1. Pathophysiology and Management of Hyperammonemia in Organ Transplant Patients 
Harish Seethapathy, Andrew Z. Fenves 
American Journal of Kidney Diseases 
DOI: /j.ajkd
Copyright © 2019 National Kidney Foundation, Inc. Terms and Conditions

2. Figure 1
Mechanisms underlying the development of hyperammonemia in transplant recipients. Intestines are the chief ammonia producing organ. Intestinal ammonia release may be dramatically increased in the presence of urease-producing bacteria. Ammonia detoxification and elimination take place in the liver and kidneys, while skeletal muscle provides significant ammonia-buffering capacity. Urea cycle defects (inherited or induced by immunosuppression), acid-base status of a patient, and muscle mass affect the ability of a transplant recipient to deal with elevated ammonia levels in the blood, leading to increased perfusion across the blood-brain barrier and consequent astrocyte injury. Abbreviations: OTC, ornithine transcarbamylase; GS, glutamine synthetase.
American Journal of Kidney Diseases DOI: ( /j.ajkd )
Copyright © 2019 National Kidney Foundation, Inc. Terms and Conditions