AKI in the ICU: Epidemiology and Risk Stratification
AKI in the ICU: Epidemiology and Risk Stratification
Given how common AKI is and how significant its impact on survival is, one might expect more detailed information to be available on its cause. However, until recently, there have been two major obstacles to obtaining robust assessments of etiology and therefore it has been difficult to properly characterize risk for AKI. First, the lack of standard criteria for diagnosis of AKI has meant that observational studies cannot easily be compared to determine what demographic variables are associated with a general risk of AKI as against those that are specific to the underlying condition that leads to an exposure known to produce AKI. For example, risk factors for AKI in the setting of cardiac surgery tend to confound risks of AKI with risks for cardiovascular disease. A related problem comes from the observation that CKD puts patients at risk for AKI. In most epidemiological studies it has not been possible to separate susceptibility for AKI from risk factors for CKD. In a study of 5383 critically ill patients, gender and race were not found to alter AKI susceptibility, whereas age was a consistent risk factor. Interestingly, surgical admissions were at greater risk than medical and ICU admissions for cardiovascular, neurological, and respiratory disease/infection, whereas those for trauma, malignancy, and other causes were at decreased risk. Similarly, we reported recently on 1836 patients hospitalized for community-acquired pneumonia. In this study, one-third (34%) of the patients developed AKI. Baseline susceptibilities for AKI in this setting included age, white race, and baseline comorbidities such as CKD, cardiac disease, and diabetes.
However, risk for disease represents the interaction between susceptibility (i.e., features intrinsic to the patient) and exposure (i.e., the causative factor or factors). Exposures known to produce AKI in susceptible populations include sepsis, ischemia, heart failure, liver disease, major surgery (especially vascular and cardiac), myonecrosis, urinary tract obstruction, and various nephrotoxins. In the critically ill, sepsis is the major cause of AKI, accounting for nearly 50% of cases. Several studies have reported that sepsis-induced AKI is associated with short- and long-term risk of death.
The second obstacle to establishing accurate information on causes of AKI and therefore on risk assessment is that we continue to have an incomplete understanding of the pathogenesis of AKI in many of the circumstances in which it is seen. Although there are many reasons for this, we and others have argued that the lack of suitable animal models is a major factor. Thus, for AKI occurring in many common settings (e.g., sepsis, cardiac surgery, radio contrast), a better understanding of pathogenesis is needed.
Etiology and Risk Assessment
Given how common AKI is and how significant its impact on survival is, one might expect more detailed information to be available on its cause. However, until recently, there have been two major obstacles to obtaining robust assessments of etiology and therefore it has been difficult to properly characterize risk for AKI. First, the lack of standard criteria for diagnosis of AKI has meant that observational studies cannot easily be compared to determine what demographic variables are associated with a general risk of AKI as against those that are specific to the underlying condition that leads to an exposure known to produce AKI. For example, risk factors for AKI in the setting of cardiac surgery tend to confound risks of AKI with risks for cardiovascular disease. A related problem comes from the observation that CKD puts patients at risk for AKI. In most epidemiological studies it has not been possible to separate susceptibility for AKI from risk factors for CKD. In a study of 5383 critically ill patients, gender and race were not found to alter AKI susceptibility, whereas age was a consistent risk factor. Interestingly, surgical admissions were at greater risk than medical and ICU admissions for cardiovascular, neurological, and respiratory disease/infection, whereas those for trauma, malignancy, and other causes were at decreased risk. Similarly, we reported recently on 1836 patients hospitalized for community-acquired pneumonia. In this study, one-third (34%) of the patients developed AKI. Baseline susceptibilities for AKI in this setting included age, white race, and baseline comorbidities such as CKD, cardiac disease, and diabetes.
However, risk for disease represents the interaction between susceptibility (i.e., features intrinsic to the patient) and exposure (i.e., the causative factor or factors). Exposures known to produce AKI in susceptible populations include sepsis, ischemia, heart failure, liver disease, major surgery (especially vascular and cardiac), myonecrosis, urinary tract obstruction, and various nephrotoxins. In the critically ill, sepsis is the major cause of AKI, accounting for nearly 50% of cases. Several studies have reported that sepsis-induced AKI is associated with short- and long-term risk of death.
The second obstacle to establishing accurate information on causes of AKI and therefore on risk assessment is that we continue to have an incomplete understanding of the pathogenesis of AKI in many of the circumstances in which it is seen. Although there are many reasons for this, we and others have argued that the lack of suitable animal models is a major factor. Thus, for AKI occurring in many common settings (e.g., sepsis, cardiac surgery, radio contrast), a better understanding of pathogenesis is needed.
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