Acute kidney injury (AKI)

Abstract

Acute kidney injury (AKI) can generally be considered as sudden reduction in kidney function occurring over hours to days, and is commonly but not always associated with a reduction in urine output. Its definition was based on rises in serum creatinine and reductions in urine output criteria. Its incidence, prevalence, and aetiology vary according to the country/region profile (low income, high income, tropical, etc.), age (children, adult, or elderly), and clinical setting (outpatients versus inpatient, hospital versus intensive care unit). The incidence of AKI is increasing in the hospital setting, and is more common with increasing age, male sex, pre-existing CKD, and comorbidity (congestive cardiac failure, diabetes, hypertension). The majority of cases result from multiple insults: dehydration, drugs in conjunction with inflammation and/or sepsis. AKI may have a spectrum of being an incidental finding with no signs or symptoms to a moderate to severe condition with increased morbidity and mortality due to accumulation of nitrogenous waste products and fluid–electrolyte disorders. The aetiologies of AKI are numerous and can broadly be classified as pre-renal, intrinsic renal, and post-renal (obstructive). A thorough evaluation of the patients with AKI for diagnosis and treatment are required. There are no specific treatments, but eliminating aetiological reasons and protection from further kidney function loss are crucial. A balanced haemodynamic management along with a balanced fluid–electrolyte replacement and arranging drug dosages are important. Various modes of renal replacement therapies may be used for treating severe cases.