Membranous glomerulonephritis overview

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Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Membranous glomerulonephritis from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X-ray

CT

Ultrasound

MRI

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

Overview

Historical Perspective

Membranous glomerulonephritis was first discovered by David Jones, renal pathologist from Syracuse University in New York, in 1957.

Classification

There is no established system for the classification of MGN. however it can be divided in two groups based on etiology of MGN.

Pathophysiology

Membranous glomerulonephritis is caused by immune complex formation in the glomerulus. The immune complexes are formed by binding of antibodies to antigens in the glomerular basement membrane. The antigens may be part of the basement membrane, or deposited from elsewhere by the systemic circulation. The immune complex serves as an activator that triggers a response from the complement system and form a membrane attack complex which stimulates release of proteases and oxidants by the mesangial and epithelial cells, damaging the capillary walls and causing them to become leaky. It is thought that MGN is mediated by genetic factors like PLA2R, enviromental factors, drug (captopril) side effects, infections like hepatitis B and hepatitis C

Causes

The main causes of Membranous Glomerulonephritis are Infectious causes like Hepatitis B, drugs like captopril and autoimmune diseases like systemic lupus erythematosus.

Differentiating Hereditary pancreatitis from Other Diseases

MGN must be differentiated from other diseases that cause proteinuria, weight loss, and renal failure, such as MPGN, MCD, and FSGC.

Epidemiology and Demographics

The Incidence rate of Membranous Glomerulonephritis is 27 per 100.000. The prevalence rate of Membranous Glomerulonephritis is 690 per 100,000

Risk Factors

The most potent risk factor in the development of [disease name] is drugs. Other risk factors include penicilliamine and captopril.

Screening

There is insufficient evidence to recommend routine screening for membranous glomerulonephritis.

Natural History, Complications, and Prognosis

Common complications of membranous glomerulonephritis include renal failure.

Diagnosis

Diagnostic Criteria

The most efficient and sensitive test is ANA, ds-DNA antibodies specific test that is utilized for diagnosis of membranous glomerulonephritis. The gold standard test for the diagnosis of biopsy.

History and Symptoms

The hallmark of membranous glomerulonephritis is nephrotic syndrome. A positive history of forthy urine and headache are suggestive of membranous glomerulonephritis.

Physical Examination

Common physical examination findings of membranous glomerulonephritis include edematous feets and headache.

Laboratory Findings

The major laboratory workup includes blood workup, auto-immune workup and urine workup.

Electrocardiogram

There are no ECG findings associated with membranous glomerulonephritis.

X-ray

There are no x-ray findings associated with membranous glomerulonephritis.

Ultrasound

There are no echocardiography and ultrasound findings associated with membranous glomerulonephritis.

CT scan

There are no CT scan findings associated with membranous glomerulonephritis.

MRI

There are no MRI findings associated with membranous glomerulonephritis.

Other Imaging Findings

There are no other imaging findings associated with membranous glomerulonephritis

Other Diagnostic Studies

The patients with compromised renal functions are indicated for biopsy

Treatment

Medical Therapy

lipid lowering and Anticoagulation for better blood flow. Diuretics to reduce edema. Angiotensin inhibition ACE inhibitor or an angiotensin II receptor blocker (ARB) are recomended to reduce renal vascular damage.

Surgery

Surgery is not the first-line treatment option for patients with MGN. Surgery is usually reserved for patients requiring renal transplant.

Primary Prevention

There are no established measures for the primary prevention of MGN.

Secondary Prevention

There are no established measures for the secondary prevention of MGN.

References


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