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Acute kidney injury: Clinical
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|Blood Urea Nitrogen||35 mg/dL|
|Creatinine, Serum||2.0 mg/dL|
With acute kidney injury, or AKI, there’s a decrease in kidney function that typically happens over a few days. This leads to the retention of urea and other nitrogenous waste products- such as ammonia and uric acid and dysregulation of extracellular volume and electrolytes.
The most commonly used diagnostic criteria for AKI are the Kidney Disease: Improving Global Outcomes or KDIGO guidelines. The KDIGO guidelines define AKI as an increase in serum creatinine of at least 0.3 milligrams per deciliter within 48 hours or as an increase in serum creatinine by 1.5 times the baseline serum creatinine within the last 7 days or when the urine volume has been less than 0.5 milliliters per kilogram per hour for six hours. Based on these criteria, there are three stages of AKI, where stage 1 is mild and stage 3 is severe AKI. In stage 1 AKI, there’s an increase in serum creatinine to 1.5 to 1.9 times the baseline serum creatinine or an increase in serum creatinine by 0.3 milligrams per deciliter or a decrease in urine output to below 0.5 milliliters per kilogram per hour for 6 to 12 hours. In stage 2 AKI, there’s an increase in serum creatinine to 2 to 2.9 times the baseline serum creatinine or a decrease in urine output to less than 0.5 milliliters per kilogram per hour for more than 12 hours. In stage 3 AKI, there’s an increase in serum creatinine to 3 times the baseline serum creatinine or an increase in serum creatinine to more than 4 milligrams per deciliter or a decrease in urine output to less than 0.3 milliliters per kilogram per hour for more than 24 hours or anuria- meaning less than 100 milliliters per day of urine- for more than 12 hours or where renal replacement therapy has been initiated. All individuals are classified according to whichever criteria places them in the most severe stage of injury.
Once diagnosed, the causes of AKI can be split into prerenal, intrarenal, and post-renal causes. In prerenal AKI, there’s decreased blood flow into the kidneys. This can happen in hypovolemic states like an acute hemorrhage, gastrointestinal losses- like with diarrhea and vomiting, renal losses- like with diuretics or osmotic diuresis in hyperglycemia, dermal losses- like with burns and finally sequestration of fluid- also known as third-spacing- like with acute pancreatitis or sepsis. On the clinical examination, there’s tachycardia, hypotension, reduced skin turgor, and cool extremities.
Acute kidney injury (AKI) is a sudden, potentially reversible decline in renal function. AKI results in the accumulation of water, nitrogenous wastes, sodium, and other metabolic wastes in the body, and can also lead to electrolyte imbalances. Common causes include dehydration, sepsis, and some drug therapy.
AKI often presents with reduced urine output, but there can be other signs such as edema, and those associated with the accumulation of metabolic wastes such as anorexia, seizures, and altered mental status. Left untreated, it can lead to chronic kidney disease (CKD)
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