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Acute kidney injury, AKI, also known as acute renal failure, is a sudden, rapid loss of kidney function, typically within days or weeks.
The function of the kidneys is to filter blood plasma, removing metabolic wastes in urine, while also adjusting urine composition to maintain balance of various blood parameters. In AKI, metabolic wastes accumulate; and fluid, electrolyte and acid-base disorders may develop quickly. Of the many possible complications, most serious are potassium overload – hyperkalemia, and excess of fluid volume, or hypervolemia. Usually, both kidneys must fail for AKI to be diagnosed.
While AKI can be caused by a rapidly progressing intrinsic kidney disease, it is most commonly a consequence of an underlying condition outside the kidney.
Causes are classified as prerenal, renal and postrenal, with prerenal being most common.
Urine formation occurs in the functional units of kidneys, called the nephrons. Blood enters the nephrons via the afferent arteriole, passes through a ball of capillaries called the glomerulus, where filtration takes place, then leaves via the efferent arteriole. Blood pressure inside the glomerulus must be high enough to enable filtration. This is achieved by having the afferent arteriole significantly larger than the efferent arteriole, creating a blood flow with a large inlet and small outlet.
Prerenal AKI is usually due to an inadequate blood flow to the kidneys. Major causes include extracellular fluid volume depletion and decreased blood pressure, both of which reduce the glomerular filtration rate. Normally, autoregulatory mechanisms within the kidney, which dilate the afferent arteriole in response to volume loss, can compensate for a certain degree of low blood flow. AKI develops when hypoperfusion is severe, or when these mechanisms are compromised in patients with preexisting chronic kidney disease. Medications that cause dilation of the efferent arteriole or constriction of the afferent arteriole, reduce the pressure inside the glomerulus, and may contribute to development of AKI.
In patients with prerenal AKI but otherwise healthy kidneys, renal function typically returns to normal after the underlying condition is resolved, or the offending drug is discontinued.
Renal causes refer to intrinsic problems within the kidney, such as inflammation or necrosis of any of its components: the glomeruli, renal tubules, and interstitium.
Postrenal causes include various types of obstruction in the storage or voiding parts of the urinary system. These range from microscopic obstruction within renal tubules, to blockage of ureters by kidney stones, to urethral obstruction due to enlarged prostate in men.
Some AKI may involve problems at MORE than one level. For example, renal hypoperfusion, a prerenal cause, may sometimes be severe enough to induce ischemia of renal tubule cells, leading to intrinsic kidney disease. As the cells die, cellular debris may clog the tubules, becoming a postrenal cause.
Initially, symptoms of AKI are commonly masked by those of the underlying condition. In a later stage, symptoms are due to accumulation of nitrogenous wastes and disturbances of fluid and electrolyte balance. Urine output may or may not be reduced.
Diagnosis is based on renal function tests, such as serum creatinine and urea, serum electrolytes, urinary sediment, urine output and urinalysis.
Cause must be determined. Prerenal causes are usually apparent. Ultrasound is commonly performed to detect postrenal blockage.
Treatments aim to address the underlying cause, although some patients may also require fluid and electrolyte management, or dialysis.