ACUTE RENAL FAILURE
Acute renal failure (ARF), also known as “acute kidney injury” (AKI), is a reversible acute decline in renal function with rapid onset (Devarajan, 2017). The most extensively used and standardized definitions for pediatric ARF are pediatric RIFLE (pRIFLE; risk for renal dysfunction, injury to the kidney, failure of kidney function, loss of kidney function, and end-stage renal disease), Acute Kidney Injury Network (AKIN), and kidney disease improving global outcomes (KDIGOs) classifications (Sutherland et al., 2015). ARF is marked by a decrease in glomerular filtration rate, an inability of the kidneys to regulate fluid and electrolyte homeostasis as well as an increase in serum creatinine and blood urea nitrogen levels (Andreoli, 2009). The exact incidence of pediatric ARF is unknown. Nursing care of pediatric patients with ARF focuses on determination and treatment of the underlying cause of ARF along with early medical management.
The incidence of ARF is rising in relation to increased use of advanced medical technology for children who are critically ill or experience chronic conditions (Devarajan, 2017). Worldwide, one in three children experience ARF during an occurrence of hospitalization (Susantitaphong et al., 2013). Pediatric ARF can arise from multiple causes with clinical manifestations that range from minimal elevation in serum creatinine to anuric renal failure (Devarajan, 2017).
The pathophysiology behind an acute kidney insult is classified into three phases: development, extension, and resolution. During the development phase, a kidney insult leads to injury and may be subclinical (Hayes, 2017). Repair processes commence during the extension phase. Adaptive repair results in correction of the renal structure without long-term consequence (Hayes, 2017). Maladaptive repair often results in change of renal structure and in turn reduced kidney function (Hayes, 2017). Net result of renal injury and repair are represented in the extension phase (Hayes, 2017). Overall, renal recovery results from adaptive repair whereas progression leads to change in kidney function and/or structure that can be detected by histopathology, imaging studies, or biomarkers (Basile et al., 2016).
Diagnosis of ARF is based on characteristic signs and symptoms: edema, decreased urine output, hematuria, hypertension, and laboratory results. Diagnosis of ARF by laboratory results is based on serum creatinine levels. Normal serum creatinine level for an infant is 0.2 to 0.4 mg/dL, 18 to 35 µmol/L (Devarajan, 2017). Diagnostic use of serum creatinine levels can present issues. ARF serum creatinine is an insensitive and delayed measure of decreased kidney 10function as serum creatinine may not increase until a 50% or higher reduction in glomerular filtration rate is present (Andreoli, 2009; Devarajan, 2017). Additionally, if dialysis is initiated as a treatment, serum creatinine levels cannot be measured accurately. An abnormal urinalysis can also indicate ARF. Although individuals with prerenal ARF may display a normal urinalysis, urinalysis is most often used to determine the underlying cause of ARF. Regardless of the limitations posed by serum creatinine levels in the diagnosis of ARF, it is presently the best laboratory test for diagnosis in pediatrics.
The risk of ARF is highest among children cared for in an intensive care unit (Devarajan, 2017). Pediatric patients requiring critical care or dialysis have the highest ARF mortality rates (Sutherland et al., 2015