insults to the renal vasculature, glomeruli, or interstitium Causes of postrenal AKI include congenital or acquired anatomic obstructions of the urinary tract such as posterior urethral valves, stones, masses, and functional or anatomic bladder outlet obstruction TABLE 100.13 ESTIMATION OF GLOMERULAR FILTRATION RATE BY THE SCHWARTZ FORMULA C cr = k × L/S cr C cr = creatinine clearance in mL/min/1.73 m2 k a = proportionality constant L = length (cm) S cr = serum creatinine (mg/dL) ak values: Low–birth-weight infants during the first year of life = 0.33 Full-term babies during first year of life = 0.45 Children and adolescent girls = 0.55 Adolescent boys = 0.7 Adapted from Schwartz GJ, Feld LG, Langford DJ A simple estimate of glomerular filtration rate in full-term infants during the first year of life J Pediatr 1984;104:849–854; Schwartz GJ, Gauthier B A simple estimate of glomerular filtration rate in adolescent boys J Pediatr 1985;106:522–526; and Schwartz GJ, Haycock GB, Edelmann CM Jr, et al A simple estimate of glomerular filtration rate in children derived from body length and plasma creatinine Pediatrics 1976;58:259–263 Goals of Treatment The goals of treatment include mitigating and/or correcting any fluid or electrolyte disturbances resulting from AKI as well as removing the underlying cause, if possible Measures should be taken to induce nitrogenous waste elimination and achieve electrolyte homeostasis whether by the kidneys themselves or through RRT when needed Clinical Considerations Clinical recognition Children with AKI may present with a variety of complaints related either directly to kidney dysfunction or to the underlying cause itself Patients and caregivers may notice changes in the urine output or quality They may present with concern for changes in appearance or physical function related to volume overload Other presenting symptoms of AKI may be nonspecific such as malaise and nausea In other instances, the initial complaint will be related to an underlying systemic or infectious cause for the AKI Triage considerations AKI includes a wide spectrum of disease and severity Initial triage should be based on overall clinical appearance and hemodynamic stability Patients with hypertensive crisis, respiratory distress from volume overload, or life-threatening dysrhythmias from electrolyte disturbances warrant emergent stabilization Children with more mild presentations may undergo further evaluation into underlying causes at the onset Clinical assessment A thorough history is necessary to reveal the underlying etiology of AKI A detailed history of fluid balance should be obtained The quality and quantity of urine should be identified Recent medications should be reviewed to identify potential causes of drug-induced nephrotoxicity Important classes of medications that increase the risk for AKI include nonsteroidal anti-inflammatory drugs (NSAIDs), angiotensinconverting enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARBs), aminoglycoside antibiotics, and calcineurin inhibitors The patient should be evaluated for hypertension, and the physical examination should assess hydration status and perfusion as well as evaluate for edema and evidence of third spacing The patient’s weight should be compared to a “dry weight” or recent weight prior to the onset of illness, when possible The examination may reveal signs of systemic vasculitis associated with nephritis, such as rashes or arthritis The presence of a palpable bladder or mass, which may be compressing the urinary tract or stemming from the kidneys themselves, should be assessed for during the abdominal examination Laboratory assessment of AKI serves two purposes First, it should determine the severity of renal dysfunction and identify associated electrolyte, metabolic, or hematologic abnormalities, which may require urgent intervention Secondly, a focused investigation should be aimed at determining the underlying cause of AKI based on the clinical presentation of the patient Initial serum laboratory studies should include serum creatinine, electrolytes, and complete blood cell counts Children with AKI may demonstrate hyperkalemia, hypo- or hypernatremia, AG acidosis, hypocalcemia, and/or hyperphosphatemia depending on the degree of dysfunction and the chronicity of the underlying etiology Serial assessment of renal function and electrolytes will be required to determine the disease course and to monitor for the development of electrolyte derangements and changes in renal function Although the results may not affect the course of management within the ED, laboratory studies aimed at assessing for an underlying cause may assist specialists with treatment in a more rapid fashion In cases of suspected glomerulonephritis, serum complement studies, serologic testing for streptococcal infection, and autoimmune antibodies such as antinuclear, anti-DNA, antineutrophil cytoplasmic, and antiglomerular basement (anti-GBM) antibodies may be considered in conjunction with specialist consultation Initial urine studies should include urinalysis with microscopic assessment An elevated urine specific gravity may be consistent with prerenal physiology The presence of nitrite or leukocyte esterase suggests a urinary tract infection Detection of large heme by dipstick is found in glomerulonephritis and myoglobinuria, and differentiation between these two disorders relies upon the presence or absence of red blood cells in the urine sediment, respectively Heavy proteinuria by dipstick, which detects albumin excretion, would be suggestive of glomerular disease and should be followed by a quantitative urine protein to creatinine ratio (normal less than 0.2, nephrotic range greater than to 3) Microscopic examination of the urine sediment may be normal or nearly normal, consistent with prerenal AKI and some cases of acute tubular necrosis (ATN) ATN may also be associated with granular, muddy brown, and/or tubuloepithelial cell casts The finding of red blood cell casts is pathognomonic of glomerulonephritis, and concomitant white blood cells or white blood cell casts would be consistent with an exudative nephritis such as postinfectious glomerulonephritis or renal vasculitis Urine sediment associated with acute interstitial nephritis (AIN) varies and includes microscopic hematuria, sterile pyuria, and white blood cell casts The degree of proteinuria associated with AIN is also variable, though is typically not severe except in nonsteroidal anti-inflammatory drug (NSAIDS)-induced AIN, which may be associated with nephrotic range proteinuria If interstitial nephritis is suspected, the urine should be evaluated for the presence of eosinophils, though sensitivity and specificity of urine eosinophilia is limited An assessment of urine chemistries may also be useful in distinguishing prerenal AKI from ATN, and initial studies to consider include urine electrolytes and urine creatinine The fractional excretion of sodium (FENa) is calculated as follows: FENa (%) = [(urine Na × serum creatinine)/(serum Na × urine creatinine)] × 100 In general, a value below 1% suggests prerenal disease and reflects reabsorption of almost all of the filtered sodium to maintain intravascular volume, an appropriate response to decreased renal perfusion A value greater than 2% is consistent with ATN or other tubular disorders Of note, the FENa may be less than 1% in normal subjects reflecting normal tubular handling of sodium in the setting of relatively low sodium intake It may also be low in some cases of AIN, postischemic ATN, and acute glomerulonephritis The fractional excretion of urea is similarly calculated as the FENa with substitution of urine urea nitrogen and BUN and is generally less than 35% in prerenal states Diuretics increase urine sodium excretion but have less effect on urea excretion Therefore, the FENa may be less reliable and the fractional excretion of urea more informative if diuretics have been provided prior to the collection of urine Radiographic assessment should be considered in all patients with AKI of unclear etiology This is most certainly true in those who present with acute anuria, as urinary tract obstruction is a possible etiology and would require intervention Given its safety and general availability, ultrasonography of the kidneys and urinary tract should be considered in all children with AKI Ultrasound can provide assessment of the renal parenchyma and may identify conditions of acquired or congenital obstruction of the urinary tract Doppler investigation of the renal vessels should be performed if there is concern for vascular compromise or thrombosis, though further imaging may be necessary, given the limitations of this modality Management The initial management of AKI in the ED is largely supportive and should focus on addressing fluid or electrolyte abnormalities while avoiding further renal insult If prerenal physiology is suspected, appropriate volume resuscitation with isotonic fluids should be provided