title: Cytokine elevation and transaminitis after laparoscopic donor nephrectomy.
abstract: Acute kidney injury frequently occurs in the critically ill and often progresses into multiorgan dysfunction syndrome, resulting in high mortality. We previously showed that nephrectomized mice had increased interleukin (IL)-6 and tumor necrosis factor (TNF)-α that directly contributed to systemic inflammation and hepatic injury. In this study, we examined whether patients undergoing laparoscopic donor nephrectomy have increased postoperative cytokine levels with injury to the liver and whether the remaining kidney sustains injury. Serial serum and urine samples were collected from 32 patients undergoing laparoscopic donor nephrectomy and 17 patients undergoing nonrenal laparoscopic surgery. Serum IL-6, IL-18, TNF-α and monocyte chemotactic protein-1 (MCP-1) (markers of systemic inflammation) and urinary neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), MCP-1, and IL-18 (markers of acute kidney injury) were quantified by enzyme-linked immunosorbent assay. We also analyzed serum creatinine, aspartate transaminase (AST), and alanine transaminase to assess liver injury. Patients who underwent donor nephrectomy not only demonstrated increased serum creatinine but also had significant increases in serum IL-6, MCP-1, and AST. Serum TNF-α also trended upward in donor nephrectomy patients. Finally, the donor nephrectomy group showed increased urinary NGAL but not KIM-1 at 24 h. Taken together, our findings of increased serum IL-6, MCP-1, and AST after donor nephrectomy suggest that an acute reduction of kidney function induces systemic inflammation and may have distant effects on the liver. Further studies are needed to correlate increased urinary NGAL after donor nephrectomy both as a potential marker for renal tubular stress and/or hypertrophy in the contralateral kidney.
authors.affiliation: Department of Anesthesiology, College of Physicians and Surgeons of Columbia University, New York, NY 10032-3784, USA.
authors.forename: Steven
authors.initials: S
authors.lastname: Yap
authors.forename: Sang Won
authors.initials: SW
authors.lastname: Park
authors.forename: Brian
authors.initials: B
authors.lastname: Egan
authors.forename: H Thomas
authors.initials: HT
authors.lastname: Lee
mesh_terms: D058186:Acute Kidney Injury / Q000097:blood / Q000453:epidemiology / Q000652:urine; D000209:Acute-Phase Proteins; D000328:Adult; D001219:Aspartate Aminotransferases / Q000097:blood*; D015415:Biomarkers / Q000097:blood / Q000652:urine; D016022:Case-Control Studies; D018932:Chemokine CCL2 / Q000097:blood*; D003404:Creatinine / Q000097:blood; D005260:Female; D005919:Glomerular Filtration Rate / Q000502:physiology; D000072596:Hepatitis A Virus Cellular Receptor 1; D006801:Humans; D020382:Interleukin-18 / Q000097:blood* / Q000652:urine; D015850:Interleukin-6 / Q000097:blood* / Q000652:urine; D016030:Kidney Transplantation; D010535:Laparoscopy; D000071068:Lipocalin-2; D054834:Lipocalins / Q000097:blood; D008107:Liver Diseases / Q000097:blood / Q000453:epidemiology / Q000652:urine; D019520:Living Donors; D008297:Male; D008562:Membrane Glycoproteins / Q000097:blood; D008875:Middle Aged; D009392:Nephrectomy; D011184:Postoperative Period; D011518:Proto-Oncogene Proteins / Q000097:blood; D011991:Receptors, Virus / Q000097:blood; D012307:Risk Factors; D014409:Tumor Necrosis Factor-alpha / Q000097:blood* / Q000652:urine
chemical_list: D000209:Acute-Phase Proteins; D015415:Biomarkers; C111835:CCL2 protein, human; D018932:Chemokine CCL2; C491143:HAVCR1 protein, human; D000072596:Hepatitis A Virus Cellular Receptor 1; D020382:Interleukin-18; D015850:Interleukin-6; C489506:LCN2 protein, human; D000071068:Lipocalin-2; D054834:Lipocalins; D008562:Membrane Glycoproteins; D011518:Proto-Oncogene Proteins; D011991:Receptors, Virus; D014409:Tumor Necrosis Factor-alpha; D003404:Creatinine; D001219:Aspartate Aminotransferases