obsolete nephrotic syndrome with lesion of membranous glomerulonephritis

Nephrotic Syndrome with Membranous Glomerulonephritis: An Obsolete Description

Membranous nephropathy (MN) is a kidney disease characterized by the thickening of glomerular basement membranes due to immune complex deposition, leading to massive proteinuria (>3.5 g/day) and clinically presenting with peripheral edema, hypertension, frothy urine, and manifestations of thromboembolic phenomena [10]. This condition was previously described as a distinct entity, but it is now recognized as one of the many glomerular diseases causing nephrotic syndrome.

Historical Context

In the past, membranous nephropathy was considered a single disease entity with diverse causes. However, current understanding suggests that it is not a single disease, but rather a pattern of injury in the kidney [3]. The condition can be primary/idiopathic or secondary, and its presentation has evolved over time.

Current Understanding

Membranous nephropathy is now recognized as an autoimmune condition that causes the immune system to attack the tiny filtering units (glomeruli) in the kidneys [14]. This leads to changes in the glomerular basement membrane, resulting in massive proteinuria. The condition is characterized by a thickening of the glomerular basement membrane and subepithelial immunoglobulin-containing deposits without or with only marginal cell proliferation or mesangial expansion [12].

Clinical Presentation

The clinical presentation of membranous nephropathy includes peripheral edema, hypertension, frothy urine, and manifestations of thromboembolic phenomena. Laboratory investigations show hypoalbuminemia, dyslipidemia, and acute kidney injury [10]. The condition is often associated with other autoimmune diseases.

Evolution of Understanding

The understanding and management of membranous nephropathy have rapidly evolved over the past decade. Identification of target antigens has allowed for more precise molecular diagnoses, and the ability to monitor circulating autoantibodies has added a new vantage point in terms of disease monitoring [1]. The condition is now recognized as one of the many glomerular diseases causing nephrotic syndrome.

References

[1] Context: Description of obsolete nephrotic syndrome with lesion of membranous glomerulonephritis

[3] Context: Description of obsolete nephrotic syndrome with lesion of membranous glomerulonephritis

[10] Context: Description of obsolete nephrotic syndrome with lesion of membranous glomerulonephritis

[12] Context: Description of obsolete nephrotic syndrome with lesion of membranous glomerulonephritis

[14] Context: Description of obsolete nephrotic syndrome with lesion of membranous glomerulonephritis

Based on the search results, it appears that you are looking for information on the signs and symptoms of a condition that is no longer considered current medical practice. However, I can provide you with some information on the classic presentation of nephrotic syndrome associated with membranous glomerulonephritis (MGN).

Classic Presentation:

• Edema: Severe swelling, particularly around the eyes and in the ankles and feet [13][14]
• Proteinuria: Excess protein in the urine due to kidney damage, leading to water retention [11][12][14]
• Hematuria: Blood in the urine, which may appear pink or light brown due to red blood cells [11][12]

Other Possible Symptoms:

• Arterial Hypertension: High blood pressure, affecting 20-50% of patients [3]
• Microscopic Hematuria: Presence of red blood cells in the urine, affecting 25-50% of patients [3]
• Changes in Renal Function: Abnormalities in kidney function, affecting 25% of patients [3]

Important Note:

Please keep in mind that these symptoms are associated with a condition that is no longer considered current medical practice. Modern medicine has evolved, and the presentation of nephrotic syndrome may differ from what was previously observed.

References:

[1] WG Couser (2017) - Primary membranous nephropathy [3] M Dantas (2023) - Other findings in membranous glomerulonephritis [11] A Nikolopoulou (2019) - Patients present with heavy proteinuria, microscopic hematuria, and acute kidney injury [12] Y Radhakrishnan (2024) - Membranous nephropathy is characterized by deposition of immune complexes leading to thickening of glomerular basement membrane [13] A Nikolopoulou (2019) - Patients present with heavy proteinuria, microscopic hematuria, and acute kidney injury [14] H Trujillo (2020) - Review of membranous nephropathy with emphasis on recent clinical trials and pathophysiologic advances

Diagnostic Tests for Membranous Nephropathy (MN)

Membranous nephropathy (MN) is a kidney disease characterized by the deposition of immune complexes on the basement membrane of the glomeruli, leading to proteinuria and nephrotic syndrome. The diagnosis of MN can be challenging, but various diagnostic tests are available to aid in its identification.

Kidney Biopsy

The gold standard for diagnosing MN is a kidney biopsy, which involves taking a small sample of tissue from the kidney (Radhakrishnan

Treatment Options for Membranous Nephropathy (MN) with Nephrotic Syndrome

Membranous nephropathy (MN) is a common cause of nephrotic syndrome in adults, characterized by deposition of immune complexes along the subepithelial region of the glomerular basement membranes (GBMs). The treatment of MN has evolved over the years, and various drug options are available to manage this condition.

Immunosuppressive Therapies

• Cyclophosphamide: This is a traditional immunosuppressive agent used in the treatment of MN. However, its use has declined due to concerns about toxicity and the availability of newer agents (7).
• Steroids: Corticosteroids, such as prednisone, are often used in combination with other immunosuppressants to reduce proteinuria and slow disease progression (8).
• Calcineurin inhibitors: Tacrolimus and cyclosporine A have been shown to be effective in inducing remission in MN patients. They work by inhibiting the activity of calcineurin, a key component in the activation of T-cells (6, 5).

Targeted Therapies

• Rituximab: This monoclonal antibody targets CD20-positive B-cells and has been shown to be effective in reducing proteinuria and improving renal function in MN patients (2, 9).
• Methylprednisolone: This corticosteroid is often used in combination with other immunosuppressants to reduce inflammation and slow disease progression (10).

Other Treatment Options

• Angiotensin-converting enzyme inhibitors (ACEIs): These medications can help reduce proteinuria by blocking the conversion of angiotensin I to angiotensin II (11).
• Angiotensin receptor blockers (ARBs): Similar to ACEIs, ARBs can also help reduce proteinuria and slow disease progression (11).

It is essential to note that each patient's response to treatment may vary, and the choice of therapy should be individualized based on factors such as renal function, proteinuria levels, and underlying comorbidities.

References: (2) Idiopathic Membranous Nephropathy Treatment Study Group: Methylprednisolone plus chlorambucil as compared with methylprednisolone alone for the treatment of idiopathic membranous nephropathy with nephrotic syndrome in adults. (5) KDIGO Guideline on Glomerulonephritis (6) KDIGO Guideline on Glomerulonephritis (7) Membranous Nephropathy (MN) (8) Idiopathic Membranous Nephropathy Treatment Study Group: Methylprednisolone plus chlorambucil as compared with methylprednisolone alone for the treatment of idiopathic membranous nephropathy with

Based on the search results, it appears that membranous nephropathy (MN) is a common cause of nephrotic syndrome in adults, particularly in older adults. However, there are other conditions that can also present with similar symptoms.

Differential Diagnosis:

• Focal Segmental Glomerulosclerosis (FSGS): This is another common cause of nephrotic syndrome, especially in children and young adults [12].
• Membranoproliferative Glomerulonephritis (MPGN): This condition can also present with nephrotic syndrome and is characterized by the deposition of immune complexes along the glomerular basement membrane [6].
• Lupus Nephritis: Systemic lupus erythematosus (SLE) can cause nephrotic syndrome due to membranous or proliferative glomerulonephritis [4].
• Diabetic Nephropathy: This is a common cause of nephrotic syndrome in diabetic patients, characterized by thickening of the glomerular basement membrane and mesangial expansion [5].

Key Features:

• Age: Membranous nephropathy is more common in older adults, while FSGS is more common in children and young adults.
• Proteinuria: Both membranous nephropathy and FSGS can present with massive proteinuria (>3.5 g/day).
• Edema: Peripheral edema is a common feature of both conditions.

Diagnostic Approach:

• Kidney Biopsy: A kidney biopsy is often required to confirm the diagnosis, particularly in cases where the clinical presentation is atypical or there are multiple potential causes [13].
• Immunofluorescence: This can help identify specific immune complexes and complement components that may be present in the glomeruli.

References:

[1] Membranous nephropathy (MN) is a unique glomerular lesion that is the most common cause of idiopathic nephrotic syndrome in nondiabetic white adults. [2] [3] Eighty percent of patients present with nephrotic syndrome, and the remainder are diagnosed earlier in the disease course after an incidental finding on imaging studies. [4] [5] Known causes of secondary MGN are described under 4 broad categories: (1) drugs/medications, (2) infections, (3) autoimmune disorders, and (4) malignancy. [6] [7] Membranous nephropathy is the most common cause of nephrotic syndrome in older adults but is rare in children. [8] [9] Membranous nephropathy (MN), also known as membranous glomerulopathy, is one of the many glomerular diseases causing nephrotic syndrome. [10] [11] Other factors influencing edema formation in nephrotic syndrome are the patient’s dominant posture (e.g., standing or sitting for prolonged periods) or whether lymphatic or venous insufficiency or congestive heart failure is present.