Kidney‐pancreas transplantation in the setting of donor ethylene glycol poisoning

Abstract

T he safety of kidney or kidneypancreas transplantation in the setting of donor ethylene glycol (EG) poisoning has not been well established. While renal transplantation has been reported from a donor after EG toxicity, 1 there are no reports of successful simultaneous pancreas-kidney (SPK) transplantation in this setting in the literature. This article describes a case of successful kidney-pancreas transplantation in the setting of donor death from EG. Ethylene glycol is an odorless, colorless alcohol with a sweet taste used as antifreeze for automotives. Ingestion may be accidental, most commonly affecting children and household pets, or may be associated with attempted suicide. Approximately 5,000 people in the United States are treated for EG poisoning per year, with about 30 to 40 resulting in fatalities. 2 The hallmarks of EG poisoning are central nervous system (CNS) depression, profound metabolic acidosis, cardiopulmonary compromise, and acute renal failure.Ethylene glycol has 3 primary toxic effects, that are most easily classifi ed by their differing time courses (Figure 1). The fi rst stage runs from 30 minutes to 12 hours after ingestion and is marked by CNS depression and gastritis by the unmetabolized EG, an effect similar to ethanol intoxication. 3 Central nervous system symptoms of intoxication with lethargy, seizures, and coma predominate during this initial stage. The second stage takes over as EG is metabolized in the liver. Two rapid oxidations, fi rst to glycoaldehyde (by alcohol dehydrogenase) and then to glycolic acid (by aldehyde dehydrogenase) are followed by the relatively slow oxidation to glyoxylic acid, leading to buildup of metabolite glycolic acid. 4 The presence of large amounts of glycolic acid leads to anion gap metabolic acidosis usually within 12 to 24 hours of ingestion of EG. Symptoms in this stage can range from hypotension and tachypnea to frank cardiopulmonary collapse with pulmonary edema and multiorgan failure. 5 The third stage of EG toxicity involves renal failure, usually appearing about 24 to 72 hours after ingestion. The metabolite glyoxylic acid can be converted to up to 4 different metabolites, depending on the relative presence of co-metabolites. The metabolites are: glycine (relatively nontoxic, formed in the presence of pyridoxine), alpha-hydroxy-beta-ketoadipate (formed in the presence of thiamine), formic acid (not usually present in large amounts), and oxalate. 6 Oxalate binds serum calcium ions to form the compound calcium oxalate, that precipitates in crystalline form. Not only does this have the capacity of causing hypocalcemia, possibly leading to tetany and prolonged QTc, but can also result in the deposition of the crystals in the renal cortex. 7 These insoluble calcium-oxalate crystals are deposited in the proximal convoluted tubule and interstitium, causing physical trauma to cells, obstructing the tubule, and inciting an infl ammatory reaction. Ultimately, these mechanisms lead to necrosis of the proximal tubule. This mechanism of acute renal failu...

Ethylene Glycol Poisoning Should Not Contraindicate Liver Donation

“…Because the third stage of EG toxicity involves calcium oxalate crystal deposition often in the renal cortex, causing acute kidney injury, one must be weary before using kidneys as allografts. 7 However, there have been reports of successful transplantation of a kidney 8 and of a kidney and pancreas 7 in this setting. Because there is a need for all viable allografts to be used, organs from EG overdosed donors should not be dismissed.…”