Rubin Tuder

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Effects of acid aspiration-induced acute lung injury on kidney function.

Jeffrey B Hoag; Manchang Liu; R Blaine Easley; Martin F Britos-Bray; Priya Kesari; Heitham Hassoun; Mark Haas; Rubin M Tuder; Hamid Rabb; Brett A Simon (Profiled Authors: Rubin Tuder; Ronald Easley; Mark Haas; Manchang Liu; Heitham Hassoun; Hamid Rabb; Bret Simon)

Dept. of Medicine and Anesthesiology, The Johns Hopkins Univ., 600 North Wolfe St., Tower 711, Baltimore, MD 21287-8711, USA.
American journal of physiology. Renal physiology 2008;294(4):F900-8.

Acute lung injury (ALI) in combination with acute kidney injury carries a mortality approaching 80% in the intensive care unit. Recently, attention has focused on the interaction of the lung and kidney in the setting of ALI and mechanical ventilation (MV). Small animal models of ALI and MV have demonstrated changes in inflammatory mediators, water channels, apoptosis, and function in the kidney early in the course of injury. The purpose of this investigation was to test the hypothesis that ALI and injurious MV cause early, measurable changes in kidney structure and function in a canine HCl aspiration model of ALI when hemodynamics and arterial blood gas tensions are carefully controlled. Intratracheal HCl induced profound ALI as demonstrated by increased shunt fraction and airway pressures compared with sham injury. Sham-injured animals had similar mean arterial pressure and arterial Pco(2) and HCO(3) levels compared with injured animals. Measurements of renal function including renal blood flow, urine flow, serum creatinine, glomerular filtration rate, urine albumin-to-creatinine ratio, and kidney histology scores were not different between groups. With maintenance of hemodynamic parameters and alveolar ventilation, ALI and injurious MV do not alter kidney structure and function early in the course of injury in this acid aspiration canine model. Kidney injury in large animal models may be more similar to humans and may differ from results seen in small animal models.

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