Renal replacement therapy

Abstract

Endogenous toxins accumulate in blood as a result of many biochemical processes.1 If their concentration exceeds certain levels, they cause illness. Some toxins are volatile (e.g., CO2, ketones) and can be excreted by the lungs through ventilation; others are lipophilic (e.g., bile acids, bilirubin) and can be excreted by the liver via the biliary system; yet others are water soluble and nonvolatile and are excreted by the kidneys. 2 When acute kidney injury (AKI) occurs, these water-soluble substances (potassium, phosphate, urea, creatinine) and endogenous toxins (methylguanidine, guanidinosuccinic acid, hippuric acid, uric acid, phenols, beta-2 microglobulin, purines, myo-inositol, etc.), which are normally excreted by the kidney, accumulate in blood. If accumulation progresses, AKI becomes severe; and if their removal is not addressed by either renal recovery or the initiation of artificial renal replacement therapy, the patient dies from uncontrolled hyperkalemia or uremia. Unfortunately, AKI requiring renal replacement therapy (RRT) is relatively common in critically ill patients treated in the intensive care unit (ICU) and involves close to 5% of all admissions.3 When a decision is made that artificial renal replacement therapy is needed, the physician has a variety of techniques at his/her disposal: intermittent hemodialysis (IHD), continuous renal replacement therapy (CCRT), slow extended daily dialysis (SLEDD), and peritoneal dialysis, each with its technical variations. All of these techniques rely on the principle that unwanted solutes and water can be removed through a semipermeable membrane-based separating process. The principles of such process have been extensively studied and described.4,5 © 2010 Springer-Verlag US.