What Is Membranous Nephropathy?
Membrane nephropathy is a pathomorphological diagnostic term that is a common cause of adult nephrotic syndrome. Its characteristic pathological change is the deposition of a large number of immune complexes on the epithelial side of the glomerular capillaries. The clinical manifestations are nephrotic syndrome (large amount of proteinuria, hypoalbuminemia, high edema, hyperlipidemia), or asymptomatic, non-nephrotic range proteinuria.
- nickname
- Membranous glomerulonephritis
- English name
- membranous nephropathy
- Visiting department
- Nephrology
- Multiple groups
- Middle-aged and elderly
- Common causes
- Associated with antiphospholipase A2 receptors and multisystem diseases
- Common symptoms
- Nephrotic syndrome
Basic Information
Causes of membranous nephropathy
- Membrane nephropathy can be divided into idiopathic and secondary membranous nephropathy according to the cause.
- Idiopathic membranous nephropathy
- Most are related to anti-phospholipase A 2 receptor antibodies. Anti-phospholipase A 2 receptor antibodies bind to the corresponding antigens on podocytes to form an in situ immune complex, which in turn activates complement through an alternative pathway to form a C5b-9 membrane attack. The complex damages podocytes, destroys the glomerular filtration barrier, and produces proteinuria.
- 2. Secondary membranous nephropathy
- Secondary to many systemic diseases, such as systemic lupus erythematosus, rheumatoid arthritis, hepatitis B virus infection, and drugs, poisons, tumors or environmental factors, etc., the drugs that cause secondary membranous nephropathy are mainly gold preparations, Mercury, penicillamine, ibuprofen, diclofenac, etc.
Clinical manifestations of membranous nephropathy
- Age
- More common in people over 40 years of age, the onset is often more insidious.
- 2. Nephrotic syndrome
- The clinical manifestations are nephrotic syndrome (large amount of proteinuria, hypoalbuminemia, high edema, hyperlipidemia), or asymptomatic, non-nephrotic range proteinuria.
- 3. Microscopic hematuria
- May be accompanied by a small amount of microscopic hematuria.
- 4. Hypertension and / or renal impairment
- Some patients have hypertension and / or renal impairment.
- 5. Signs
- Edema of both lower extremities or face, in severe cases, peritoneal effusion and pleural effusion may occur, mostly leakage; some patients may have no clinical symptoms and proteinuria may be found during routine physical examination.
Membranous nephropathy
- Auxiliary inspection
- (1) Quantitative urine protein is usually> 3.5g / day, but rarely exceeds 15g / day;
- (2) Hypoalbuminemia plasma autoprotein <30g / L;
- (3) Hyperlipidemia is mainly caused by elevated cholesterol;
- (4) Negative autoantibodies and normal serum complement levels;
- (5) Hepatitis B and C virus markers were negative.
- 2. Kidney biopsy
- Pathological examination of renal biopsy such as light microscope, immunopathology, electron microscope.
Membrane nephropathy diagnosis
- Diagnosis depends on clinical manifestations and pathological changes of renal biopsy. Renal biopsy pathological changes are as follows:
- Light mirror
- Glomerular capillaries and basement membrane lesions are characteristic changes of membranous nephropathy. Glomerular without proliferative and inflammatory exudative lesions; Mesangial area widening and segmental cell proliferation may occur in the late stage; it may also be manifested as glomerular capillarium segment collapse, abandonment, or even glomerular damage .
- 2. Immunopathology
- IgG is distributed along the glomerular capillaries in granular form. Most patients can 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 epithelial side of the basement membrane of the glomerular capillaries. Phase I: The epithelial side of the electronic denser is small, with a scattered distribution, and the basement membrane structure is intact. In stage II, the dense substance on the epithelial side increased, the basement membrane-like substance proliferated, and the epithelial side protruded to form a spike. Phase III: The basement membrane-like substance further surrounds the electronic dense substance into the membrane, and the basement membrane is significantly thickened and irregular stratification occurs. Stage IV: The electron dense substance in the basement membrane began to absorb, and the electronic translucent area appeared, and the basement membrane changed like a worm. If electron denses are seen in the mesangial area and under the endothelium, attention should be paid to the existence of secondary etiology.
Membrane nephropathy treatment
- Non-immunotherapy
- For young patients with a quantitative urine protein <3.5g / day, normal or mildly reduced plasma albumin, and normal renal function.
- (1) Control of blood pressure Blood pressure is controlled below 125 / 70mmHg, and the drug is preferably angiotensin-converting enzyme inhibitor (ACEI) or angiotensin II receptor antagonist (ARB).
- (2) Anticoagulation therapy can prevent anticoagulation therapy for the high incidence of venous thrombosis in patients with membranous nephropathy. Patients with high risk factors (continuous urine protein> 8g / day, plasma autoprotein <20g / L, application of diuretics or long-term bed rest, etc.) should be actively treated with anticoagulation. Low-molecular-weight heparin injection is the first choice for drugs. If patients have chronic hypoproteinemia, consider switching to oral warfarin anticoagulation therapy, but close monitoring of coagulation function is needed.
- (3) Low protein diet The protein intake of patients with a large amount of proteinuria should be limited to 0.8g / (kg · d), and sufficient calories should be given at the same time. The total calories should generally be guaranteed at 146.54kJ (35kcal) / (kg · d).
- (4) Others include treatment of edema and hyperlipidemia.
- 2. Immunotherapy
- Immunosuppressive therapy depends on the extent and duration of proteinuria and the state of renal function. High-risk patients with proteinuria> 3.5g / day with impaired renal function or proteinuria> 8g / day should be considered immunotherapy.
- Membrane nephropathy immunotherapy regimen and its efficacy evaluation are also very controversial. Generally speaking, glucocorticoids (hereinafter referred to as hormones) alone are not effective, and hormone + cyclophosphamide (CTX) or cyclosporine A (CsA) treatment, Can make some patients achieve clinical remission. Judgment of curative effect may not necessarily be to achieve complete remission (urine protein 0.3g / day), partial remission (urine protein 3.5g / day or urinary protein decrease> 50%, serum albumin> 30g / L) can also be achieved Effectively improve the prognosis of patients.