Heme pigment released from myoglobin or hemoglobin can cause AKI through intravascular volume depletion (seen in rhabdomyolysis), renal vasoconstriction, direct proximal tubular injury, and tubular obstruction. In rhabdomyolysis, myoglobin is released in the circulation from damaged skeletal muscle. Major causes of rhabdomyolysis include trauma, drugs and toxins, seizures, metabolic and electrolyte disorders, endocrinopathies (diabetic ketoacidosis, hyperglycemic hyperosmolar syndrome, hypothyroidism), and exercise. Rhabdomyolysis-induced AKI is more likely to occur with serum creatine kinase levels >5000 U/L. In addition to elevated serum creatine kinase and serum creatinine levels, hyperkalemia, hypocalcemia, hyperphosphatemia, hyperuricemia, metabolic acidosis, increased lactate dehydrogenase concentration, and increased aspartate and alanine aminotransferase levels can occur. Urinary findings include FENa <1% (due to renal vasoconstriction), myoglobinuria, pigmented (red) granular casts, and a positive urine dipstick for blood with absence of erythrocytes.
In addition to correcting the underlying cause, prevention and management of AKI involve aggressive intravenous isotonic fluid resuscitation aimed at maintaining urine output >200 to 300 mL/h. Limited studies suggest that alkalinization of the urine with intravenous bicarbonate to increase the urine pH >6.5 may prevent tubular cast formation. If urine alkalinization is used, it should be discontinued if the patient develops symptomatic hypocalcemia or alkalosis, or if urine pH does not increase to >6.5 after several hours. Dialysis may be necessary for severe electrolyte and acid-base abnormalities. Most patients have partial or complete renal recovery. Normal saline is the recommended initial fluid of choice, and patients can require 10 liters of fluid per day.
Intravenous bicarbonate should only be used after diuresis is established with volume repletion. It should not be used if pH is >7.5, serum bicarbonate is >30 mEq/L (30 mmol/L), and/or severe hypocalcemia is present. Intravenous bicarbonate can cause symptomatic hypocalcemia and can promote deposition of calcium phosphate in the renal tubules.
Patients may have hypocalcemia. Hypocalcemia is due to sequestration of calcium in damaged cells. Rebound hypercalcemia occurs during the recovery phase due to release of calcium from damaged muscles and is worsened by exogenous calcium treatment. Calcium should only be given in patients who are symptomatic or in patients at risk for arrhythmia due to severe hyperkalemia with electrocardiogram changes.