The regulation of ischemic acute renal failure by extrarenal organs

Purpose of review: Recent work suggests that extrarenal organs, such as the liver, lung, spleen, brain, lymphoid tissues, and bone marrow, regulate acute renal failure. We now review several examples of such regulation. Recent findings: First, we demonstrate kidney-liver crosstalk during ischemic renal failure. Renal ischemia induces the renal production of interleukin 6 and the renal expression of interleukin 10 receptors; interleukin 6 stimulates the production of interleukin 10 by the liver; interleukin 10 ameliorates renal injury. The potential mechanisms of interleukin 6 and 10 are discussed. Second, we review the possible effects of the acute phase response on renal ischemic injury. We point out potential analogies between the recently reported association of increased interleukin 6 and C-reactive protein with myocardial ischemia, and renal ischemia. Third, we briefly review the salutary effects of hepatocyte growth factor, produced by the lung, spleen, and liver, on ischemic renal injury. Finally, we discuss how renal ischemia elicits an inflammatory response of neutrophils, macrophages, and T cells that may exacerbate the injury. Granulocyte-colony stimulating factor, produced by the kidney in response to ischemia, may participate in eliciting this inflammation. Such inflammation may be exacerbated by cytokines and growth factors released by the brain after traumatic injury. Summary: We discuss the existing evidence for extrarenal regulation of acute renal failure. This suggests that concurrent disease of those extrarenal organs might alter the course of acute renal failure.