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 patients with acute kidney injury (AKI).
Apply knowledge of the pathophysiology of AKI to develop a treatment plan.
Develop strategies to minimize the occurrence of drug-induced AKI.
Monitor and evaluate the safety and effectiveness of the treatment 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. AKI often coexists with other clinical syndromes such as shock and sepsis.
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/h for at least 6 hours. Only one of the three criteria needs to be met for diagnosis of AKI.1
Kidney disease is being increasingly viewed as a continuum.2 Once kidney disease persists longer than 90 days, patients have progressed to chronic kidney disease (CKD).2
Approximately 7% to 18% of all hospitalized patients and more than half of critically ill patients develop AKI, and mortality increases with greater AKI severity.2,3 Despite improvements in the medical care of individuals with AKI, in-hospital mortality is greater than 40% when AKI is not resolved.4
Community-acquired AKI occurs outside the hospital setting. Its incidence is 20 to 200 cases per 1 million population,2 and it accounts for 1% to 4% of hospital admissions.5
ETIOLOGY AND PATHOPHYSIOLOGY
There are three categories of causes of AKI that share some pathophysiologic mechanisms: prerenal, intrinsic, and postrenal AKI. Specific syndromes within these categories have unique pathophysiologic features and treatment strategies.
Prerenal AKI occurs in approximately 10% to 25% of patients with AKI. Renal hypoperfusion can occur secondary to systemic vasodilation or intravascular volume depletion due to conditions such as hemorrhage, dehydration, GI fluid losses, and fluid depletion related to major surgery. Early preventive measures, such as fluid resuscitation, can prevent progression and improve recovery because it can restore renal blood flow before structural kidney damage occurs.4 Conditions of reduced cardiac output (eg, heart failure [HF], myocardial infarction) can decrease effective circulation or increase central venous pressure. Sepsis and liver disease can also reduce effective circulatory blood flow, resulting in decreased glomerular perfusion and prerenal AKI....