Lack of a systematic definition of acute renal failure (ARF) previously led to significant confusion clinically and in the medical literature. In 2004, the Acute Dialysis Quality Initiative (ADQI) group published the RIFLE classification of ARF, based on changes from the patient's baseline either in serum creatinine level, glomerular filtration rate (GFR), or urine output (UO).
The RIFLE classification of ARF is as follows[1] :
- Risk (R) - Increase in serum creatinine level X 1.5 or decrease in GFR by 25%, or UO < 0.5 mL/kg/h for 6 hours
- Injury (I) - Increase in serum creatinine level X 2.0 or decrease in GFR by 50%, or UO < 0.5 mL/kg/h for 12 hours
- Failure (F) - Increase in serum creatinine level X 3.0, decrease in GFR by 75%, or serum creatinine level ≥ 4 mg/dL with acute increase of >0.5 mg/dL; UO < 0.3 mL/kg/h for 24 hours, or anuria for 12 hours
- Loss (L) - Persistent ARF, complete loss of kidney function >4 weeks
- End-stage kidney disease (E) - Loss of kidney function >3 months
Since baseline serum creatinine level and GFRs may not be readily available, the consensus committee recommended the use of the Modification of Diet in Renal Disease (MDRD) equation to estimate the patient’s GFR/1.73 mm based on serum creatinine level, age, gender, and race. The proportional decrease in GFR should be calculated from 75 mL/min per 1.73 mm2, the agreed upon lower limit of normal.
ARF is a common entity in the emergency department (ED). Emergency physicians play a critical role in recognizing early ARF, preventing iatrogenic injury, and reversing the course of ARF.
Incidence in the United States
The annual incidence of community-acquired acute renal failure (ARF) is approximately 100 cases per 1 million population, and it is diagnosed in only 1% of hospital admissions at presentation.
Using the RIFLE classification, hospital-acquired ARF of the Risk, Injury, and Failure categories has been found in 9%, 5%, and 4% of hospital admissions,[2]respectively, and in approximately 17%, 12%, and 7% of critical care admissions.[3, 4]
This high incidence of hospital-acquired ARF is multifactorial; it is related to an aging population with increased risks of ARF, the high prevalence of nephrotoxic exposures possible in a hospital setting, and increasing severity of illness.
Imaging studies in acute renal failure (ARF) are most important in the emergent workup of suspected postrenal azotemia.
The distinction between community- and hospital-acquired acute renal failure (ARF) is important for the differential diagnoses, treatment, and eventual outcome of patients with ARF.
Because most cases of community-acquired acute renal failure (ARF) are secondary to volume depletion, as many as 90% of cases are estimated to have a potentially reversible cause. Hospital-acquired ARF often occurs in an intensive-care-unit (ICU) setting and is commonly part of multiorgan failure.
This dichotomy in the etiology of ARF explains the increased mortality rate, dialysis requirements, and rates of progression to end-stage renal failure seen in hospital-acquired ARF compared with community-acquired ARF.
Mortality rates for ARF have changed little since the advent of dialysis at 50%.[5]This curious statistic simply reflects the changing demographics of ARF from community- to hospital-acquired settings.
Currently, the mortality rate for hospital-acquired ARF is reported to be as high as 70% and is directly correlated to the severity of the patient's other disease processes. The mortality rate among patients presenting to the ED with prerenal ARF may be as low as 7%.
With the advent of dialysis, the most common causes of death associated with ARF are sepsis, cardiac failure, and pulmonary failure. Interestingly, patients who are older than age 80 years with ARF have mortality rates similar to those of younger adult patients.
Pediatric patients with ARF represent a different set of etiologies and have mortality rates averaging 25%.
ARF is not a benign disease. One study noted a 31% mortality rate in patients with ARF not requiring dialysis, compared with a mortality rate of only 8% in matched patients without ARF. Even after adjusting for comorbidity, the odds ratio for dying of ARF was 4.9 compared with patients without ARF.
There seems to be a stepwise relationship between the RIFLE category of renal injury and mortality. Compared with non-acute kidney injury (AKI), the relative risk (RR) of death for Risk is 2.40; for Injury, 4.15; and for Failure, 6.4.[6]
Mortality rates are generally lower for nonoliguric ARF (>400 mL/d) than for oliguric (< 400 mL/d) ARF, reflecting the fact that nonoliguric ARF is usually caused by drug-induced nephrotoxicity and interstitial nephritis, which have few other systemic complications.
Creatinine
Serum creatinine measurement provides the ED physician with an accurate and consistent estimation of GFR. Correct interpretation of serum creatinine measurement extends beyond just knowing normal values for the specific laboratory.
The serum creatinine level varies by method of measurement, either Jaffe or iminohydrolase. The upper limit of the normal creatinine level can be 1.6-1.9 mg/dL or 1.2-1.4 mg/dL, respectively. This becomes important when patients present with changes in creatinine measured in different laboratories.
Differing methods report markedly different results when interfacing with certain chemicals.
The Jaffe method of measuring creatinine reports falsely elevated serum creatinine in the presence of the following noncreatinine chromogens: glucose, fructose, uric acid, acetone, acetoacetate, protein, ascorbic acid, pyruvate, cephalosporin antibiotics. High levels of bilirubin cause reports of falsely low creatinine by the Jaffe method.
Extremely high glucose levels and the antifungal agent flucytosine interfere with the iminohydrolase method.
The serum creatinine level, a reflection of creatinine clearance, is a function of creatinine production and excretion rates.
Creatinine production is determined by muscle mass. The serum creatinine level must always be interpreted with respect to patient's weight, age, and sex.
For example, GFR decreases by 1% per year after age 40 years, yet serum creatinine level generally remains stable. Balance is achieved via a decrease in muscle mass with age, which matches the fall in GF.
Men generally have a higher muscle mass per kilogram of body weight and thus a higher serum creatinine level than women.
The GFR can be estimated by the following formulas:
- Cockcroft-Gault equation: GFR mL/min = (140 - Age y)(Weight kg)(0.85 if female)/(72 X Serum Creatinine mol/L
- Modification of Diet in Renal Disease (MDRD) equation: GFR, in mL/min per 1.73 mm 2 = 186.3 X ((Serum Creatinine) exp[-1.154]) X (Age exp[-0.203]) X (0.742 if female) X (1.21 if African American)
The ADQI consensus committee on acute renal failure (ARF) favors the (MDRD) equation to estimate GFR.
An important consideration and limitation is that significant decrements in GFR can occur while creatinine levels remain in the normal range.
Changes in serum creatinine level reflect changes in GFR. Rate of change in serum creatinine level is an important variable in estimating GFR. Stable changes in serum creatinine level correlate with changes in GFR by the following relationships:
- If creatinine 1 mg/dL is baseline for a given patient with normal GFR
- Creatinine 2 mg/dL - 50% reduction in GFR
- Creatinine 4 mg/dL - 70–85% reduction in GFR
- Creatinine 8 mg/dL - 90–95% reduction in GFR
As suggested by these data, knowledge of a patient's baseline creatinine level becomes very important. Small changes with low baseline levels of creatinine may be much more important clinically than large changes with high basal creatinine.
Certain diseases and medications can interfere with the correlation of serum creatinine with GFR. Acute glomerulonephritis causes increased tubular secretion of creatinine, falsely depressing the rise in serum creatinine level when ARF occurs in acute glomerulonephritis. Trimethoprim and cimetidine cause decreased creatinine secretion and a falsely elevated creatinine with no change in GFR.
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