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- W2941806721 abstract "Neurologic complications are common after solid-organ transplantation, occurring in one-third of patients. Immunosuppression-related neurotoxicity (involving calcineurin inhibitors and corticosteroids), opportunistic central nervous system infections, seizures, and delirium are some of the causes of neurologic symptoms following solid-organ transplantation. An uncommon often missed complication posttransplantation involves buildup of ammonia levels that can lead to rapid clinical deterioration even when treated. Ammonia levels are not routinely checked due to the myriad of other explanations for encephalopathy in a transplant recipient. A treatment of choice for severe hyperammonemia involves renal replacement therapy (RRT), but there are no guidelines on the mode or parameters of RRT for reducing ammonia levels. Hyperammonemia in a transplant recipient poses specific challenges beyond the actual condition because the treatment (RRT) involves significant hemodynamic fluctuations that may affect the graft. In this review, we describe a patient with posttransplantation hyperammonemia and discuss the pathways of ammonia metabolism, potential factors underlying the development of hyperammonemia posttransplantation, and choice of appropriate therapeutic options in these patients. Neurologic complications are common after solid-organ transplantation, occurring in one-third of patients. Immunosuppression-related neurotoxicity (involving calcineurin inhibitors and corticosteroids), opportunistic central nervous system infections, seizures, and delirium are some of the causes of neurologic symptoms following solid-organ transplantation. An uncommon often missed complication posttransplantation involves buildup of ammonia levels that can lead to rapid clinical deterioration even when treated. Ammonia levels are not routinely checked due to the myriad of other explanations for encephalopathy in a transplant recipient. A treatment of choice for severe hyperammonemia involves renal replacement therapy (RRT), but there are no guidelines on the mode or parameters of RRT for reducing ammonia levels. Hyperammonemia in a transplant recipient poses specific challenges beyond the actual condition because the treatment (RRT) involves significant hemodynamic fluctuations that may affect the graft. In this review, we describe a patient with posttransplantation hyperammonemia and discuss the pathways of ammonia metabolism, potential factors underlying the development of hyperammonemia posttransplantation, and choice of appropriate therapeutic options in these patients. Clinical Vignette: A 65-year-old white man with a medical history significant for hypothyroidism and atrial fibrillation underwent bilateral sequential lung transplantation for severe interstitial lung disease. He was receiving tacrolimus, azathioprine, and prednisone for immunosuppression. 28 days posttransplantation, he was admitted with hyponatremia (serum sodium, 116 mEq/L) secondary to syndrome of inappropriate antidiuretic hormone secretion. He was treated with fluid restriction and hypertonic saline solution. He was on treatment with the antidepressant venlafaxine, which was stopped. His serum sodium level normalized over the next few days. On hospital day 5, he experienced an acute episode of shortness of breath, and his mental status was altered. An arterial blood gas while using a high-flow nonrebreather showed pH of 7.52, Pco2 of 31mm Hg, and Po2 of 67mm Hg. His mental status deteriorated, and he was intubated and placed on mechanical ventilation. Serum ammonia level was 506μmol/L. Liver function test results and serum creatinine, electrolyte, and lactate levels were normal. Thyroid-stimulating hormone level was very low (0.03mIU/L) and he was started on treatment with high-dose levothyroxine. Continuous venovenous hemodiafiltration was initiated for clearance of ammonia. He also received sodium benzoate, sodium phenylacetate, rifaximin, and lactulose. His ammonia levels gradually decreased to 144μmol/L after 18 hours and to 75μmol/L after 36 hours on continuous renal replacement therapy (CRRT). Continuous venovenous hemodiafiltration was stopped and his ammonia levels remained stable. His mental status returned to baseline over the course of the next few days and he was extubated. Clinical Vignette: A 65-year-old white man with a medical history significant for hypothyroidism and atrial fibrillation underwent bilateral sequential lung transplantation for severe interstitial lung disease. He was receiving tacrolimus, azathioprine, and prednisone for immunosuppression. 28 days posttransplantation, he was admitted with hyponatremia (serum sodium, 116 mEq/L) secondary to syndrome of inappropriate antidiuretic hormone secretion. He was treated with fluid restriction and hypertonic saline solution. He was on treatment with the antidepressant venlafaxine, which was stopped. His serum sodium level normalized over the next few days. On hospital day 5, he experienced an acute episode of shortness of breath, and his mental status was altered. An arterial blood gas while using a high-flow nonrebreather showed pH of 7.52, Pco2 of 31mm Hg, and Po2 of 67mm Hg. His mental status deteriorated, and he was intubated and placed on mechanical ventilation. Serum ammonia level was 506μmol/L. Liver function test results and serum creatinine, electrolyte, and lactate levels were normal. Thyroid-stimulating hormone level was very low (0.03mIU/L) and he was started on treatment with high-dose levothyroxine. Continuous venovenous hemodiafiltration was initiated for clearance of ammonia. He also received sodium benzoate, sodium phenylacetate, rifaximin, and lactulose. His ammonia levels gradually decreased to 144μmol/L after 18 hours and to 75μmol/L after 36 hours on continuous renal replacement therapy (CRRT). Continuous venovenous hemodiafiltration was stopped and his ammonia levels remained stable. His mental status returned to baseline over the course of the next few days and he was extubated." @default.
- W2941806721 created "2019-05-03" @default.
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- W2941806721 date "2019-09-01" @default.
- W2941806721 modified "2023-10-18" @default.
- W2941806721 title "Pathophysiology and Management of Hyperammonemia in Organ Transplant Patients" @default.
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- W2941806721 doi "https://doi.org/10.1053/j.ajkd.2019.03.419" @default.
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