Goodpasture syndrome medical therapy: Difference between revisions
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==Medical Therapy== | ==Medical Therapy== | ||
Goodpasture’s syndrome responds well to treatment with [[corticosteroid]]s [[immunosuppressant]]s, and [[plasmapheresis]]. Treatment of Goodpasture's should begin before serum creatinine levels are greater than 5.7mg/dl, before the development of anuria, and the need for renal dialysis. [[Corticosteriod]]s are given for at least 6 months in tapering doses, [[immunosuppressant]]s asre given for 2 to 3 months, and [[plasmapheresis]] is given for 10 to 14 treatments. | Goodpasture’s syndrome responds well to treatment with [[corticosteroid]]s [[immunosuppressant]]s, and [[plasmapheresis]]. Treatment of Goodpasture's should begin before serum creatinine levels are greater than 5.7mg/dl, before the development of anuria, and the need for renal dialysis. [[Corticosteriod]]s are given for at least 6 months in tapering doses, [[immunosuppressant]]s asre given for 2 to 3 months, and [[plasmapheresis]] is given for 10 to 14 treatments.<ref name="pmid25018939">{{cite journal| author=| title=Chapter 14: Anti-glomerular basement membrane antibody glomerulonephritis. | journal=Kidney Int Suppl (2011) | year= 2012 | volume= 2 | issue= 2 | pages= 240-242 | pmid=25018939 | doi=10.1038/kisup.2012.27 | pmc=4089639 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25018939 }} </ref> | ||
An alternative treatment used for Goodpasture's is [[rituximab]]. The use of [[rituximab]] for 2 to 4 weeks is beneficial in the recovery of renal function in patients undergoing renal dialysis. However, its use as an induction therapy for Goodpasture's is not ideal because of its slow activation time. | An alternative treatment used for Goodpasture's is [[rituximab]]. The use of [[rituximab]] for 2 to 4 weeks is beneficial in the recovery of renal function in patients undergoing renal dialysis. However, its use as an induction therapy for Goodpasture's is not ideal because of its slow activation time.<ref name="pmid27049372">{{cite journal| author=Couser WG| title=Pathogenesis and treatment of glomerulonephritis-an update. | journal=J Bras Nefrol | year= 2016 | volume= 38 | issue= 1 | pages= 107-22 | pmid=27049372 | doi=10.5935/0101-2800.20160016 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27049372 }} </ref> | ||
==References== | ==References== | ||
Revision as of 17:09, 17 October 2016
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
The mainstay of therapy for Goodpasture syndrome is corticosteriods, cyclophosphamide and plasmapheresis.
Medical Therapy
Goodpasture’s syndrome responds well to treatment with corticosteroids immunosuppressants, and plasmapheresis. Treatment of Goodpasture's should begin before serum creatinine levels are greater than 5.7mg/dl, before the development of anuria, and the need for renal dialysis. Corticosteriods are given for at least 6 months in tapering doses, immunosuppressants asre given for 2 to 3 months, and plasmapheresis is given for 10 to 14 treatments.[1]
An alternative treatment used for Goodpasture's is rituximab. The use of rituximab for 2 to 4 weeks is beneficial in the recovery of renal function in patients undergoing renal dialysis. However, its use as an induction therapy for Goodpasture's is not ideal because of its slow activation time.[2]
References
- ↑ "Chapter 14: Anti-glomerular basement membrane antibody glomerulonephritis". Kidney Int Suppl (2011). 2 (2): 240–242. 2012. doi:10.1038/kisup.2012.27. PMC 4089639. PMID 25018939.
- ↑ Couser WG (2016). "Pathogenesis and treatment of glomerulonephritis-an update". J Bras Nefrol. 38 (1): 107–22. doi:10.5935/0101-2800.20160016. PMID 27049372.