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.