History, physical examination, and basic studies usually allow proper classification of the child with AKI (Table 1652). Prerenal azotemia is characterized by precipitating factors and oliguria. Intrinsic tubular injury is associated with precipitating factors but urine output may be low, normal, or high, depending on the severity of the injury. Glomerular and vascular disorders may present with hematuria, edema, hypertension, and oliguria. The urine output with postrenal AKI may be low or normal and may be associated with flank masses or a distended bladder on examination. Depending on the underlying cause and severity of illness, AKI can be associated with signs of dehydration or volume overload.
A urinalysis (UA) should be obtained in all children with AKI.In prerenal azotemia, the UA is unremarkable with a high specific gravity reflecting appropriate renal retention of water in thesetting of renal hypoperfusion. However neonates are not able
Urethral obstruction (stricture, posterior urethral valves) Ureteral obstruction Ureterocele Extrinsic tumor compressing bladder outlet Neurogenic bladder (myelomeningocele, spinal cord injury)
Acute tubular necrosis Nephrotoxins (medications, contrast, myoglobin) Infection (sepsis) Interstitial nephritis Glomerular injury (primary glomerulonephritis, vasculitis, hemolytic uremic syndrome) Vascular (renal vein thrombosis, arterial emboli, malignant hypertension) to concentrate urine as well. With intrinsic tubular injury andpostrenal AKI, the UA may show mild hematuria and/or proteinuria with a specific gravity of 1.015 or less. With glomerularand vascular injury, the amount of hematuria and proteinuriais usually moderate to severe. In oliguric states, differentiationbetween prerenal azotemia and acute tubular necrosis may beaided by determining the urine osmolality and fractional excretionof sodium (see Table 165-2). Renal ultrasound is often helpful in determining the AKI category (see Table 165-2). Renal biopsy is indicated in select cases only.
Common electrolyte abnormalities seen with AKI includehyperkalemia, metabolic acidosis, hypocalcemia, and hyperphosphatemia. These labs may need to be monitored frequently,depending on the initial results and clinical course. A complete blood count should be obtained as anemia is frequentlyobserved. Other studies may be obtained as clinically indicated.
In some cases the underlying disorder can be treated. Examples include volume repletion in dehydration, stopping an offending nephrotoxic medication, and relieving urinary tract obstruction. In all cases efforts should be made to limit additional renal injury (e.g., ensuring adequate renal perfusion and avoiding nephrotoxic medications). Medication dosages should be adjusted for decreased renal function as appropriate.
Fluid therapy depends on the volume status and urine output. If hypovolemia is present, intravascular volume should be expanded by intravenous administration of saline. If hypervolemia is present, 1 to 2 mg/kg of furosemide and fluid restriction may be attempted. If the patient is relatively euvolemic, then the total fluid input should be adjusted to meet the total
Urine output Low Low, normal, or high Low or normal
Urinalysis Normal RBCs, WBCs, protein, casts Variable
Urine Na+ (mEq/L) <15 <20–30 >40 >50 Variable, may be >40
FENa* (%) <1 <2.5 >2 >2.5 Variable, may be >2
Urine osmolality >500 >350 ∼300 ∼300 Variable, may be (mOsm/L)
Renal ultrasound Normal Increased echogenicity, decreased Hydronephrosis corticomedullary differentiation