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Fatal hyperammonemia after repeat renal transplantation.
Roy K Kiberenge1, Humphrey Lam2
1Department of Anesthesiology, University of Iowa, Iowa City, IA, USA.
Journal of Clinical Anesthesia
|January 10, 2015
Summary
A kidney transplant recipient developed severe hyperammonemia despite normal liver function. The condition rapidly worsened, leading to brain herniation, with no clear cause found in diagnostic tests.
Area of Science:
- Nephrology
- Neurology
- Metabolic Disorders
Background:
- Recurrent kidney transplantation can present complex post-operative challenges.
- Symptomatic hyperammonemia is a critical condition often associated with liver dysfunction.
Observation:
- A 35-year-old male, post-repeat kidney transplant, exhibited gastrointestinal symptoms and altered mental status.
- Despite ammonia-clearing therapies, the patient's ammonia levels escalated, resulting in unresponsiveness and cerebral herniation.
Findings:
- The patient presented with severe hyperammonemia and normal liver function, a rare clinical scenario.
- Standard urine and serum organic acid analyses did not identify a urea cycle disorder.
- Histopathological examination failed to reveal the underlying cause of the hyperammonemia.
Implications:
- This case highlights the potential for unexplained hyperammonemia in kidney transplant recipients.
- Further investigation into non-urea cycle metabolic derangements or novel etiologies is warranted.
- Early recognition and management of hyperammonemia are crucial to prevent neurological damage.
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