Covid-19流行期间移植实践
Lentine et al, AJKD © National Kidney Foundation
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在这个作者面试中，AJKD社交媒体编辑器，蒂莫西yau @maximal_change，与Krista Lentine @Kristalentine，Roslyn Mannon @mannonmom，和米歇尔约瑟夫森[...]
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Allograft survival in de novo and recurrent membranous nephropathy (MN). Kaplan-Meier curves for postbiopsy cumulative kidney allograft survival in patients with de novo versus recurrent MN. Figure 2 from 
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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. Figure 1 from 
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