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{{Membranous glomerulonephritis}}
{{Membranous glomerulonephritis}}
{{CMG}}; {{AE}} {{SAH}}
{{CMG}}; {{AE}} {{SAH}} {{Pervaiz Laghari}}
 


==Overview==
==Overview==
Pharmacologic medical therapy is recommended among patients who has infectious, [[autoimmune]] causes of membranous glomerulonephritis. The drugs like [[prednisone]] and [[cyclophospamide]] are recomended for the treatment of autoimmune cause of membranous glomerulonephritis. Drug like [[Angiotensin-II receptor blocker|Angiotensin receptor inhibitior (ACEi)]] is recomended for managment of hypertension.
==Medical Therapy==
==Medical Therapy==
Following recommendations are advised while dealing with patient suffering membranous glomerulonephritis '''MGN'''<ref name="pmid29891261">{{cite journal| author=Vial R, Daniel L, Devos M, Bouchacourt B, Cazajous G, Sichez H et al.| title=[Chronic lymphoid leukemia and renal complication: Report on 10 cases from Marseille over 16 years]. | journal=Rev Med Interne | year= 2018 | volume=  | issue=  | pages=  | pmid=29891261 | doi=10.1016/j.revmed.2018.05.006 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29891261  }}</ref><ref name="pmid29879319">{{cite journal| author=Tang KT, Tseng CH, Hsieh TY, Chen DY| title=Induction therapy for membranous lupus nephritis: a systematic review and network meta-analysis. | journal=Int J Rheum Dis | year= 2018 | volume= 21 | issue= 6 | pages= 1163-1172 | pmid=29879319 | doi=10.1111/1756-185X.13321 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29879319 }}</ref><ref name="pmid29879066">{{cite journal| author=Wu W, Shang J, Tao C, Wang S, Hu X, Zhang S et al.| title=The prognostic value of phospholipase A2 receptor autoantibodies on spontaneous remission for patients with idiopathic membranous nephropathy: A meta-analysis. | journal=Medicine (Baltimore) | year= 2018 | volume= 97 | issue= 23 | pages= e11018 | pmid=29879066 | doi=10.1097/MD.0000000000011018 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29879066 }}</ref><ref name="pmid29867982">{{cite journal| author=Turrent-Carriles A, Herrera-Félix JP, Amigo MC| title=Renal Involvement in Antiphospholipid Syndrome. | journal=Front Immunol | year= 2018 | volume= 9 | issue=  | pages= 1008 | pmid=29867982 | doi=10.3389/fimmu.2018.01008 | pmc=5966534 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29867982  }}</ref><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="pmid29847754">{{cite journal| author=Morris CA, Patel MJ, Fenves AZ, Masia R| title=Case 17-2018: A 40-Year-Old Woman with Leg Swelling and Abdominal Distention and Pain. | journal=N Engl J Med | year= 2018 | volume= 378 | issue= 22 | pages= 2124-2132 | pmid=29847754 | doi=10.1056/NEJMcpc1712228 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29847754  }}</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>
Following is the treatment of 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><ref name="pmid15847250">{{cite journal |vauthors=Ozsoy RC, Koopman MG, Kastelein JJ, Arisz L |title=The acute effect of atorvastatin on proteinuria in patients with chronic glomerulonephritis |journal=Clin. Nephrol. |volume=63 |issue=4 |pages=245–9 |date=April 2005 |pmid=15847250 |doi= |url=}}</ref>
 
*Pharmacologic medical therapy is recommended among patients who has infectious, autoimmune causes of membranous glomerulonephritis.
* lipid lowering and Anticoagulation for better blood flow.
*First-line therapy for MN is [[Immunosupressive drug|immunosupressive therapy]]. Patients with [[autoimmune]] are treated with [[immunosuppressive]] therapy.
* Diuretics to reduce edema.
*Other pharmacologic medical therapies for membranous glomerulonephritis is treatment of [[proteinuria]] which include [[antihypertensive]] therapy, anticoagulation therapy, anti-lipid therapy.  
* Angiotensin inhibition
'''1. Patients with autoimmune etiology'''
* ACE inhibitor or an angiotensin II receptor blocker (ARB) are recomended to reduce renal vascular damage.


=== Proteinuria goal: ===
'''1.1 Immunosuppressive therapy:'''
* The optimal proteinuria goal in patients with chronic kidney disease is less than 1000 mg/day.
:* Preferred regimen (1): [[Prednisone]] 0.5 mg/kg per day with [[cyclophosphamide]] IV for 3-5 months
:* Preferred regimen (2): [[Methylprednisolone]] 0.4 mg/kg per day given with [[cyclophosphamide]] 2.0 to 2.5 mg/kg per day given IV for 2, 4, and 6 months
:* Preferred regimen (3): [[Tacrolimus]] 0.05 mg/kg per day for PO for 12 months with a six-month taper
:* Preferred regimen (4): [[Rituximab]] 3.5g/day IV for 6-12 months
'''2. Treatment for proteinuria:'''<ref name="pmid291333562">{{cite journal |vauthors=Whelton PK, Carey RM, Aronow WS, Casey DE, Collins KJ, Dennison Himmelfarb C, DePalma SM, Gidding S, Jamerson KA, Jones DW, MacLaughlin EJ, Muntner P, Ovbiagele B, Smith SC, Spencer CC, Stafford RS, Taler SJ, Thomas RJ, Williams KA, Williamson JD, Wright JT |title=2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines |journal=Hypertension |volume=71 |issue=6 |pages=e13–e115 |date=June 2018 |pmid=29133356 |doi=10.1161/HYP.0000000000000065 |url=}}</ref>


* However, this goal is often not attainable in patients with idiopathic MN. As noted above, the renal prognosis in idiopathic MN is markedly improved in patients who attain at least partial remission of proteinuria, defined as protein excretion below 3.5 g/day plusa 50 percent or greater reduction in protein excretion from the peak value [17]. Partial remission was independently associated with a slower decrease in renal function over time (-0.17 versus -0.86 mL/min per month with no remission) and a lower incidence of renal failure (9 versus 29 percent, adjusted hazard ratio [HR] 0.17).
'''2.1 Antihypertensive therapy'''
 
:* Preferred regimen (1) [[angiotensin|Losartan]] PO for 50 mg q daily (100mg per day)  
* Attainment of partial remission can result from one or more of the following: angiotensin inhibition, immunosuppressive therapy, and spontaneous remission, which is not uncommon in idiopathic MN.
'''2.2 Anticoalgulation tharapy'''
'''Goal blood pressure:'''
:* [[heparin|Low molecular weight or unfractionated heparin]], followed by PO [[warfarin]]
* The goal blood pressure in patients with MN is the same as it is in other patients with proteinuric chronic kidney disease. Attainment of this goal can slow the progression of proteinuric chronic kidney disease and can provide cardiovascular protection since chronic kidney disease is associated with a marked increase in cardiovascular risk. The data supporting these recommendations are presented separately.
'''2.3 Anti-lipid therapy'''
 
* Attainment of the blood pressure goal in patients with MN usually requires more than angiotensin inhibition alone. Correction of volume overload is of particular importance and usually requires loop diuretics. Diuretics should be pushed until the blood pressure goal is reached or the patient has attained "dry weight" which, in the presence of persistent hypertension, is defined as the weight at which further fluid removal leads to symptoms (fatigue, orthostatic hypotension) or to decreased tissue perfusion as evidenced by an otherwise unexplained elevation in the blood urea nitrogen and/or serum creatinine concentration.
 
* A low-salt diet is an important component of antihypertensive therapy (especially when using angiotensin inhibitors) and edema control in patients with MN. In addition, a high-salt diet can increase proteinuria, and in some individuals, a high-salt diet rather than increased immunologic activity should be considered as an underlying cause of worsening proteinuria.
 
=== Lipid lowering: ===
* Hyperlipidemia, with often dramatic elevations in the serum cholesterol concentration, is commonly present in patients with nephrotic syndrome. The mainstay of therapy for such hypercholesterolemia is statins. This issue is discussed in detail elsewhere.
 
=== Anticoagulation: ===
* Patients with nephrotic syndrome, particularly those with MN, are at increased risk for thrombotic events, such as deep vein and renal vein thrombosis or pulmonary embolism.
 
* The risk in MN was illustrated in a series of 898 patients in the Glomerular Disease Collaborative Network and the Toronto Glomerulonephritis Registry [23]. Clinically evident and radiologically confirmed venous thromboembolic events occurred in 7.2 percent of patients. The median time to the first thromboembolic event was 3.8 months; 74 percent occurred within the first two years of diagnosis and 86 percent occurred within three years. A low serum albumin concentration at the time of diagnosis, but not the degree of proteinuria, independently predicted 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.
 
* A separate issue is the possible role of prophylactic anticoagulation in patients at high risk for thromboembolism. This issue, including the definition of high risk, is discussed elsewhere.
 
=== First-line immunosuppressive therapy: ===
* Cyclophosphamide plus glucocorticoids or a calcineurin inhibitor with low-dose or no glucocorticoids.
* 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, as noted in a randomized head-to-head comparative trial that primarily enrolled moderate-risk patients (mean protein excretion 7 to 8 g/day and mean serum creatinine 1.05 mg/dL [93 micromol/L]) [28].
* Side effects
* 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 was defined as less than 3.5 g/day plus at least a 50 percent reduction from baseline (75 versus 22 percent with placebo). Renal function was the same in both groups. One year after the cessation of therapy, relapse of proteinuria was common, but 39 percent of treated patients were still in remission, compared to 13 percent with placebo. (See 'Relapsing disease' below.)
* The efficacy of tacrolimus (without glucocorticoids) was demonstrated in a randomized trial of 48 patients with MN who were treated with tacrolimus (0.05 mg/kg per day for 12 months with a six-month taper) or placebo [33]. The rate of complete or partial remission was significantly higher with tacrolimus at both 12 months (82 versus 24 percent) and 18 months (94 versus 35 percent).
* Rituximab may have benefit among patients with a moderate risk of progression who have not previously received immunosuppressive therapy.


'''2.3.1 Life-style modification'''
:*Decrease salt intake
:*Weight loss
'''2.3.2 Statins'''
:*[[Atorvastatin clinical studies|Atorvastatin]] PO 10mg q daily
==References==
==References==
{{Reflist|2}}
{{Reflist|2}}
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Latest revision as of 06:44, 21 October 2020

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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] Pervaiz Laghari, MD[3]


Overview

Pharmacologic medical therapy is recommended among patients who has infectious, autoimmune causes of membranous glomerulonephritis. The drugs like prednisone and cyclophospamide are recomended for the treatment of autoimmune cause of membranous glomerulonephritis. Drug like Angiotensin receptor inhibitior (ACEi) is recomended for managment of hypertension.

Medical Therapy

Following is the treatment of membranous glomerulonephritis.[1][2][3][4]

  • Pharmacologic medical therapy is recommended among patients who has infectious, autoimmune causes of membranous glomerulonephritis.
  • First-line therapy for MN is immunosupressive therapy. Patients with autoimmune are treated with immunosuppressive therapy.
  • Other pharmacologic medical therapies for membranous glomerulonephritis is treatment of proteinuria which include antihypertensive therapy, anticoagulation therapy, anti-lipid therapy.

1. Patients with autoimmune etiology

1.1 Immunosuppressive therapy:

  • Preferred regimen (1): Prednisone 0.5 mg/kg per day with cyclophosphamide IV for 3-5 months
  • Preferred regimen (2): Methylprednisolone 0.4 mg/kg per day given with cyclophosphamide 2.0 to 2.5 mg/kg per day given IV for 2, 4, and 6 months
  • Preferred regimen (3): Tacrolimus 0.05 mg/kg per day for PO for 12 months with a six-month taper
  • Preferred regimen (4): Rituximab 3.5g/day IV for 6-12 months

2. Treatment for proteinuria:[5]

2.1 Antihypertensive therapy

  • Preferred regimen (1) Losartan PO for 50 mg q daily (100mg per day)

2.2 Anticoalgulation tharapy

2.3 Anti-lipid therapy

2.3.1 Life-style modification

  • Decrease salt intake
  • Weight loss

2.3.2 Statins

References

  1. ↑ 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. ↑ 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. ↑ Wasserstein AG (April 1997). "Membranous glomerulonephritis". J. Am. Soc. Nephrol. 8 (4): 664–74. PMID 10495797.
  4. ↑ Ozsoy RC, Koopman MG, Kastelein JJ, Arisz L (April 2005). "The acute effect of atorvastatin on proteinuria in patients with chronic glomerulonephritis". Clin. Nephrol. 63 (4): 245–9. PMID 15847250.
  5. ↑ Whelton PK, Carey RM, Aronow WS, Casey DE, Collins KJ, Dennison Himmelfarb C, DePalma SM, Gidding S, Jamerson KA, Jones DW, MacLaughlin EJ, Muntner P, Ovbiagele B, Smith SC, Spencer CC, Stafford RS, Taler SJ, Thomas RJ, Williams KA, Williamson JD, Wright JT (June 2018). "2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines". Hypertension. 71 (6): e13–e115. doi:10.1161/HYP.0000000000000065. PMID 29133356.

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