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Kidney Week

Abstract: FR-PO0390

Monocyte Imbalance Predicts AKI After Pulmonary Endarterectomy in Patients with Chronic Thromboembolic Pulmonary Hypertension

Session Information

Category: Acute Kidney Injury

  • 102 AKI: Clinical, Outcomes, and Trials

Author

  • Mohammed, Bilal Khan, Northwestern University Feinberg School of Medicine, Chicago, Illinois, United States
Background

Acute kidney injury (AKI) is a common and serious complication after pulmonary thromboendarterectomy (PTE) for chronic thromboembolic pulmonary hypertension (CTEPH), yet the perioperative immune mechanisms driving its onset remain undefined. This study evaluated whether early innate immune dysregulation predicts postoperative AKI in patients undergoing PTE.

Methods

Ten consecutive PTE patients were prospectively profiled (n=3 developed AKI; n=7 did not). Simultaneous pulmonary arterial (PA) and systemic blood samples were collected pre-incision (Pre-Cx), post-clamp release (Post-Cx), and on postoperative days (POD) 1 and 2. Peripheral blood mononuclear cells were isolated by density gradient centrifugation and analyzed by flow cytometry to quantify monocyte subsets [classical (CM), intermediate (INT-M), and non-classical (NCM)] and neutrophils. Neutrophil-to-monocyte ratios (N:M, N:CM, N:INT-M, N:NCM) were derived. Statistical analyses included Mann–Whitney U, permutation analysis, Cliff’s delta, bootstrap confidence intervals, and two-way ANOVA for group × time interactions. Clinical data (hemodynamics, chronicity, reperfusion lung injury, ICU/hospital stay) were compared between groups.

Results

AKI patients had lower preoperative SvO2(60 ± 12% vs 70 ± 6%, p=0.049) and longer ICU (20 ± 17 vs 6 ± 3 days, p=0.049) and hospital stays (26 ± 20 vs 9 ± 3 days, p=0.038). CM counts showed a significant group × time interaction (p=0.017), with blunted recovery in AKI. INT-M expansion was exaggerated (p=0.04), while NCM declined in both groups. On POD-1, AKI patients exhibited marked increases in N:M (+1.24), N:INT-M (+7.7), and N:NCM (+484) ratios (Cliff’s δ ≥0.7, p=0.03), normalizing by POD-2.

Conclusion

Failure of monocyte recovery and transient neutrophil–monocyte imbalance characterize postoperative AKI after PTE in CTEPH. These immune shifts identify a distinct perioperative inflammatory phenotype that may enable early AKI risk stratification and guide targeted interventions after pulmonary thromboendarterectomy.