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{{Membranous glomerulonephritis}}
{{Membranous glomerulonephritis}}
{{CMG}}; {{AE}}
{{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==
* Given the high rate of gradual spontaneous improvement in patients with idiopathic membranous nephropathy, only selected patients with more severe or progressive disease should receive immunosuppressive therapy.
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>
* In contrast, almost all patients are candidates for more general therapies for nephrotic syndrome, such as angiotensin inhibition, lipid lowering, and, in selected patients, anticoagulation. Other aspects of therapy include diuretics to control edema and maintenance of adequate nutrition.
*Pharmacologic medical therapy is recommended among patients who has infectious, autoimmune causes of membranous glomerulonephritis.
* Angiotensin inhibition
*First-line therapy for MN is [[Immunosupressive drug|immunosupressive therapy]]. Patients with [[autoimmune]] are treated with [[immunosuppressive]] therapy.
* Administration of an ACE inhibitor or an angiotensin II receptor blocker (ARB) is recommended in virtually all patients with proteinuric chronic kidney disease since such therapy may significantly reduce the rate of disease progression, acting at least in part by lowering the intraglomerular pressure.
*Other pharmacologic medical therapies for membranous glomerulonephritis is treatment of [[proteinuria]] which include [[antihypertensive]] therapy, anticoagulation therapy, anti-lipid therapy.  
* The evidence for a renal protective effect with an ACE inhibitor or an ARB is relatively weak among patients with MN. Possible benefits with use of an ACE inhibitor or ARB were noted in a study from the Spanish Group for the Study of Glomerular Disease (GLOSEN), which retrospectively examined the outcomes of 328 patients with MN and nephrotic-range proteinuria (>3.5 g/day)[12]. Although none were treated with immunosuppressive medication, 67 percent of patients received either an ACE inhibitor or ARB, and 32 percent developed complete or partial remission, defined as reduction of protein excretion to <0.3 g/day in at least three consecutive visits, or to <3.5 g/day with normal serum albumin, respectively. The mean time to achieve partial or complete remission was approximately 15 and 39 months. However, because this was not a randomized controlled trial, it is not possible to draw definitive conclusions about the benefit of ACE inhibitors or ARBs on the frequency of spontaneous remission [20]. Furthermore there was a significant rise in the serum creatinine among patients who did not remit in this study, suggesting that there is a significant hazard associated with withholding immunosuppressive therapy in all patients while waiting for spontaneous remission.
'''1. Patients with autoimmune etiology'''
Proteinuria goal
 
The optimal proteinuria goal in patients with chronic kidney disease is less than 1000 mg/day.
 
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).
 
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.
 
Goal blood pressure
 
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.
 
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.
'''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:'''<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>


First-line immunosuppressive therapy
'''2.1 Antihypertensive therapy'''
* Cyclophosphamide plus glucocorticoids or a calcineurin inhibitor with low-dose or no glucocorticoids.
:* Preferred regimen (1) [[angiotensin|Losartan]] PO for 50 mg q daily (100mg per day)  
* Rituximab may be used with resistant patients.
'''2.2 Anticoalgulation tharapy'''
* A random urine protein-to-creatinine ratio should not be used as initial and follow-up test to measure the progress of treatment.
:* [[heparin|Low molecular weight or unfractionated heparin]], followed by PO [[warfarin]]
* 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.
'''2.3 Anti-lipid therapy'''
* 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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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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