Membranous glomerulonephritis (MGN) is a kidney disorder that occurs due to the thickening of the glomerular basement membrane within the kidneys.
Protein leakage into urine can cause chronic kidney disease progression.
Classification of MGN as follows:
Primary MGN
Secondary MGN
MGN is caused by the deposition of immune complexes along the glomerular basement membrane.
The feature is diffuse thickening without significant inflammation or cell proliferation. The podocytes are damaged by the immune deposits that increased permeability allows proteins to pass into the urine.
Idiopathic MGN patients may have spontaneous remission, proteinuria, or kidney failure.
Epidemiology
About 10 to 15 % of the cases of glomerular diseases and 25 to 30% of the cases of end-stage renal disease are found in the U.S.
United States reports approximately 12 cases per million for membranous nephropathies.
In 1% to 7% of pediatric kidney biopsies cases it shows presence of MGN, out of which 50% cases are on risk of progressive kidney disease.
Membranous nephropathy causes about 1.9 ESKD cases per million annually in US.
Anatomy
Pathophysiology
Anti-PLA2R antibodies found in glomeruli and membranous nephropathy with autoimmune liver disease.
In membranous nephropathy, immune complexes deposit in the glomerular basement membrane through in situ production/deposition.
The vascular endothelial cells transport through immune complexes from capillaries to peritubular interstitial space.
This process includes the release of pro-inflammatory cytokines, which initiate the migration of monocytes and neutrophils from the bloodstream into the kidney.
Etiology
The causes of MGN are:
Toxins
Infections
Malignancies
Genetics
Prognostic Factors
Early treatment leads to complete or partial remission with membranous glomerulonephritis.
Higher serum creatinine indicates worse outcomes. Poor prognosis is related to gender, older age, high proteinuria level, and abnormal kidney function.
Granulomatosis presents with upper airway lesions, glomerulonephritis, hemorrhage, and kidney failure.
Around 30% of patients experience spontaneous remission while another 30% shows stable proteinuria.
Clinical History
Collect details including presenting symptoms, complaints, and medical history to understand clinical history of patient.
Patients should take a low-sodium diet control to reduce blood pressure and edema.
Patients should record their blood pressure at home regularly and follow good hygiene practices.
Nutritional counselling plays vital role in recovery process of patient as it promotes the nutritional diet.
To deal with fatigue and stress issues patient should follow occupational or physical therapy which is useful to manage fatigue and maintain functional stability.
Proper awareness about MGN should be provided and its related causes with management strategies.
Appointments with a nephrologist and preventing recurrence of disorder is an ongoing life-long effort.
In the initial assessment phase, the goal is to prevent further kidney damage and diagnose any life-threatening complications in the patient.
Pharmacologic therapy is effective in the treatment phase as it includes use of diuretics, corticosteroids, ACE inhibitors, and immunosuppressants agent.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and intervention therapies.
The regular follow-up visits with the nephrologist are scheduled to check the improvement of patients along with treatment response.
Membranous glomerulonephritis (MGN) is a kidney disorder that occurs due to the thickening of the glomerular basement membrane within the kidneys.
Protein leakage into urine can cause chronic kidney disease progression.
Classification of MGN as follows:
Primary MGN
Secondary MGN
MGN is caused by the deposition of immune complexes along the glomerular basement membrane.
The feature is diffuse thickening without significant inflammation or cell proliferation. The podocytes are damaged by the immune deposits that increased permeability allows proteins to pass into the urine.
Idiopathic MGN patients may have spontaneous remission, proteinuria, or kidney failure.
About 10 to 15 % of the cases of glomerular diseases and 25 to 30% of the cases of end-stage renal disease are found in the U.S.
United States reports approximately 12 cases per million for membranous nephropathies.
In 1% to 7% of pediatric kidney biopsies cases it shows presence of MGN, out of which 50% cases are on risk of progressive kidney disease.
Membranous nephropathy causes about 1.9 ESKD cases per million annually in US.
Anti-PLA2R antibodies found in glomeruli and membranous nephropathy with autoimmune liver disease.
In membranous nephropathy, immune complexes deposit in the glomerular basement membrane through in situ production/deposition.
The vascular endothelial cells transport through immune complexes from capillaries to peritubular interstitial space.
This process includes the release of pro-inflammatory cytokines, which initiate the migration of monocytes and neutrophils from the bloodstream into the kidney.
The causes of MGN are:
Toxins
Infections
Malignancies
Early treatment leads to complete or partial remission with membranous glomerulonephritis.
Higher serum creatinine indicates worse outcomes. Poor prognosis is related to gender, older age, high proteinuria level, and abnormal kidney function.
Granulomatosis presents with upper airway lesions, glomerulonephritis, hemorrhage, and kidney failure.
Around 30% of patients experience spontaneous remission while another 30% shows stable proteinuria.
Collect details including presenting symptoms, complaints, and medical history to understand clinical history of patient.
Intravenous preparation decreases cumulative toxicity risk with lower total dose in medications.
NSAIDs can reduce proteinuria but are now less used compared to ACE inhibitors and ARBs.
Avoid immunosuppressive treatment for asymptomatic proteinuria.
Asymptomatic nephrotic patients with normal kidney function may experience remission.
Secondary membranous nephropathy may be cured to treat the underlying cause such as hepatitis with antivirals
Nephrology
Patients should take a low-sodium diet control to reduce blood pressure and edema.
Patients should record their blood pressure at home regularly and follow good hygiene practices.
Nutritional counselling plays vital role in recovery process of patient as it promotes the nutritional diet.
To deal with fatigue and stress issues patient should follow occupational or physical therapy which is useful to manage fatigue and maintain functional stability.
Proper awareness about MGN should be provided and its related causes with management strategies.
Appointments with a nephrologist and preventing recurrence of disorder is an ongoing life-long effort.
It reduces angiotensin II levels to decrease aldosterone secretion.
Nephrology
Intervention procedures include renal biopsy and plasmapheresis in severe cases.
Dialysis and kidney transplantation is suggested in advanced stages of kidney failure.
Nephrology
In the initial assessment phase, the goal is to prevent further kidney damage and diagnose any life-threatening complications in the patient.
Pharmacologic therapy is effective in the treatment phase as it includes use of diuretics, corticosteroids, ACE inhibitors, and immunosuppressants agent.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and intervention therapies.
The regular follow-up visits with the nephrologist are scheduled to check the improvement of patients along with treatment response.
Membranous glomerulonephritis (MGN) is a kidney disorder that occurs due to the thickening of the glomerular basement membrane within the kidneys.
Protein leakage into urine can cause chronic kidney disease progression.
Classification of MGN as follows:
Primary MGN
Secondary MGN
MGN is caused by the deposition of immune complexes along the glomerular basement membrane.
The feature is diffuse thickening without significant inflammation or cell proliferation. The podocytes are damaged by the immune deposits that increased permeability allows proteins to pass into the urine.
Idiopathic MGN patients may have spontaneous remission, proteinuria, or kidney failure.
About 10 to 15 % of the cases of glomerular diseases and 25 to 30% of the cases of end-stage renal disease are found in the U.S.
United States reports approximately 12 cases per million for membranous nephropathies.
In 1% to 7% of pediatric kidney biopsies cases it shows presence of MGN, out of which 50% cases are on risk of progressive kidney disease.
Membranous nephropathy causes about 1.9 ESKD cases per million annually in US.
Anti-PLA2R antibodies found in glomeruli and membranous nephropathy with autoimmune liver disease.
In membranous nephropathy, immune complexes deposit in the glomerular basement membrane through in situ production/deposition.
The vascular endothelial cells transport through immune complexes from capillaries to peritubular interstitial space.
This process includes the release of pro-inflammatory cytokines, which initiate the migration of monocytes and neutrophils from the bloodstream into the kidney.
The causes of MGN are:
Toxins
Infections
Malignancies
Early treatment leads to complete or partial remission with membranous glomerulonephritis.
Higher serum creatinine indicates worse outcomes. Poor prognosis is related to gender, older age, high proteinuria level, and abnormal kidney function.
Granulomatosis presents with upper airway lesions, glomerulonephritis, hemorrhage, and kidney failure.
Around 30% of patients experience spontaneous remission while another 30% shows stable proteinuria.
Collect details including presenting symptoms, complaints, and medical history to understand clinical history of patient.
Intravenous preparation decreases cumulative toxicity risk with lower total dose in medications.
NSAIDs can reduce proteinuria but are now less used compared to ACE inhibitors and ARBs.
Avoid immunosuppressive treatment for asymptomatic proteinuria.
Asymptomatic nephrotic patients with normal kidney function may experience remission.
Secondary membranous nephropathy may be cured to treat the underlying cause such as hepatitis with antivirals
Nephrology
Patients should take a low-sodium diet control to reduce blood pressure and edema.
Patients should record their blood pressure at home regularly and follow good hygiene practices.
Nutritional counselling plays vital role in recovery process of patient as it promotes the nutritional diet.
To deal with fatigue and stress issues patient should follow occupational or physical therapy which is useful to manage fatigue and maintain functional stability.
Proper awareness about MGN should be provided and its related causes with management strategies.
Appointments with a nephrologist and preventing recurrence of disorder is an ongoing life-long effort.
It reduces angiotensin II levels to decrease aldosterone secretion.
Nephrology
Intervention procedures include renal biopsy and plasmapheresis in severe cases.
Dialysis and kidney transplantation is suggested in advanced stages of kidney failure.
Nephrology
In the initial assessment phase, the goal is to prevent further kidney damage and diagnose any life-threatening complications in the patient.
Pharmacologic therapy is effective in the treatment phase as it includes use of diuretics, corticosteroids, ACE inhibitors, and immunosuppressants agent.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and intervention therapies.
The regular follow-up visits with the nephrologist are scheduled to check the improvement of patients along with treatment response.
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