Diagnosis And Treatment Of Membranous Nephropathy

What is membranous nephropathy?

Membranous nephropathy is a pathomorphological diagnosis term, which refers to a group of diseases in which the deposition of immune complexes under the glomerular visceral epithelial cells leads to a series of lesions in the glomerular basement membrane, and the typical manifestation is diffuse glomerular basement membrane Sexually heterogeneous thickening and "spike" formation.

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20%~25% of membranous nephropathy is secondary to other diseases such as hepatitis B or other infections, autoimmune diseases (systemic lupus erythematosus, Sjögren syndrome, rheumatoid arthritis, etc.), drugs (gold preparations), penicillamine, etc.), tumors, etc. Active treatment of the primary disease or removal of the pathogenic factors can alleviate or even disappear. However, the etiology of most membranous nephropathy is not clear. Therefore, according to the etiology of membranous nephropathy, membranous nephropathy is clinically divided into idiopathic membranous nephropathy and secondary membranous nephropathy. Among them, idiopathic membranous nephropathy accounts for 80% of membranous nephropathy, and more than 30% of patients will develop persistent proteinuria and develop into end-stage renal disease.

What are the clinical manifestations of membranous nephropathy?

The clinical manifestations of membranous nephropathy mainly include:

(1) It is more common in those over 40 years old, and the onset is often hidden.
(2) Nephrotic syndrome: massive proteinuria, hypoalbuminemia, hyperlipidemia, and high edema.
(3) Microscopic hematuria.
(4) Some patients are accompanied by hypertension or renal impairment.
(5) Signs: lower extremities or face edema, severe ascites, pleural effusion, mostly transudate; some patients may have no clinical symptoms, and proteinuria is found during routine physical examination.

It should be noted that if patients with idiopathic membranous nephropathy are not treated in time, 1/3 of them will develop the end-stage renal disease within 10 years of onset, and ultimately they can only rely on hemodialysis or kidney transplantation to continue their lives.

How to distinguish between secondary membranous nephropathy and idiopathic membranous nephropathy?

Secondary membranous nephropathy refers to a definite cause, which can be seen in rheumatic diseases such as lupus and rheumatoid arthritis, infectious diseases such as hepatitis B virus and EB virus, taking gold preparations, penicillamine, heavy metals, and environmental factors, etc. And tumors and other reasons generally can be alleviated by treating the primary disease. The etiology of idiopathic membranous nephropathy is not very clear yet, and the treatment needs to be combined with renal biopsy pathological examination and proteinuria level for comprehensive treatment.

How is membranous nephropathy diagnosed?

The typical renal pathological changes of membranous nephropathy are diffuse thickening of the glomerular basement membrane and "spike" changes in the basement membrane. Immunofluorescence test shows that immunoglobulin and complement are deposited along the capillary wall. Diagnosis depends on clinical manifestations and pathological changes of renal biopsy. The pathological changes of renal biopsy are as follows:

(1) light mirror

Glomerular capillary loop basement membrane lesion is a characteristic change of membranous nephropathy. Glomerular non-proliferative and inflammatory exudative lesions; in the late stage, mesangial area widening and segmental cell hyperplasia may appear; glomerular capillary loops may also be segmentally collapsed, abandoned, or even the entire glomerulus is destroyed.

(2) Immunopathology

IgG is distributed along glomerular capillary loops in granular form, and most patients may be accompanied by C3 deposition, and IgM and IgA deposition can still be seen in a few cases.

(3) electron microscope

Electron-dense deposits were seen on the basement membrane epithelial side of the glomerular capillary loop. Stage I: The electron-dense objects on the epithelial side are small and scattered, and the basement membrane structure is complete. In stage II, the dense matter on the epithelial side increases, the basement membrane-like substance proliferates, and the protrusions on the epithelial side form spikes. Stage III: The basement membrane-like substance further surrounds the electron-dense material into the membrane, and the basement membrane is obviously thickened and irregularly layered. Stage IV: Electron-dense substances in the basement membrane begin to absorb, electron-lucent areas appear, and the basement membrane shows insect-like changes. If electron density is seen in the mesangium and subendothelium, attention should be paid to the presence of a secondary etiology.

How should membranous nephropathy be treated?

The treatment of secondary membranous nephropathy is generally based on the primary disease causing the onset, symptomatic treatment, and comprehensive treatment based on the actual clinical situation of the patient. Idiopathic membranous nephropathy is mainly treated with angiotensin-converting enzyme inhibitors and angiotensin Ⅱ receptor antagonists to reduce proteinuria in patients. At the same time, patients are provided with anticoagulant therapy, lipid-lowering therapy, symptomatic and supportive therapy, and Hormone combined with immune preparation drug therapy.

For patients with refractory conditions caused by hormone absorption disorders, diuretics and albumin supplementation should be provided to patients to reduce gastrointestinal edema; for patients with acute renal failure, active renal treatment is required to correct reversible factors; Those with non-standard hormones and immunosuppressants need to adjust the dose according to the patient's symptoms, strictly follow the doctor's advice and adopt a personalized treatment plan.

Therapeutic drugs: (1) calcineurin inhibitors, such as cyclosporine, tacrolimus, and mycophenolate mofetil, which have a faster onset of action; (2) multi-target immunosuppressive therapy, glucocorticoids are often used clinically Hormone + mycophenolate mofetil + calcineurin inhibitor treatment can exert their respective curative effects through different drugs to achieve a synergistic effect; (3) biological agent treatment such as rituximab (monoclonal antibody) treatment.

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