Common laboratory findings include hemoconcentration (elevated hematocrit and total solids) associated with dehydration. Blood glucose may be decreased secondary due to increased metabolic demands or even possibly due to sepsis. Blood urea nitrogen and creatinine may be elevated especially during an acute renal failure crisis. A pre-renal component may be contributing to the azotemia through dehydration, poor perfusion and hemoconcentration. Urine sediment should be examined for casts for the detection of renal tubular damage.

Hepatocellular damage usually results in elevated liver enzyme concentrations. Mild icterus may also occur. Muscle damage can cause very high levels of creatinine phosphokinase (CPK) levels which peak at 24 to 48 hours and then decline.

Coagulation abnormalities caused by thrombocytopenia, coagulation factor disruption, and blood sludging may be present. Disseminated intravascular coagulation (DIC) is characterized by thrombocytopenia, decreased fibrinogen levels, prolongation of activated partial thromboplastin time (APTT), prothrombin time (PTT), and activated clotting (ACT). Shistocytes may be present on a blood smear lending support to DIC. Also, blood smears commonly show nucleated red blood cells, however, this is usually transient.

Electrolytes abnormalities such as hypernatremia may be present due to pure water loss. Hyperkalemia or hypokalemia could also be present. Hypophosphatemia and hypocalcemia may occur 24-48 hours later.