Acute Kidney Injury
As many as 70% of ICU patients have some degree of acute renal dysfunction, and about 5% require renal replacement therapy (1). The acute renal dysfunction that occurs in critically ill patients is called acute kidney injury, and this chapter describes the diagnostic and therapeutic considerations related to this entity.
I. Diagnostic Considerations
Acute kidney injury (AKI) is defined as an abrupt (within 48 hrs) decrease in renal function that is clinically significant (i.e., can have adverse consequences) (2).
A. Diagnostic Criteria
The Acute Kidney Injury Network has proposed the following criteria for the diagnosis of AKI (2):
An increase in serum creatinine of ≥0.3 mg/dL within 48 hours, or
An increase in serum creatinine of ≥50% within 48 hours, or
A decrease in hourly urine output to <0.5 mL/kg (oliguria) for more than 6 hours.
Ideal body weight is recommended for weight-based urine output measurements (3).
B. Etiologies
The common predisposing conditions for AKI are listed in Table 26.1 (1). These conditions can be categorized by their location in relation to the kidneys; i.e., prerenal, renal, or postrenal.
Table 26.1 Common Causes of Acute Kidney Injury | ||||||||||||||
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1. Prerenal Disorders
Prerenal disorders are extrarenal, and promote AKI by decreasing renal blood flow (e.g., hypovolemia). Correcting these disorders may, or may not, improve renal function, depending on the severity and duration of the flow impairment in the kidneys.
2. Renal Disorders
The principal renal disorders that produce AKI are acute tubular necrosis (ATN) and acute interstitial nephritis (AIN).
ATN is responsible for over 50% of cases of AKI (4), and is the result of injury involving the epithelial cell lining of the renal tubules. Common inciting conditions include septic shock, trauma, major surgery, radiocontrast dye, nephrotoxic drugs, and rhabdomyolysis.
AIN involves inflammatory injury in the renal parenchyma, and is described later in the chapter.
3. Postrenal Obstruction
Postrenal obstruction is responsible for 10% of cases of AKI (4). The obstruction can involve the most distal portion of the renal collecting ducts (papillary necrosis), the ureters (from a retroperitoneal mass), or the urethra (strictures or prostatic enlargement). Obstructing renal calculi do not cause AKI unless there is a solitary functional kidney.
C. Diagnostic Evaluation
The evaluation of AKI begins with a bedside ultrasound evaluation of the kidneys for evidence of postrenal obstruction (hydronephrosis). If there is no obstruction, the measurements in Table 26.2 can help to distinguish prerenal from intrinsic renal disorders, but only in the setting of oliguria.
Table 26.2 Urinary Measurements for the Evaluation of Oliguria | ||||||||||||||||||
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1. Spot Urine Sodium
In prerenal disorders (e.g., hypovolemia), there is an
increase in sodium reabsorption in the renal tubules, which results in a low urine sodium concentration (<20 mEq/L).
The renal tubular dysfunction in ATN impairs sodium reabsorption, resulting in a high urine sodium concentration (>40 mEq/L).
EXCEPTIONS: A prerenal disorder can be associated with a high urine sodium if there is ongoing diuretic therapy, or the patient has chronic renal disease with an obligatory sodium loss in urine (5).
2. Fractional Excretion of Sodium
The fractional excretion of sodium (FENa) is the fraction of filtered sodium that is excreted in the urine, and is equivalent to the fractional sodium (Na) clearance divided by the fractional creatinine (Cr) clearance, as expressed by the following equation:
(U/P is the urine-to-plasma ratio.)
In prerenal disorders, the FENa is <1%, reflecting sodium conservation.
In renal disorders like ATN, the FENa is typically >2%, indicating inappropriate sodium loss in the urine (6).
3. Fractional Excretion of Urea
The fractional excretion of urea (FEU) is conceptually
similar to the FENa, but it is not influenced by diuretics (10), which is a major advantage over the FENa. The FEU is equivalent to the fractional urea clearance divided by the fractional creatinine clearance, as expressed by the following equation:
similar to the FENa, but it is not influenced by diuretics (10), which is a major advantage over the FENa. The FEU is equivalent to the fractional urea clearance divided by the fractional creatinine clearance, as expressed by the following equation:
(U/P is the urine-to-plasma ratio.) The FEU is low (<35%) in prerenal disorders, and high (>50%) in intrinsic renal disorders.
4. Uncertainty
Distinguishing between prerenal and intrarenal causes of AKI can be difficult, especially when there is both a prerenal and renal component that coexist (e.g., in trauma, where hypovolemia and rhabdomyolysis can both contribute to AKI). Uncertainty in the setting of oliguria should prompt a fluid challenge (see next section).
II. Initial Management
The following are recommendations for the initial encounter with a patient who develops AKI, especially when associated with oliguria.
A. What to Do
As just mentioned, it is often difficult to rule out a pre-renal component in oliguric AKI, and uncertainty should prompt a fluid challenge. (See Chapter 7, Section III-A, for recommendations on fluid challenges.)
If volume infusion is not indicated, or does not correct the problem, then proceed as follows:
Reduce fluid intake as much as possible.
Discontinue potentially nephrotoxic drugs. Com-mon offenders are listed in Table 26.3.
Adjust the dose of drugs that are excreted in the urine.
Table 26.3 Drugs Most Often Implicated in Acute Kidney Injury | ||||||||||
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B. What Not to Do
Do not give furosemide to correct oliguria (3). Intra-venous furosemide does not improve renal function in AKI, and does not convert oliguric to non-oliguric renal failure (1,3,12). Furosemide can increase urine output during the recovery phase of AKI (13), and can be used at that time if volume overload is a problem.Related posts:
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