Acute kidney injury (AKI) is defined as an abrupt decrease in glomerular filtration rate (GFR). Incidence varies from 20% to as high as 70% in critically ill patients. Classically, AKI has been divided into three broad pathophysiologic categories: prerenal AKI, intrinsic AKI, and postrenal (obstructive) AKI. The clinical manifestations of AKI vary among a wide range of symptoms and metabolic abnormalities. A sudden decrease in GFR will result in rising concentrations of solutes in the blood, which are normally excreted by the kidneys. Recently, new urinary and serum biomarkers have gained a place in the diagnosis, classification, and prognosis prediction of AKI. The best treatment for AKI is prevention. Patients with prerenal azotemia should have intravascular volume deficits corrected and cardiac function optimized. Obstructive (postrenal) kidney disease is treated by mechanical relief of the block. The primary management of acute interstitial nephritis is discontinuation of the inciting agent. Renal replacement therapy (RRT) has emerged as a supportive mechanism rather than just as a lifesaving measure. Continuous techniques are preferable in treating critically ill patients, although every modality has its benefits, indications, and contraindications.
Part of the book: Intensive Care