Acute Kidney Injury

I. DEFINITION

Acute kidney injury (AKI) is an abrupt reduction in renal function leading to an inability to excrete metabolic wastes and maintain proper fluid and electrolyte balance. AKI results in increased serum levels of creatinine, urea nitrogen and may result in increased serum potassium, increased serum phosphorus, metabolic acidosis, and/or oliguria. The presence and severity of AKI is defined based on elevation of serum creatinine and/or oliguria (see Table 22-1).

II. CAUSES

The etiology of AKI is usually divided into three categories: prerenal, intrinsic renal, and postrenal.

A. Prerenal Azotemia: Prerenal azotemia describes any condition in which blood flow to the kidneys is decreased. Causes of reduced renal blood flow include intravascular volume depletion, shock, sepsis, and heart failure. Prerenal azotemia is a common cause of AKI in intensive care units often related to hypotension or poor renal perfusion during complex surgery, frequently cardiac procedures with bypass. If reduced renal blood flow persists, then tubular cells may began to die in a process called acute tubular necrosis (ATN). It should be noted that histology rarely demonstrates necrosis in human renal injury, although the presence of tubular-cell casts on microscopic analysis of the urine is generally used to indicate the presence of ATN.

B. Intrinsic Renal Causes: The most common causes of intrinsic AKI (in order of frequency) are sepsis-related causes, ischemia, and toxins such as medications. While sepsis may cause renal dysfunction due to hypotension, inflammatory cytokines can cause direct renal injury and decreased renal capillary flow during sepsis. Other renal causes of AKI include glomerular disease such as acute glomerulonephritis (GN), renal vascular diseases such as hemolytic uremic syndrome (HUS), acute interstitial nephritis, and, in newborns, congenital anomalies of the kidneys. Pyelonephritis is an uncommon cause of AKI since it usually affects only one kidney.

C. Postrenal AKI: Postrenal AKI is caused by obstruction of the flow of urine at any level of the urinary tract.

III. CLINICAL FEATURES AND DIAGNOSIS

A. History: Many patients with AKI are asymptomatic and present only with alterations in laboratory findings. The patient and his or her medical record should be evaluated for recent fluid intake, last void, hematuria, stooling pattern, recent blood pressures (including
intraoperative blood pressures), heart rate, flank pain, malaise, rash, joint pain, fever, and recent medication exposures. A history of dehydration, sepsis, or previous complex surgery suggests prerenal azotemia. Exposure to tubular toxins such as amphotericin, IV contrast, or aminoglycosides, or drugs such as indomethacin that reduce renal blood flow suggest toxin-induced AKI. Bloody diarrhea with malaise suggests hemolytic uremic syndrome. Gross hematuria or bilateral flank pain suggests acute GN.

TABLE 22-1 pRIFLE Criteria

Stage	SCr-Based	Urine Output
Risk	>25% eCCl decrease	<0.5 mL/kg/h for 8 h
Injury	>50% eCCl decrease	<0.5 mL/kg/h
Failure	>75% eCCl decrease or eCCl <35 mL/min/1.73 m²	<0.5 mL/kg/h for 25 h or <0.3 mL/kg/h for 12 h
Adapted from Fortenberry JD, Paden ML, Goldstein SL. Acute kidney injury in children: an update on diagnosis and treatment. Pediatr Clin North Am 2013 Jun;60(3):669-688.

B. Physical Examination: Patients should be examined for altered mental status; hyper- or hypotension; tachycardia; face, pre-sacral (especially in the supine critically ill patient), or extremity edema; skin turgor; mucous membrane dryness; flank pain; abdominal mass; a palpable bladder; and rash. Poor skin turgor, tachycardia, and hypotension suggest prerenal azotemia. Commonly, children with AKI present with oliguria and signs of fluid overload such as edema and hypertension. Bilateral flank tenderness may indicate GN or interstitial nephritis. An enlarged bladder in a newborn suggests urinary obstruction such as posterior urethral valves.

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