The cardiopulmonary signs may be a sequelle of the CNS depression of stage 1. Renal failure develops in stage 3. Renal damage is due to tubular damage induced by EG metabolites and impaired renal blood flow due to renal edema. Calcium oxalate crystal deposition in the renal tubules probably plays a minor role in the development of renal failure but does provide a diagnostic clue and causes hypocalcemia. The history and clinical presentation often make one suspicious of a diagnosis of EG intoxication.
Successful therapy hinges on a rapid diagnosis.
The clinical findings may mimic other polysystemic diseases including ARF of another cause, acute gastroenteritis, pancreatitis, and diabetic ketoacidosis. Lab findings include azotemia, hyperphosphatemia, hyperkalemia, severe hypocalcemia, metabolic acidosis, isosthenuria, acid urine and sometimes glucosuria or proteinuria. Blood calcium may be extremely low. Always consider antifreeze poisoning in azotemic patients with a marked reduction in calcium. Calcium oxalate crystals may be observed in urine within 3 hours of ingestion.