secondary analysis of the SISPCT trial across 33 German ICUs, measuring plasma H3.1 nucleosomes in 971 patients (927 with RRT data) and relating them to 28-day mortality and time to RRT with Cox regression.

Key findings

  • 443 patients (45.6%) had sepsis and 520 (53.6%) had septic shock
  • Admission H3.1 was higher in septic shock than sepsis (median 921.84 vs 432.71 ng/mL)
  • Elevated H3.1 was associated with mortality and AKI requiring RRT (hazard ratios are not shown because the abstract is cut off)

Clinical relevance

H3.1 nucleosomes may help identify sepsis patients at risk of kidney failure and death, as a research biomarker.

Who should care

Critical Care MedicinePediatric Critical CareEmergency Medicine

Limitations

Secondary analysis of a trial from 2009-2013, no effect sizes in the abstract, and not tested as a clinical decision tool.

A neutrophil extracellular trap marker shows prognostic promise in sepsis.

This is an AI-generated summary of the published abstract, not a clinical recommendation. It may not reflect the full text or subsequent updates — verify against the original source before acting on it.

Abstract

Objectives

The release of neutrophil extracellular traps is a key immune host defense mechanism that can contribute to organ damage during sepsis if excessive. We evaluated presentation H3.1 nucleosome levels in patients with sepsis, septic shock, and sepsis-associated acute kidney injury (AKI). We sought to determine if plasma H3.1 nucleosome levels could serve as predictive biomarkers for both renal replacement therapy (RRT) requirements and 28-day mortality.

Design

A secondary analysis of prospectively collected samples from the large multicenter Effect of Sodium Selenite Administration and Procalcitonin-Guided Therapy on Mortality in Patients with Severe Sepsis or Septic Shock (SISPCT) trial.

Setting

Patients from 33 ICUs in Germany recruited between November 6, 2009, and June 6, 2013, including a 90-day follow-up period.

Patients

A total of 971 patients with complete data on plasma H3.1 admission levels with sepsis and septic shock, and 927 patients with complete data on RRT requirements.

Interventions

None.

Measurements and main results

We evaluated associations between H3.1 levels and mortality and the time to commencement of RRT using multivariable Cox regression. A total of 443 patients (45.6%) presented with sepsis, and 520 patients (53.6%) had septic shock. Admission H3.1 levels were higher in patients with septic shock than sepsis (median, 921.84 vs. 432.71 ng/mL; p < 0.001). In a multivariable analysis for 28-day mortality, a one unit increase in log10 H3.1 levels was associated with a 48% increase in 28-day mortality (adjusted hazard ratio [HR], 1.48, 95% CI, 1.07-2.04; p = 0.02). Plasma H3.1 was also higher in patients with stage 3 AKI requiring RRT with septic shock vs. sepsis (1832 vs. 801.4 ng/mL; p = 0.01). In a multivariable Cox regression controlling for maximum lactate, procalcitonin, and C-reactive protein levels, plasma H3.1 levels were significantly higher in patients who developed AKI requiring RRT when compared with patients who did not develop AKI, with one log10 increase of H3.1 increasing the risk of 28-day RRT by 80% (adjusted HR, 1.8; 95% CI, 1.34-2.40; p < 0.001).

Conclusions

Elevated levels of H3.1 nucleosomes at admission are associated with mortality and AKI requiring RRT.

Trial registration

The trial was registered in clinicaltrials.gov , identifier: NCT00832039.

DOI

10.1097/ccm.0000000000007270

PMID

42545097

PMCID

PMC13632813

Research metadata (titles, abstracts, authors, publication dates) is sourced from Europe PMC, which aggregates content from PubMed/MEDLINE, PubMed Central, and other providers under the U.S. National Library of Medicine (NLM/NCBI). NLM does not claim copyright on abstracts; the original journal publishers or authors may hold rights to the full articles. AI-generated summaries are derived only from the abstract, never the full text, and are always labeled as AI-generated.

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