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Academic literature on the topic 'GBM Patients'

Author: Grafiati

Published: 6 September 2023

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Books on the topic "GBM Patients"

1

Group, Diagram, ed. Collins gem patience card games. HarperCollins, 1996.

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2

Herbelin, Yehonathan. Gam ani hayiti sham: I was there. Kineret, 2019.

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3

Elʻazar, Mosheh ben Shelomoh. Sefer Maʻaneh rakh: Bo yevoʼar ekh yitnaheg ha-adam ... she-lo yikhʻos ṿeshe-lo yaḳpid ṿe-lo yitraʻem ... ṿe-gam ... ʻal ezeh ha-ofanim mutar li-kheʻos ... ṿe-gam yevoʼar ... kol darkhe ha-teshuvah she-mefuzarim ben ha-sefarim ... Sifre Or ha-ḥayim, 2000.

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4

Health policy in Britain: The politics and organisation of the National Health Service. 2nd ed. Macmillan, 1985.

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5

Health policy in Britain: The politics and organisation of the National Health Service. 3rd ed. Macmillan, 1992.

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6

Health policy in Britain: The politics and organisation of the National Health Service. 3rd ed. Macmillan, 1992.

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7

Cui, Zhao, Neil Turner, and Ming-hui Zhao. Antiglomerular basement membrane disease. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0073_update_001.

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Cyclophosphamide and plasma exchange are the standard of care in rapidly progressive glomerulonephritis or lung haemorrhage caused by antiglomerular basement membrane (anti-GBM) disease, and it is unusual to encounter patients at earlier stages. Steroids are universally used in addition. There is some evidence that plasma exchange may not be a critical part of treatment at an earlier stage. There is no more than anecdotal evidence for other therapies. Slower-onset therapies such as antibodies to B cells are rarely appropriate. If untreated, patients with severe anti-GBM disease will not recove

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8

Cui, Zhao, Neil Turner, and Ming-hui Zhao. Alport post-transplant antiglomerular basement membrane disease. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0075.

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Alport antiglomerular basement membrane (anti-GBM) disease is a rare example of disease caused by allo-sensitization after renal transplantation, first described in 1992. Because the recipient lacks a specific glomerular basement membrane (GBM) protein, they can become sensitized to the normal molecule present in the GBM of the donor kidney. The disease is restricted to the allograft. Interestingly severe disease arises from this only arises rarely, certainly less than 1 in 20, probably closer to 1 in 50. It characteristically causes late graft loss in a first transplant with accelerated tempo

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9

Cattran, Daniel C., and Heather N. Reich. Membranous glomerulonephritis. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0064_update_001.

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It has been clear for several decades from comparison with the rodent model disease Heymann nephritis that membranous glomerulonephritis (MGN) is an immune condition in which antibodies, usually autoantibodies, bind to targets on the surface of podocytes. However, the antigen in Heymann nephritis, megalin, is not present on human podocytes. The first potential antigen was identified by studying rare examples of maternal alloimmunization, leading to congenital membranous nephropathy in the infant caused by antibodies to neutral endopeptidase. More recently, the target of autoantibody formation

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10

Group, Diagram, and Group Diagram. Patience Card Games (Collins Gem). HarperCollins Publishers, 1996.

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