Causes of AKI

• As much of the extracellular fluid goes to the damaged muscle, this causes hypovolemia and decreased renal perfusion.

• AKI usually occurs if there is some underlying predisposing factor such as dehydration, sepsis, or acidosis.

  • AKI results from volume depletion causing renal ischemia/ formation of tubular casts, tubular obstruction from myoglobin, and tubular injury from free iron.

  • As the heme pigment is released from myoglobin, it causes tubular obstruction, damage to the tubular epithelial cells, and vasoconstriction.

• Many electrolyte imbalances occur such as increased hyperkalemia, hyperphosphatemia, hyperuricemia (release of purines from muscle cells), and hypocalcemia (calcium enters damaged muscle cells). Metabolic acidosis is also common.

Prevention of AKI

• Prevention is composed of two main principles: correcting volume depletion and preventing the formation of tubular casts. Furthermore, addressing the underlying cause of the rhabdomyolysis is important.

• Rehydration should be started early and aggressively. Sufficient hydration can prevent renal hypoperfusion causing ischemic injury. Also, it increases urine flow, decreasing cast formation by diluting the heme pigment and washing out existing casts.

  • IV isotonic solutions should be started ASAP, with the volume depending on the underlying cause. If the patient is already at risk of AKI, it can be started at a rate of 1-2 L/hr. Fluids can be stopped when CPK is under 5000.

• Bicarbonate can also be given in severe cases as it increases urine pH, decreasing renal damage from the heme pigments.

• A loop diuretic is only used if the patient is fluid overloaded.

Treatment of AKI

• Monitor and address electrolyte imbalances: hyperkalemia, hyperphosphatemia, hyperuricemia, hypocalcemia

• Besides addressing electrolytes, tissue hypoperfusion, and fluid resuscitation, there is no specific treatment.

• Hemodialysis can be considered in cases of volume overload, hyperkalemia, severe acidemia, uremia.