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Ann Thorac Surg 2003;75:899-905
© 2003 The Society of Thoracic Surgeons


Original article: cardiovascular

Neutrophil CD11b upregulation during cardiopulmonary bypass is associated with postoperative renal injury

Christine S. Rinder, MDa,b*, Manuel Fontes, MDb, Joseph P. Mathew, MDb, Henry M. Rinder, MDa, Brian R. Smith, MDa Multicenter Study of Perioperative Ischemia (McSPI) Research Group

a Department of Laboratory Medicine, New Haven, Connecticut, USA
b Department of Anesthesiology, Yale University School of Medicine, New Haven, Connecticut, USA

Accepted for publication September 16, 2002.

* Address reprint requests to Dr Rinder, Department of Anesthesiology, Yale School of Medicine, PO Box 208051, 333 Cedar St, New Haven, CT 06520-8051, USA.
e-mail: christine.rinder{at}yale.edu

BACKGROUND: Renal injury remains a persistent complication of cardiopulmonary bypass (CPB) that, when sufficient to require dialysis, increases mortality eight-fold. The high prevalence of renal failure in sepsis and adult respiratory distress syndrome has been linked to the systemic inflammatory response associated with those disorders. We hypothesized that components of the inflammatory response to CPB may similarly contribute to post-CPB acute renal injury.

METHODS: Markers of leukocyte and platelet activation peri-CPB were measured in 75 patients undergoing cardiac operation with CPB and were correlated with acute renal injury, defined as an increase (>= 50%) in peak serum creatinine post-CPB.

RESULTS: Eleven patients sustained post-CPB acute renal injury. This subset of patients demonstrated significantly greater increases in neutrophil CD11b density (p = 0.01), as well as higher total neutrophil counts (p = 0.045), compared with patients with preserved renal function. Hemodynamic instability sufficient to require postoperative hemodynamic support also predicted an increased risk of acute renal injury. However, neutrophil CD11b upregulation did not correlate with this or any other clinical variables associated with renal risk, suggesting that this marker of the neutrophil inflammatory response may independently predict renal injury. By contrast other inflammatory markers, neutrophil myeloperoxidase levels, monocyte CD11b, base line C-reactive protein, and platelet CD62P expression did not differ between the two patient groups.

CONCLUSIONS: Upregulation of the neutrophil adhesion receptor CD11b and high circulating neutrophil numbers are associated with acute renal injury after CPB, suggesting a contribution by activated neutrophils to the pathophysiology of this complication.




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