Direct peritoneal resuscitation reduces inflammation in the kidney after acute brain death.

Abstract

Brain death is associated with significant inflammation within the kidneys, which may contribute to reduced graft survival. Direct peritoneal resuscitation (DPR) has been shown to reduce systemic inflammation after brain death. To determine its effects, brain dead rats were resuscitated with normal saline (targeted intravenous fluid) to maintain a mean arterial pressure of 80 mmHg; DPR animals also received 30 cc of intraperitoneal peritoneal dialysis solution. Rats were euthanized at 0, 2, 4, and 6 h after brain death. Pro-inflammatory cytokines were measured using ELISA. Levels of IL-1β, TNF-α, and IL-6 in the kidney were significantly increased as early as 2 h after brain death and significantly decreased with DPR. Levels of leukocyte adhesion molecules ICAM and VCAM increased after brain death and were decreased with DPR (ICAM 2.33 ± 0.14 vs. 0.42 ± 0.04, P = 0.002; VCAM 82.6 ± 5.8 vs. 37.3 ± 1.9, P = 0.002 at 4 h) as were E-selectin and P-selectin (E-selectin 25,605 vs. 16,144, P = 0.005; P-selectin 82.5 ± 3.3 vs. 71.0 ± 2.3, P = 0.009 at 4 h). Use of DPR reduces inflammation and adhesion molecule expression in the kidneys, and is associated with reduced macrophages and neutrophils on immunohistochemistry. Using DPR in brain dead donors has the potential to reduce the immunologic activity of transplanted kidneys and could improve graft survival.