Acute Kidney Injury

Christine B. Sethna

Nataliya Chorny

Smarika Sapkota

James Schneider

KEY POINTS

Acute kidney injury (AKI) is common during critical illness and is associated with significant morbidity and mortality.

AKI is defined by the pRIFLE criteria: graded levels of risk assessment (risk, injury, failure) and outcomes (loss and end-stage renal disease).

The incidence of AKI is rising primarily because of increased use of intensive care and advanced technologies such as cardiac surgery, bone marrow transplantation, and care of very low-birth-weight premature infants.

In the intensive care unit, the most common etiologies of AKI are sepsis, multiple organ dysfunction syndrome, cardiac surgery, and nephrotoxic medication.

Biomarkers may aid in early diagnosis and prevention.

The etiology of AKI is classified into categories of prerenal, intrinsic, and postrenal.

Treatment of AKI is largely supportive and includes optimizing renal perfusion through fluid management and avoidance of nephrotoxins.

Pediatric acute kidney injury (AKI) in the intensive care unit (ICU) is a dynamic process that is multifactorial and complex. Traditionally, AKI is classified into three categories based on the anatomical location of the injury: prerenal AKI, intrinsic renal AKI, and postrenal AKI. Prerenal AKI results from decreased perfusion to the kidney either from volume depletion or decreased circulating volume. Intrinsic AKI is characterized by kidney dysfunction from injury to the glomerular, tubular, or vascular structures of the kidney. Postrenal AKI is caused by obstruction of the lower urinary tract. Despite the growing understanding of the causes and mechanisms of AKI development, very few preventive and therapeutic measures exist.

The clinical landscape of AKI has undergone a dramatic change in recent years. The incidence of pediatric AKI is continuously rising and the etiology of disease has shifted due to the increased use of intensive care and advanced technologies.

AKI is a known independent risk factor for increased mortality and morbidity in critically ill children. Therefore, a focus on preventive and therapeutic strategies is paramount. The discovery of early biomarkers is opening up an exciting new era in the diagnosis of AKI. Hopefully, this advance in diagnostic markers will lead to an improvement in prevention and intervention for patients with AKI.

DEFINITION OF AKI

AKI, formerly known as acute renal failure (ARF), is defined as the abrupt onset of renal dysfunction resulting from injurious endogenous or exogenous processes characterized by a decrease in glomerular filtration rate (GFR) and an increase in serum creatinine. This leads to an inability to regulate acid and electrolyte balance as well as failure to excrete waste and fluid. There has been a shift in terminology from “ARF” to “AKI” in order to more accurately describe renal dysfunction as a continuum rather than an absolute failure in kidney function. More than 30 definitions of AKI that appeared in published literature prior to 2004 resulted in variations in the reported incidence and morbidity and mortality rates for AKI (1). To overcome this, standardized definitions for AKI

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