Acute Kidney Injury
Upon completion of the chapter, the reader will be able to:
Assess a patient’s kidney function based on clinical presentation, laboratory results, and urinary indices.
Identify pharmacotherapeutic outcomes and endpoints of therapy in a patient with acute kidney injury (AKI).
Apply knowledge of the pathophysiology of AKI to the development of a treatment plan.
Design a diuretic regimen to treat volume overload in AKI.
Develop strategies to minimize the occurrence of drug and radiocontrast-induced AKI.
Monitor and evaluate the safety and efficacy of the therapeutic plan.
Acute kidney injury (AKI) is a potentially life-threatening syndrome that occurs primarily in hospitalized patients and frequently complicates the course of critically ill patients. It is characterized by a rapid decrease in glomerular filtration rate (GFR) and the resultant accumulation of nitrogenous waste products (eg, creatinine), with or without a decrease in urine output.
The term AKI has replaced the term acute renal failure (ARF) because it more completely encompasses the entire spectrum of acute injury to the kidney, from mild changes in kidney function to end-stage kidney disease requiring renal replacement therapy (RRT). Furthermore, the definition of ARF was inconsistent in the literature.1 Efforts to standardize the definition of ARF led to a change in terminology to AKI and development of a consensus definition.
KEY CONCEPT AKI is defined as an increase in serum creatinine (SCr) of at least 0.3 mg/dL (27 μmol/L) within 48 hours, a 50% increase in baseline SCr within 7 days, or a urine output of less than 0.5 mL/kg/hour for at least 6 hours. Only one criterion needs to be met for diagnosis of AKI.2
EPIDEMIOLOGY AND ETIOLOGY
Approximately 5% to 7% of all hospitalized patients develop AKI. AKI is 5 to 10 times more prevalent in the hospital setting than in the community setting.3 About 5% to 20% of critically ill patients develop AKI,3 and 30% to 40% of survivors progress to chronic kidney disease (CKD).4 Despite improvements in the medical care of individuals with AKI, mortality generally exceeds 15% for patients in general wards to 50% for ICU patients.5
There are three categories of AKI: prerenal, intrinsic, and postrenal AKI. The pathophysiologic mechanisms differ for each of the categories.
Prerenal AKI occurs in approximately 10% to 25% of patients diagnosed with AKI and is characterized by reduced blood delivery to the kidney. A common cause is intravascular volume depletion due to conditions such as hemorrhage, dehydration, or GI fluid losses. Early volume restoration can prevent progression and improve recovery because no structural damage to the kidney has occurred.6 Conditions of reduced cardiac output (eg, congestive heart failure [CHF], myocardial infarction) and hypotension ...