FENa, Fractional excretion of sodium; RBCs, red blood cells; WBCs, white blood cells. *FENa (%) = [(urine sodium/plasma sodium) ÷ (urine creatinine/plasma creatinine)] × 100.
output, which may be higher or lower than normal, depending on the urine output. Assessment of intake and output should be augmented with serial measurements of body weight.
A large part of AKI treatment involves management of itscomplications. Electrolyte disorders are treated as appropriate. Potassium intake and medications that increase potassiumshould be restricted. Intravenous calcium will lower risk of arrhythmia while measures are initiated to shift potassium intocells (bicarbonate, beta-agonists, insulin/dextrose) and hastenremoval (diuretics, sodium-potassium exchange resins, dialysis).Preferred treatment of hypocalcemia involves oral supplementation and calcitriol, and IV supplementation is reserved for severecases. Hypertension may be treated with diuretics, calcium channel blockers, and vasodilators. Angiotensin-converting enzyme(ACE) inhibitors are usually avoided in the setting of AKI.
Major indications for acute dialysis are listed in Table 165-3. Medical therapy may be attempted before initiating renalreplacement therapy. There is no set blood urea nitrogen orcreatinine level at which dialysis is started for uremia. Renal replacement options in children include peritoneal dialysis,hemodialysis, and continuous renal replacement therapy. Themode used is chosen on an individual basis.
Recovery from AKI depends on the etiology, severity, availability of specific treatments, and other aspects of the patient’s course. Nonoliguric AKI usually recovers well, whereas the outcome with oliguric AKI is more variable. Even with a seemingly good recovery, history of AKI may place the child at increased risk for future renal complications, including chronic kidney disease (CKD).
Congenital anomalies of the kidney and urinary tract (CAKUT) are the most common causes of CKD that present between birth and 10 years of age. After age 10 acquired diseases, such as focal segmental glomerulosclerosis and glomerulonephritis (GN), are more common causes of incident CKD. The risk of progression to end-stage renal disease (ESRD) is related to the underlying cause and severity of CKD. During puberty, renal function may deteriorate if the damaged kidneys are not able to grow and adapt to increased demands. CKD is staged to facilitate appropriate evaluation and monitoring (Table 165-4). The GFR can be estimated in children using the Schwartz formula (see Chapter 161). Most complications of CKD do not manifest until at least stage 3 CKD. In stage 4 CKD, the complications become more numerous and severe. Children with stage 5 CKD (ESRD) are typically treated with either dialysis or renal transplantation.