Sorbents in acute renal failure and the systemic inflammatory response syndrome

Renal replacement therapy in acute renal failure is currently focused on the use of modifications of dialysis (continuous arteriovenous hemofiltration and hemodiafiltration) to remove middle molecular weight toxins, Introduction Acute renal failure is manifested by the sudden cessation of renal function, retention of products of protein and mineral metabolism, alterations in fluid and acid-base homeostasis, and extremely high mortality. The latter has remained virtually unchanged over the last 30 years [1, 2], and has only been altered recently by advances in dialysis techniques [3] requiring large volumes of substitution fluid in the process of hemodiafiltration. The leading cause of acute renal failure and admission to the ICU in the USA is sepsis, with over 750,000 cases per annum an consisting of small proteins, and cytolkines involved in absolute mortality rate of 28.6%, and a projected annual the systemic inflammatory response syndrome (SIRS). Conventional high-flux dialyzers are not efficient at removing these molecules, prompting the investigation of sorbents to augment or replace dialysis. Sorbents have been developed to modulate SIRS by targeting cytokines such as IL-1, IL-6, IL-10, IL-18 and TNF, among others. Extensive pre-clinical studies are underway to demonstrate the clinical utility and safety of either adding sorbent hemoadsorption devices to hemodialysis, or the use of such devices alone in SIRS, sepsis, acute renal failure, cardiopulmonary bypass and end-stage renal disease. Copyright (C) 2003 S. Karger AG, Basel.