Acute Kidney Injury in Critically Ill Children

Abstract

Acute kidney injury (AKI) (previously called acute renal failure) is characterized by the abrupt inability of the kidneys to adequately excrete waste products and regulate fl uid and electrolyte homeostasis appropriately. This results in an at least partially reversible increase in the blood concentration of creatinine and nitrogenous waste products. Renally eliminated medication will accumulate, and nephrotoxic drugs may provide a “second hit” to the already injured kidneys. Furthermore, fl uid management and nutrition will be hampered by oliguria. AKI is typically classifi ed as pre-renal, intrinsically renal, or post-renal. Pre-renal AKI may occur as a consequence of a reduced renal blood fl ow due to several conditions leading to intravascular volume depletion and/or compromised cardiac output. Since the kidneys are intrinsically normal, pre-renal injury is considered reversible once the hemodynamic conditions have been restored to normal. When pre-renal injury persists for a longer period of time, hypoperfusion of the kidneys will lead to hypoxic or ischemic acute tubular necrosis (ATN), a form of intrinsic AKI. During the evolution of pre-renal to intrinsically renal injury several compensatory pathways in the kidney are activated to maintain renal perfusion. These compensatory pathways include intra-renal generation of vasodilatory prostaglandins and angiotensin II, which increases eff erent arteriolar resistance, thereby increasing intraglomerular pressure to maintain or even raise the glomerular fi ltration rate. There are, however, certain clinical circumstances (e.g., administration of cyclo-oxygenase inhibitors, angiotensin converting enzyme inhibitors or nephrotoxic drugs) that may inhibit or interfere with one of the compensatory mechanisms and thus precipitate AKI . In intrinsic AKI, the pathology lies within the kidney itself. In the critically ill patient it is often caused by ATN or interstitial nephritis, elicited by a wide range of drugs or infectious agents. Other causes are glomerulonephritis and hemolytic uremic syndrome. Post-renal AKI is caused by an obstruction of the urinary outfl ow tract such as intraluminal obstruction due to urethral valves or coagulated blood, functional obstruction due to a neurogenic bladder or extraluminal obstruction which may result from malignant conditions. This form of AKI can be restored by removal of the actual obstruction or by insertion of a urinary deviation proximal to the obstruction. Altogether, AKI occurs with variable severity and in many clinical scenarios.