• Bertrand L Jaber, Brian J G Pereira, Joseph V Bonventre, and Vaidyanathapuram S Balakrishnan.
• Division of Nephrology, Caritas St. Elizabeth's Medical Center, Boston, Massachusetts 02135, USA. Bertrand_jaber@cchcs.org
• Kidney Int. 2005 Jan 1; 67 (1): 14-33.

AbstractAcute inflammatory disorders are the result of an interaction between genetic and environmental factors, and are often characterized by an imbalance between pro- and anti-inflammatory host immune responses. Over the past decade, polymorphisms of host response genes have been explored as genetic risk and prognostic markers in the course and severity of acute inflammatory disorders. Increasing evidence supports an important role for inflammatory mechanisms in the pathogenesis of acute renal failure (ARF) following both ischemic and nephrotoxic injury. The use of genetic epidemiology may become a useful tool to identify patients with an altered susceptibility to developing hospital-acquired ARF, and stratify those who may benefit from preventive therapies that modulate host immune responses in a favorable way. This review summarizes the existing experimental and clinical studies supporting the role of inflammation in ARF and critically appraises studies that have examined polymorphism of immune response genes as potential determinants of susceptibility to and severity of acute inflammatory disorders. Conclusions are drawn on the application of genetic epidemiology to the field of ARF and the rationale for further research on the role of genetic markers in ARF.

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