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Following recommendations are advised while dealing with patient suffering membranous glomerulonephritis '''MGN'''<ref name="pmid29852477">{{cite journal| author=Bomback AS, Fervenza FC| title=Membranous Nephropathy: Approaches to Treatment. | journal=Am J Nephrol | year= 2018 | volume= 47 Suppl 1 | issue= | pages= 30-42 | pmid=29852477 | doi=10.1159/000481635 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29852477 }}</ref><ref name="pmid22859855">{{cite journal| author=Waldman M, Austin HA| title=Treatment of idiopathic membranous nephropathy. | journal=J Am Soc Nephrol | year= 2012 | volume= 23 | issue= 10 | pages= 1617-30 | pmid=22859855 | doi=10.1681/ASN.2012010058 | pmc=3458460 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22859855 }}</ref><ref name="pmid10495797">{{cite journal |vauthors=Wasserstein AG |title=Membranous glomerulonephritis |journal=J. Am. Soc. Nephrol. |volume=8 |issue=4 |pages=664–74 |date=April 1997 |pmid=10495797 |doi= |url=}}</ref> | Following recommendations are advised while dealing with patient suffering membranous glomerulonephritis '''MGN'''<ref name="pmid29852477">{{cite journal| author=Bomback AS, Fervenza FC| title=Membranous Nephropathy: Approaches to Treatment. | journal=Am J Nephrol | year= 2018 | volume= 47 Suppl 1 | issue= | pages= 30-42 | pmid=29852477 | doi=10.1159/000481635 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29852477 }}</ref><ref name="pmid22859855">{{cite journal| author=Waldman M, Austin HA| title=Treatment of idiopathic membranous nephropathy. | journal=J Am Soc Nephrol | year= 2012 | volume= 23 | issue= 10 | pages= 1617-30 | pmid=22859855 | doi=10.1681/ASN.2012010058 | pmc=3458460 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22859855 }}</ref><ref name="pmid10495797">{{cite journal |vauthors=Wasserstein AG |title=Membranous glomerulonephritis |journal=J. Am. Soc. Nephrol. |volume=8 |issue=4 |pages=664–74 |date=April 1997 |pmid=10495797 |doi= |url=}}</ref> | ||
* [[Lipid]] lowering and [[anticoagulation]] for better blood flow | * [[Lipid]] lowering and [[anticoagulation]] for better blood flow | ||
* [[Diuretics]] to reduce [[edema]] | * [[Diuretics]] to reduce [[edema]] | ||
* [[Angiotensin inhibition]] | * [[Angiotensin inhibition]] | ||
* [[ACEi|ACE inhibitor]] or an [[angiotensin II]] receptor blocker are recomended to reduce [[renal]] [[vascular]] damage | * [[ACEi|ACE inhibitor]] or an [[angiotensin II]] receptor blocker are recomended to reduce [[renal]] [[vascular]] damage | ||
=== Treatment for proteinuria: === | === Treatment for proteinuria: === | ||
* The optimal [[proteinuria]] goal in patients with [[chronic kidney disease]] is less than 1000 mg/day | * The optimal [[proteinuria]] goal in patients with [[chronic kidney disease]] is less than 1000 mg/day<ref name="pmid29852477">{{cite journal| author=Bomback AS, Fervenza FC| title=Membranous Nephropathy: Approaches to Treatment. | journal=Am J Nephrol | year= 2018 | volume= 47 Suppl 1 | issue= | pages= 30-42 | pmid=29852477 | doi=10.1159/000481635 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29852477 }}</ref><ref name="pmid22859855">{{cite journal| author=Waldman M, Austin HA| title=Treatment of idiopathic membranous nephropathy. | journal=J Am Soc Nephrol | year= 2012 | volume= 23 | issue= 10 | pages= 1617-30 | pmid=22859855 | doi=10.1681/ASN.2012010058 | pmc=3458460 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22859855 }}</ref><ref name="pmid10495797">{{cite journal |vauthors=Wasserstein AG |title=Membranous glomerulonephritis |journal=J. Am. Soc. Nephrol. |volume=8 |issue=4 |pages=664–74 |date=April 1997 |pmid=10495797 |doi= |url=}}</ref> | ||
* Attainment of partial remission can result from one or more of the following: | * Attainment of partial remission can result from one or more of the following: | ||
=== Hpertensive managment: === | === Hpertensive managment: === | ||
* The goal blood pressure in patients with | * The goal blood pressure in patients with membranous glomerulonephritis is the same as it is in other patients with proteinuric chronic kidney disease<ref name="pmid29852477">{{cite journal| author=Bomback AS, Fervenza FC| title=Membranous Nephropathy: Approaches to Treatment. | journal=Am J Nephrol | year= 2018 | volume= 47 Suppl 1 | issue= | pages= 30-42 | pmid=29852477 | doi=10.1159/000481635 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29852477 }}</ref><ref name="pmid22859855">{{cite journal| author=Waldman M, Austin HA| title=Treatment of idiopathic membranous nephropathy. | journal=J Am Soc Nephrol | year= 2012 | volume= 23 | issue= 10 | pages= 1617-30 | pmid=22859855 | doi=10.1681/ASN.2012010058 | pmc=3458460 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22859855 }}</ref><ref name="pmid10495797">{{cite journal |vauthors=Wasserstein AG |title=Membranous glomerulonephritis |journal=J. Am. Soc. Nephrol. |volume=8 |issue=4 |pages=664–74 |date=April 1997 |pmid=10495797 |doi= |url=}}</ref> | ||
* Blood pressure can be controlled in patients with | * Blood pressure can be controlled in patients with membranous glomerulonephritis usually requires more than [[angiotensin]] inhibition alone | ||
* Volume overload cab be controlled well with [[loop diuretics]] | * Volume overload cab be controlled well with [[loop diuretics]] | ||
* A low-salt diet is an important component of [[antihypertensive]] therapy (especially when using [[angiotensin inhibitors]]) and edema control in patients with MN | * A low-salt diet is an important component of [[antihypertensive]] therapy (especially when using [[angiotensin inhibitors]]) and edema control in patients with MN | ||
* A high-salt diet can increase proteinuria. | * A high-salt diet can increase proteinuria. | ||
=== Treatment for hyperlipidemia: === | === Treatment for hyperlipidemia: === | ||
* [[Statins]] are the drug of choice for the patient with membranous glomerulonephritis | * [[Statins]] are the drug of choice for the patient with membranous glomerulonephritis<ref name="pmid29852477">{{cite journal| author=Bomback AS, Fervenza FC| title=Membranous Nephropathy: Approaches to Treatment. | journal=Am J Nephrol | year= 2018 | volume= 47 Suppl 1 | issue= | pages= 30-42 | pmid=29852477 | doi=10.1159/000481635 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29852477 }}</ref><ref name="pmid22859855">{{cite journal| author=Waldman M, Austin HA| title=Treatment of idiopathic membranous nephropathy. | journal=J Am Soc Nephrol | year= 2012 | volume= 23 | issue= 10 | pages= 1617-30 | pmid=22859855 | doi=10.1681/ASN.2012010058 | pmc=3458460 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22859855 }}</ref><ref name="pmid10495797">{{cite journal |vauthors=Wasserstein AG |title=Membranous glomerulonephritis |journal=J. Am. Soc. Nephrol. |volume=8 |issue=4 |pages=664–74 |date=April 1997 |pmid=10495797 |doi= |url=}}</ref> | ||
=== Treatment for coagulation: === | === Treatment for coagulation: === | ||
* Patients with [[nephrotic syndrome]], particularly those with membranous glomerulonephritis, are at increased risk for thrombotic events, such as deep vein and renal vein thrombosis or pulmonary embolism.<ref name="pmid29852477">{{cite journal| author=Bomback AS, Fervenza FC| title=Membranous Nephropathy: Approaches to Treatment. | journal=Am J Nephrol | year= 2018 | volume= 47 Suppl 1 | issue= | pages= 30-42 | pmid=29852477 | doi=10.1159/000481635 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29852477 }}</ref><ref name="pmid22859855">{{cite journal| author=Waldman M, Austin HA| title=Treatment of idiopathic membranous nephropathy. | journal=J Am Soc Nephrol | year= 2012 | volume= 23 | issue= 10 | pages= 1617-30 | pmid=22859855 | doi=10.1681/ASN.2012010058 | pmc=3458460 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22859855 }}</ref><ref name="pmid10495797">{{cite journal |vauthors=Wasserstein AG |title=Membranous glomerulonephritis |journal=J. Am. Soc. Nephrol. |volume=8 |issue=4 |pages=664–74 |date=April 1997 |pmid=10495797 |doi= |url=}}</ref> | * Patients with [[nephrotic syndrome]], particularly those with membranous glomerulonephritis, are at increased risk for thrombotic events, such as deep vein and renal vein thrombosis or pulmonary embolism.<ref name="pmid29852477">{{cite journal| author=Bomback AS, Fervenza FC| title=Membranous Nephropathy: Approaches to Treatment. | journal=Am J Nephrol | year= 2018 | volume= 47 Suppl 1 | issue= | pages= 30-42 | pmid=29852477 | doi=10.1159/000481635 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29852477 }}</ref><ref name="pmid22859855">{{cite journal| author=Waldman M, Austin HA| title=Treatment of idiopathic membranous nephropathy. | journal=J Am Soc Nephrol | year= 2012 | volume= 23 | issue= 10 | pages= 1617-30 | pmid=22859855 | doi=10.1681/ASN.2012010058 | pmc=3458460 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22859855 }}</ref><ref name="pmid10495797">{{cite journal |vauthors=Wasserstein AG |title=Membranous glomerulonephritis |journal=J. Am. Soc. Nephrol. |volume=8 |issue=4 |pages=664–74 |date=April 1997 |pmid=10495797 |doi= |url=}}</ref> | ||
* A low serum albumin concentration not the degree of proteinuria is suggestive of a venous thromboembolic event | * A low serum albumin concentration not the degree of proteinuria is suggestive of a venous thromboembolic event | ||
* Compared with patients who had a serum albumin concentration greater than 2.8 g/dL, the risk of an event was 2.5-fold greater in patients with a serum albumin concentration below 2.8 g/dL | * Compared with patients who had a serum albumin concentration greater than 2.8 g/dL, the risk of an event was 2.5-fold greater in patients with a serum albumin concentration below 2.8 g/dL | ||
* All patients who have a [[thromboembolic]] event should be treated initially with low molecular weight or unfractionated heparin, followed by oral anticoagulation (eg, warfarin), the same regimen used for patients without nephrotic syndrome who have deep vein thrombosis or a pulmonary embolism | * All patients who have a [[thromboembolic]] event should be treated initially with low molecular weight or unfractionated heparin, followed by oral anticoagulation (eg, warfarin), the same regimen used for patients without nephrotic syndrome who have deep vein thrombosis or a pulmonary embolism | ||
=== First-line immunosuppressive therapy: === | === First-line immunosuppressive therapy: === | ||
* [[Cyclophosphamide]] plus [[glucocorticoids]] or a [[Calcineurin inhibitor|calcineurin]] inhibitor with low-dose or no glucocorticoids | * [[Cyclophosphamide]] plus [[glucocorticoids]] or a [[Calcineurin inhibitor|calcineurin]] inhibitor with low-dose or no glucocorticoids<ref name="pmid29852477">{{cite journal| author=Bomback AS, Fervenza FC| title=Membranous Nephropathy: Approaches to Treatment. | journal=Am J Nephrol | year= 2018 | volume= 47 Suppl 1 | issue= | pages= 30-42 | pmid=29852477 | doi=10.1159/000481635 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29852477 }}</ref><ref name="pmid22859855">{{cite journal| author=Waldman M, Austin HA| title=Treatment of idiopathic membranous nephropathy. | journal=J Am Soc Nephrol | year= 2012 | volume= 23 | issue= 10 | pages= 1617-30 | pmid=22859855 | doi=10.1681/ASN.2012010058 | pmc=3458460 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22859855 }}</ref><ref name="pmid10495797">{{cite journal |vauthors=Wasserstein AG |title=Membranous glomerulonephritis |journal=J. Am. Soc. Nephrol. |volume=8 |issue=4 |pages=664–74 |date=April 1997 |pmid=10495797 |doi= |url=}}</ref> | ||
* [[Rituximab]] may be used with resistant patients | * [[Rituximab]] may be used with resistant patients | ||
* A random [[urine]] protein-to-[[creatinine]] ratio should not be used as initial and follow-up test to measure the progress of treatment | * A random [[urine]] protein-to-[[creatinine]] ratio should not be used as initial and follow-up test to measure the progress of treatment | ||
* Patients with less than 4.0 g/day on a 24-hour urine collection should not be treated with immunosuppressive therapy. They should be monitored periodically for disease progression every three months for two years and twice yearly | * Patients with less than 4.0 g/day on a 24-hour urine collection should not be treated with immunosuppressive therapy. They should be monitored periodically for disease progression every three months for two years and twice yearly | ||
* Patients with protein excretion between 4.0 and 8.0 g/day on a 24-hour urine collection undergo spontaneous complete or partial remission over a period of three to six years | * Patients with protein excretion between 4.0 and 8.0 g/day on a 24-hour urine collection undergo spontaneous complete or partial remission over a period of three to six years | ||
* [[Glucocorticoids]] alone are not effective | * [[Glucocorticoids]] alone are not effective | ||
* Other drugs include [[mycophenolate mofetil]], [[intravenous immune globulin]], and synthetic [[adrenocorticotropic hormone]] | * Other drugs include [[mycophenolate mofetil]], [[intravenous immune globulin]], and synthetic [[adrenocorticotropic hormone]] | ||
* [[Cyclophosphamide]] and chlorambucil-based regimens are equally effective | * [[Cyclophosphamide]] and chlorambucil-based regimens are equally effective | ||
* The preferred regimen is oral prednisone (0.5 mg/kg per day) or methylprednisolone (0.4 mg/kg per day) given for months 1, 3, and 5 plus oral cyclophosphamide (2.0 to 2.5 mg/kg per day) given for months 2, 4, and 6 | * The preferred regimen is oral prednisone (0.5 mg/kg per day) or methylprednisolone (0.4 mg/kg per day) given for months 1, 3, and 5 plus oral cyclophosphamide (2.0 to 2.5 mg/kg per day) given for months 2, 4, and 6 | ||
* [[Cyclosporine]] plus low-dose [[prednisone]] (maximum of 10 mg/day) | * [[Cyclosporine]] plus low-dose [[prednisone]] (maximum of 10 mg/day) | ||
* The [[cyclosporine]]-treated group had a significantly higher rate of complete (≤300 mg/day) or partial remission of proteinuria, which is defined as less than 3.5 g/day | * The [[cyclosporine]]-treated group had a significantly higher rate of complete (≤300 mg/day) or partial remission of proteinuria, which is defined as less than 3.5 g/day | ||
* Tacrolimus (0.05 mg/kg per day for 12 months with a six-month taper) | * Tacrolimus (0.05 mg/kg per day for 12 months with a six-month taper) | ||
* [[Rituximab injection|Rituximab]] may have benefit among patients with a moderate risk of progression who have not previously received immunosuppressive therapy | * [[Rituximab injection|Rituximab]] may have benefit among patients with a moderate risk of progression who have not previously received immunosuppressive therapy | ||
==References== | ==References== | ||
Revision as of 02:37, 19 July 2018
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Ahsan Hussain, M.D.[2]
Overview
Lipid lowering and anticoagulation for better blood flow. Diuretics to reduce edema. ACE inhibitor or an angiotensin II receptor blocker (ARB) are recomended to reduce renal vascular damage.
Medical Therapy
Following recommendations are advised while dealing with patient suffering membranous glomerulonephritis MGN[1][2][3]
- Lipid lowering and anticoagulation for better blood flow
- Diuretics to reduce edema
- Angiotensin inhibition
- ACE inhibitor or an angiotensin II receptor blocker are recomended to reduce renal vascular damage
Treatment for proteinuria:
- The optimal proteinuria goal in patients with chronic kidney disease is less than 1000 mg/day[1][2][3]
- Attainment of partial remission can result from one or more of the following:
Hpertensive managment:
- The goal blood pressure in patients with membranous glomerulonephritis is the same as it is in other patients with proteinuric chronic kidney disease[1][2][3]
- Blood pressure can be controlled in patients with membranous glomerulonephritis usually requires more than angiotensin inhibition alone
- Volume overload cab be controlled well with loop diuretics
- A low-salt diet is an important component of antihypertensive therapy (especially when using angiotensin inhibitors) and edema control in patients with MN
- A high-salt diet can increase proteinuria.
Treatment for hyperlipidemia:
Treatment for coagulation:
- Patients with nephrotic syndrome, particularly those with membranous glomerulonephritis, are at increased risk for thrombotic events, such as deep vein and renal vein thrombosis or pulmonary embolism.[1][2][3]
- A low serum albumin concentration not the degree of proteinuria is suggestive of a venous thromboembolic event
- Compared with patients who had a serum albumin concentration greater than 2.8 g/dL, the risk of an event was 2.5-fold greater in patients with a serum albumin concentration below 2.8 g/dL
- All patients who have a thromboembolic event should be treated initially with low molecular weight or unfractionated heparin, followed by oral anticoagulation (eg, warfarin), the same regimen used for patients without nephrotic syndrome who have deep vein thrombosis or a pulmonary embolism
First-line immunosuppressive therapy:
- Cyclophosphamide plus glucocorticoids or a calcineurin inhibitor with low-dose or no glucocorticoids[1][2][3]
- Rituximab may be used with resistant patients
- A random urine protein-to-creatinine ratio should not be used as initial and follow-up test to measure the progress of treatment
- Patients with less than 4.0 g/day on a 24-hour urine collection should not be treated with immunosuppressive therapy. They should be monitored periodically for disease progression every three months for two years and twice yearly
- Patients with protein excretion between 4.0 and 8.0 g/day on a 24-hour urine collection undergo spontaneous complete or partial remission over a period of three to six years
- Glucocorticoids alone are not effective
- Other drugs include mycophenolate mofetil, intravenous immune globulin, and synthetic adrenocorticotropic hormone
- Cyclophosphamide and chlorambucil-based regimens are equally effective
- The preferred regimen is oral prednisone (0.5 mg/kg per day) or methylprednisolone (0.4 mg/kg per day) given for months 1, 3, and 5 plus oral cyclophosphamide (2.0 to 2.5 mg/kg per day) given for months 2, 4, and 6
- Cyclosporine plus low-dose prednisone (maximum of 10 mg/day)
- The cyclosporine-treated group had a significantly higher rate of complete (≤300 mg/day) or partial remission of proteinuria, which is defined as less than 3.5 g/day
- Tacrolimus (0.05 mg/kg per day for 12 months with a six-month taper)
- Rituximab may have benefit among patients with a moderate risk of progression who have not previously received immunosuppressive therapy
References
- ↑ 1.0 1.1 1.2 1.3 1.4 1.5 Bomback AS, Fervenza FC (2018). "Membranous Nephropathy: Approaches to Treatment". Am J Nephrol. 47 Suppl 1: 30–42. doi:10.1159/000481635. PMID 29852477.
- ↑ 2.0 2.1 2.2 2.3 2.4 2.5 Waldman M, Austin HA (2012). "Treatment of idiopathic membranous nephropathy". J Am Soc Nephrol. 23 (10): 1617–30. doi:10.1681/ASN.2012010058. PMC 3458460. PMID 22859855.
- ↑ 3.0 3.1 3.2 3.3 3.4 3.5 Wasserstein AG (April 1997). "Membranous glomerulonephritis". J. Am. Soc. Nephrol. 8 (4): 664–74. PMID 10495797.