1. What is acute kidney injury (AKI)?
AKI is a sudden decrease in kidney function occurring over a period of hours to days. The acute decrease in glomerular filtration rate (GFR) is usually manifested by the accumulation of waste products including, but not limited to, urea and creatinine in the blood (azotemia), and is sometimes accompanied by oliguria.
2. What is the difference between AKI and acute renal failure (ARF)?
Although the terms AKI and ARF both described the sudden decrease in kidney function, the term AKI is now the preferred term, as it reflects the importance of smaller decrements in kidney function that do not result in complete loss of kidney function. The terms ARF or acute kidney failure now are generally used to describe AKI resulting in severe organ failure with the need for acute renal replacement therapy.
3. What is oliguria?
Oliguria (literally, scanty urine) is a reduction in urine volume to a volume that is insufficient to excrete the necessary solute load. Oliguria is generally defined as a urine volume:
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Less than 0.5 mL/kg per hour in children
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Less than 20 mL/h in adults or
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Less than 400 to 500 mL/day in adults
Anuria (literally, the absence of urine) is defined as a urine output of <100 mL/day.
4. How is AKI defined?
Although the concept of AKI is easily defined, multiple operational definitions have been used over the course of years, and coming up with a universal operational definition has been more of a challenge. Over the past 10 to 15 years, several consensus criteria for the operational definition of AKI have been developed, including the RIFLE (Risk, Injury, Failure, Loss, and End-stage) criteria developed by the Acute Dialysis Quality Initiative (ADQI) in 2004; the AKIN definition developed by the Acute Kidney Injury Network in 2007; and the Kidney Disease Improving Global Outcomes (KDIGO) definition developed by the Kidney Disease: Improving Global Outcomes Acute Kidney Injury Clinical Practice Guideline Workgroup in 2012. All three of these consensus definitions ( Table 6.1 ) define AKI based either on changes in serum creatinine concentration or on the presence of oliguria. In the RIFLE criteria, AKI is defined based on at least a 50% increase in the serum creatinine concentration developing over a period of not more than 7 days or on the basis of a urine output of <0.5 mL/kg per hour for more than 6 hours. The AKIN definition added an absolute increase in serum creatinine of at least 0.3 mg/dL to the ≥50% increase in serum creatinine, and shortened the time frame for the change in serum creatinine to 48 hours. The KDIGO definition of AKI kept the ≥ 0.3 mg/dL increase in serum creatinine over 48 hours from the AKIN definition, but restored the time frame for the 50% relative increase in serum creatinine to 7 days, as was originally proposed in the RIFLE criteria. Both the AKIN and KDIGO definitions retained the same urine output criteria as proposed in the original RIFLE criteria.
| Definition/Staging System | Increase in Serum Creatininea | Urine Output Criteriaa | |||
|---|---|---|---|---|---|
| RIFLE | AKIN/KDIGO | RIFLE | AKIN | KDIGO | |
| Risk | Stage 1 | ≥150% of baseline over 7 days | ≥0.3 mg/dL over baseline over 48 h; or ≥150% of baseline over 48 h | ≥0.3 mg/dL over baseline over 48 h; or ≥150% of baseline over 7 days | <0.5 mL/kg per hour for >6 h |
| Injury | Stage 2 | ≥200% of baseline | ≥200% of baseline | ≥200% of baseline | <0.5 mL/kg per hour for >12 h |
| Failure | Stage 3 | ≥300% of baseline; or ≥0.5 mg/dL to a level >4.0 mg/dL | ≥300% of baseline; or ≥0.5 mg/dL to a level >4.0 mg/dL | ≥300% of baseline; or ≥0.5 mg/dL to a level >4.0 mg/dL | <0.3 mL/kg per hour for >24 h; or Anuria for >12 h |
| Loss | Need for RRT due to AKI for >4 weeks | ||||
| End Stage | Need for RRT due to AKI for >3 months | ||||
5. How is the severity of AKI staged?
In addition to standardizing the definitions of AKI, the RIFLE, AKIN, and KDIGO criteria stage the severity of AKI by the magnitude of change in creatinine or the duration of oliguria (see Table 6.1). The RIFLE criteria stratified AKI into three strata of severity (Risk, Injury, and Failure) on the basis of either change in serum creatinine (≥50%, ≥100%, or ≥200% increase) or the duration of oliguria (≥6 hours, ≥12 hours, or ≥24 hours) and two outcome stages based on the duration of kidney failure (see Table 6.1). The subsequent AKIN and KDIGO criteria kept the initial three strata of severity (now called Stage 1, Stage 2, and Stage 3) but dropped the two outcome stages. In all three classification systems, the increasing severity of AKI is associated with the increasing risk of death and intensive care unit and hospital length of stay. The duration of AKI, which is not included in these staging criteria, is also associated with mortality risk. While these classification systems are important for epidemiologic studies and clinical trials, there remains uncertainty regarding the utility of AKI staging when applied prospectively in clinical practice.
6. What is acute kidney disease (AKD)?
With AKI defined as kidney dysfunction developing over less than 7 days, and chronic kidney disease (CKD) defined based on structural or functional damage to the kidney present for more than 3 months, a gap exists in patients who develop kidney dysfunction over more than 7 days but for less than 3 months. The KDIGO AKI workgroup proposed that AKD be defined as kidney disease that is present for less than 3 months, defined based on a GFR of <60 mL/min per 1.73 m , a decrease in GFR of ≥35% or an increase in serum creatinine of >50%. AKI is a subset of AKD.
7. How common is AKI?
Estimates of the incidence of AKI depend on the definition used for case finding and the population studied. It is estimated that 5% to 10% of hospitalized patients develop AKI. AKI is much more common in critically ill patients; 35% to 60% of critically ill patients will develop AKI based on the RIFLE, AKIN, or KDIGO criteria, and 5% will develop severe AKI requiring renal replacement therapy. Epidemiologic studies have demonstrated that AKI has become progressively more common, with an almost 20-fold increase in incidence over 25 years. Currently, more patients initiate renal replacement therapy for AKI than for CKD, progressing to end-stage kidney disease.
8. What are the causes of AKI?
AKI encompasses any process that causes an abrupt decrease in kidney function. The differential diagnosis includes prerenal azotemia (approximately 50% to 70% of cases), obstructive nephropathy (approximately 5% of cases, see Chapter 17) , and intrinsic forms of AKI.
10. Which patients are at risk for the development of AKI?
The most important risk factor for the development of AKI is the presence of preexisting CKD. Elderly patients are at increased risk for the development of AKI, as they often have unrecognized diminished kidney function. Other risk factors include diabetes mellitus and volume depletion. Medications that cause intrarenal vasoconstriction, such as nonsteroidal anti-inflammatory drugs (NSAIDs), also predispose to the development of AKI.
11. What is prerenal azotemia?
Prerenal azotemia is a functional form of AKI that results from diminished kidney perfusion. As there is no parenchymal injury, the hallmark of prerenal azotemia is the rapid normalization of kidney function when kidney perfusion is restored. Common etiologies of prerenal azotemia include intravascular volume depletion, congestive heart failure (cardiorenal syndrome, see Chapter 9), and advanced liver disease. The hepatorenal syndrome (see Chapter 8) is a severe form of prerenal azotemia in patients with cirrhosis of the liver and severe portal hypertension. Patients with prerenal azotemia are often (although not always) oliguric and generally manifest increased sodium reabsorption if they are not being treated with diuretics.
12. How can prerenal azotemia be differentiated from ATN?
It is important to differentiate between prerenal azotemia and intrinsic forms of AKI, as prerenal azotemia will generally improve with the correction of the underlying hemodynamic disturbance. In contradistinction, the volume loading of patients with ATN or other forms of intrinsic AKI will not result in improved kidney function and may exacerbate volume overload. Characteristic laboratory findings that help differentiate between prerenal azotemia and ATN reflect the preservation of tubular function with increased sodium reabsorption and urinary concentration in prerenal azotemia ( Table 6.2 ). Preexisting CKD or diuretic use may limit the usefulness of these indices. Novel biomarkers of tubular injury, such as neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1), have been proposed as candidates for differentiating between prerenal azotemia and intrinsic tubular damage, but are not yet validated for clinical use.
| Prerenal Azotemia | Acute Tubular Necrosis | |
|---|---|---|
| Serum BUN:creatinine ratio | >20:1 | 10:1 |
| Urine specific gravity | >1.015 | ∼1.010 |
| Urine sodium | <20 mmol/L | >40 mmol/L |
| Fractional excretion of sodium | <1% | >2% |
| Fractional excretion of urea | <35% | >50% |
| Urine osmolality | >500 mOsm/kg | ∼300 mOsm/kg |
| Urine sediment | Normal, or hyaline casts | Kidney tubular cells and “muddy brown” granular casts |
| Biomarkers of tubular injury | Negative | Positive |
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