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 development of a treatment plan.
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 those who are critically ill. 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 acute kidney injury has replaced the name acute renal failure 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).
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 serum creatinine within 7 days, or a urine output of less than 0.5 mL/kg/h for at least 6 hours. Only one criterion needs to be met for diagnosis of AKI.1
EPIDEMIOLOGY AND ETIOLOGY
Approximately 7% to 18% of all hospitalized patients develop AKI.2 More than half of those who are critically ill develop AKI,3 and 30% to 40% of survivors of AKI develop chronic kidney disease (CKD).3 Despite improvements in the medical care of individuals with AKI, mortality remains high. About 4% of hospital admissions are community-acquired AKI4 with an incidence of 20 to 200 cases per million population.2
There are three categories for the causes 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 gastrointestinal (GI) fluid losses. Early volume restoration can prevent progression and improve recovery because it can restore renal blood flow before structural damage to the kidney has occurred.5 Conditions of reduced cardiac output (eg, congestive heart failure [CHF], myocardial infarction), septic shock, and hypotension can also reduce renal blood flow, resulting in decreased glomerular perfusion and prerenal AKI. With a mild to moderate decrease in renal blood flow, intraglomerular pressure is maintained by dilation of afferent arterioles (arteries supplying blood to the glomerulus), constriction of efferent arterioles ...