Membranous proliferative glomerulonephritis

Introduction to Membrane Proliferative Glomerulonephritis Membrane-proliferative glomerulonephritis (MPGN), one of the least common types of glomerulonephritis, is generally classified into primary and secondary. The disease has various names, including mesangial. Capillary glomerulonephritis (MCGN), mesangial capillary proliferative nephritis, lobular nephritis, hypocomplementemia nephritis. The disease is a syndrome with specific pathological morphology and immunological manifestations. basic knowledge The proportion of illness: 0.03% Susceptible people: no special people Mode of infection: non-infectious Complications: malnutrition, hyperlipidemia, renal vein thrombosis, renal failure, edema

Membrane proliferative glomerulonephritis etiology

Membrane proliferative nephritis is divided into primary and secondary glomerulopathy according to its clinical and laboratory characteristics.

The cause of primary membrane proliferative nephritis is unknown. It is generally considered that type I is an immune complex disease, type II is an immune complex and an autoantibody disease, which may be related to heredity.

Autoimmune (30%):

There are three subtypes of mixed cryoglobulinemia in secondary membrane proliferative nephritis. Type I cryoglobulinemia is a single-part globulin, usually a myeloma protein, and type II is usually a single-peak IgM ball. Protein-binding IgG, also known as anti-IgG wind factor, while type III is multi-plant peak immunoglobulin, type II and type III cryoglobulinemia is prone to renal damage, its pathological features are large proliferation of mesangial cells, white blood cells In particular, mononuclear cell infiltration, glomerular basement membrane thickening has a double track phenomenon, about 1/3 of cases have small and medium arteritis, microthrombus formation in capillaries, the etiology and pathogenesis of MPGN is not very clear, type I MPGN believes that Immune complex disease caused by repeated and persistent deposition of relatively large insoluble immune complexes. Immunological complexes, cryoglobulin, complement abnormalities, and serum C3 persist in serum of patients with type II MPGN, suggesting that immune complexes are present. The role of type II MPGN, C3 nephritis factor (C3NeF) can be detected in the serum of type II MPGN patients, C3NeF is an autoantibody of C3bBb convertase, which strengthens the action of C3bBb, resulting in continuous activation of complement bypass, resulting in persistent hypo-complementemia. Denaturing the base film, the complement metabolism as the central link.

Abnormal glycoprotein deposition (30%):

Type II MPGN kidney transplantation often recurs, may cause nephritis due to the deposition of substances in the patient's serum that can cause abnormal glycoprotein formation on the basement membrane.

Genetic (30%):

The disease may be related to heredity. Patients with type II MPGN often have HLA-B7, and most patients with type I MPGN have special B cell alloantigen.

Pathogenesis

The pathogenesis of MPGN is still unclear. It is currently believed that it is related to the immunological mechanism. 50% to 60% of MPGN patients have complement C3, C1q and C4 in the blood, suggesting that both the alternative pathway and the classical pathway are activated, resulting in blood complement. Decreased, accompanied by a slight increase in immune complexes and cryoglobulinemia, deposition of immunoglobulins and complements in the glomeruli, but the relationship between complement abnormalities and disease, the role of immune complexes remains to be further Explore.

MPGN is classified into three types according to the form and deposition degree of various immune complex deposition in the glomerular basement membrane and mesangial area.

1. Type I

Mainly deposited in the subendothelial and mesangial areas, type I is associated with viral, bacterial and parasitic infections and some immune complex diseases (eg, hereditary complement deficiency, SLE, mixed cryoglobulinemia, SBE, shunt Nephritis, lymphoma, schistosomiasis, but often idiopathic, 33% to 50% of patients with type I MPGN have hypocomplementemia, 25% to 30% of patients with Clq, C4 and C5 are reduced, 15%~ 20% of patients had a decrease in factor B.

2. Type II

Known as an autoimmune disease, a uniform band-like deposition along the basement membrane of the basement membrane can be observed under electron microscopy. This type is also known as dense deposit disease (DDD) and is often accompanied by subepithelial Similar to hump-like deposits, PAS staining can sometimes be seen as strip-like deep staining on capillary rafts. Type II is mainly thought to be associated with streptococcal infection, which can cause antibody-mediated kidneys due to cross-reactivity between streptococcus and kidney antigens. Damage, type II often complicated by low plasma C3 levels, because some patients have complement activator in the blood, an autoantibody, also known as nephritis factor or C3 nephritis factor, directly against C3bBb, altered C3 bypass transformation, through with invertase Combination, blocking the action of some normal inhibitors such as factor H, increased the activation and consumption of complement, C3 nephritis factor is more common in type I and type II MPGN, especially in type II, more common with lipid nutrition Bad, because MPGN type II is mainly damage to the basement membrane, if a large number of dense sediments are deposited on the basement membrane, these deposits can activate complement, and the complement is replaced by some special substances such as nucleus. Enzyme activators, and typically you can activate the alternative pathway C3 nephritic factor that the secondary continues to increase, resulting in blood decreased complement C3, type MPGN in 70% of patients to reduce complement C3 and factor B.

3. Type III

There are deposits under the endothelium, mesangial area and subepithelial. The difference between type III and type I is whether there is deposition under the epithelium.

With the migration of time, the pathological changes of MPGN mostly progressed from hyperplasia to obvious sclerosis. When the subtype was focal MPGN, the pathological changes of the lesions diffused into the classic MPGN. Some children or adolescents began to be diffuse MPGN, and the subtypes were mostly The lobulated type, after which the movable behavior is focal or complete relief.

Membrane proliferative glomerulonephritis prevention

The course of the disease type 3 is basically the same, prevention should start from its own health, usually avoid fatigue, reasonable diet, scientific exercise, enhance physical fitness, improve the body immunity, to prevent disease, for patients who have suffered and complications, Active and effective prevention and treatment of primary disease and complications should be carried out. Once an infection is found, antibiotics that are sensitive to pathogenic bacteria, strong and non-neotoxic should be selected in time. Those with clear infection should be removed as soon as possible to prevent kidney disease. Progressive development with incomplete function.

Membrane proliferative glomerulonephritis complications Complications malnutrition hyperlipidemia renal vein thrombosis renal failure edema

Infection

When the disease manifests as nephrotic syndrome, a large amount of protein loss, malnutrition, immune dysfunction and application of glucocorticoid treatment can reduce the body's resistance, induce infectious diseases, and clinical signs are often not obvious, although there are many Antibiotics are available for selection. If the treatment is not timely or incomplete, it may cause recurrence and worsening of nephrotic syndrome, and even lead to death.

2. Thrombosis, embolization complications

Due to blood concentration (effective blood volume reduction) and hyperlipidemia, blood viscosity increases, protein loss and liver compensatory synthetic protein increase, causing body coagulation, anticoagulation and fibrinolysis system imbalance, in addition, nephrotic syndrome When the platelet function is hyperthyroidism, and the application of diuretics and glucocorticoids can aggravate the hypercoagulable state, it is prone to thrombosis and embolic complications. Among them, renal vein thrombosis is the most common, and 3/4 cases are slow to form, so the clinical symptoms are not obvious. In addition, pulmonary vascular thrombosis, embolism, lower extremity vein, inferior vena cava, coronary vascular thrombosis and cerebrovascular thrombosis are not uncommon. Thrombosis and embolization complications are important factors that directly affect the therapeutic effect and prognosis of nephrotic syndrome.

3. Renal failure

Patients with nephrotic syndrome may have decreased renal blood flow due to insufficient blood volume, induce pre-renal azotemia, and acute renal failure may occur in a small number of cases. Indirect glomerular filtration rate due to renal tubular hypertension Sudden reduction, leading to acute renal renal failure, common in patients over 50 years of age, there are no obvious incentives, oliguria or no urine, expansion of diuretic is not effective, renal biopsy pathological examination shows glomerular lesions, renal interstitial Diffuse severe edema, renal tubules can be normal or a small number of cell degeneration, necrosis, a large number of protein casts in the renal tubule.

4. Protein and fat metabolism disorders

Long-term protein loss can lead to malnutrition, pediatric growth and development retardation; immunoglobulin reduction causes low immunity and infection; metal-binding protein loss can cause trace element (iron, copper, zinc, etc.) deficiency; endocrine-binding protein deficiency It can induce endocrine disorders; decreased binding protein may increase plasma free drug concentration, accelerate excretion, affect drug efficacy, dyslipidemia leads to increased blood viscosity, promote thrombosis, embolism and cardiovascular system complications, and promote glomeruli Hardening accelerates chronic progression of kidney disease.

Membrane proliferative glomerular nephritis symptoms common symptoms urinary filtration scores significantly decreased high blood pressure pale pale short red blood cell malformation glomerular sclerosis nodular venous thrombosis low complementemia tubular urine

This group of diseases is rare in primary glomerulopathy, and is one of the few proliferative nephritis in nephrotic syndrome. The clinical manifestations of various pathological types are basically similar, no matter what the clinical manifestations of this disease are. There are almost all proteinuria and hematuria, proteinuria is non-selective, hematuria is often microscopic persistent hematuria, and 10% to 20% of patients often have episodes of gross hematuria after respiratory infection, which is serious. Glomerular hematuria with multiple urinary red blood cell malformations, more than one third of patients with hypertension, the degree of hypertension is generally mild, but there are also some cases, especially type II patients, may have severe hypertension, large The dose of hormone therapy may also induce hypertensive crisis. At least half of the patients have acute or chronic renal insufficiency. In the early stage of the disease, renal insufficiency often indicates poor prognosis. Patients often have more serious positive cells after onset. Positive pigmented anemia, manifested as pale, shortness of breath, fatigue, and the degree of anemia is not proportional to the degree of renal dysfunction, the mechanism of its occurrence is still unclear, may Complement activation of the surface of red blood cells, because of the capillary lesions may shorten the life span of red blood cells.

At the onset of the disease, at least 1/2 of the patients presented with nephrotic syndrome, about 1/4 of the patients showed asymptomatic hematuria and proteinuria, and 1/4 to 1/3 of the patients showed acute nephritis With red blood cells and red blood cell tubular urine, hypertension and renal insufficiency, about half of patients may have a history of prodromal respiratory infections, 40% have anti-"O" titers and other evidence of streptococcal infection before onset. Some patients may develop partial lipid dystrophy (Barraquar-Simmons disease), especially type II lesions, and may even occur when there is no clinical manifestation of kidney disease. Some patients may show X-linked inheritance, congenital complement. And a1-antitrypsin deficiency is also prone to occur in this disease type I. In nephrotic syndrome, renal vein thrombosis can occur. Although the disease develops highly individual differences, the disease is generally slow. Sexual progression, because the pathological and immunopathological changes of type I and type II are different and are two types of forms. Currently, they are considered to represent different diseases in clinical practice, and clinical type II is more likely to be characterized by nephritis. Like, crescentic nephritis and acute renal failure have a high concomitant rate, while type I has more features of kidney disease, often with precursor infection and anemia. Type II patients often have persistent low-complementemia and age at onset. Small, almost all patients are under the age of 20, although there are exceptions, in addition, type II is more likely to relapse after kidney transplantation.

Type III is rare, mainly occurs in children and young people, peaking at 10 to 20 years old, <2 years old, >40 years old, and the incidence of men and women is close. There is little description of the clinical manifestations of this type. Basic and long-term clinical type I The change is similar. According to Strife, type III has a lower C3 level, but no C3 nephritis factor. The prognosis of non-renal proteinuria is better than that of nephrotic syndrome. The individual difference in this type of end-stage renal disease is relatively large. In the long-term course of disease, some patients may be more stable or even gradually improve.

Examination of membrane proliferative glomerulonephritis

The patient almost always has hematuria, including microscopic or gross hematuria. Proteinuria can be mild, about 30% of which is asymptomatic proteinuria, but half of the patients have urinary protein >3.5g/24h, more than 90% of patients with proteinuria Poor selectivity, urine FDP and C3 can be elevated.

A characteristic change in laboratory tests is the reduction of blood complement. About 75% of patients with this disease have a persistent decrease in C3. Among them, type II lesions are more common, accounting for 80% to 90%, and about 10% of patients are significantly down to Below 20-30 mg/dl, in type I lesions, the mean C3 concentration decreased to 68% of normal, and type II decreased to 47% of normal, and type II lasted longer than type I, and early acting complement Ingredients (such as C1q, CA) have different degrees of decline in type I lesions, but usually normal or mildly decreased in type II, but type II is often accompanied by a decline in the late-acting complement component C5b-9. In the absence of any changes or treatment, serum C3 levels may fluctuate, and there may be a tendency to return to normal over time, indicating that there is no corresponding relationship between the changes in complement and the condition and treatment, secondary to lupus nephritis. Late liver disease, monoclonal globulin disease, leukemia and metastatic cancer nephrotic syndrome may have a decrease in C3, but other primary nephrotic syndrome, except for nephritis after streptococcal infection, rarely reduces C3, so continuous complement reduction for this Diagnosis of illness There is a big suggestive effect. Unlike the disease, the C3 level of glomerulonephritis often decreases after streptococcal infection, but it returns to normal level in 6-8 weeks. Capillary glomerulonephritis nephropathy In the syndrome, the complement is continuously reduced, more than 2 months, and the C3 is low. It is the result of the reduction of complement pathway activation and synthesis. C3 is decreased and the classical pathways C1q and C4 are generally normal, indicating that the alternative pathway may be activated, but secondary to In cryoglobulinemia, mesangial capillary glomerulonephritis, C4 is more pronounced than C3.

There is a heat-stable factor in the blood of this group of patients, also known as C3 nephritis factor (C3NF), which is an antibody to its own C3 convertase. More than 60% of type II is positive for C3NF, and only 10% for type I. 20% positive may be one of the causes of persistent low C3emia in these patients. C3NF and its analogues can also be found in other glomerular diseases associated with nephritis. Other factors that degrade C3 are especially acute nephritis. It can be detected in lupus nephritis.

The level of serum properdin is usually normal. If the level of C3 is decreased, the level of properdin can also be slightly decreased. The serum level of factor B is usually normal or slightly decreased. The circulating immune complex and cryoglobulin can be positive, more than 75%. Type I has a specific B cell alloantigen, suggesting a genetic basis for susceptibility, and HLA-AB7 and familial BIH deficiency are associated with type II disease.

Clinically, some patients may have azotemia, which often suggests acute nephritic syndrome, glomerular filtration rate is often reduced, but it can also be normal, even kidney biopsy shows severe damage to glomeruli, GFR sometimes normal, often With sodium and water retention, leading to high blood pressure, more than half of patients may have positive cell anemia, anemia can be very serious, its severity is not proportional to azotemia, red blood cell and platelet life can be shortened, 40% to 60% The patient's anti-streptococcal antibody titer is increased.

1. Type I membrane proliferative glomerulonephritis pathology and biopsy examination:

(1) Light microscopy: The main changes in type I membrane proliferative glomerulonephritis are diffuse capillary wall thickening and intravascular cell proliferation, as well as single nucleus leukocyte and neutrophil infiltration, mesangial area and capillaries. The wall exhibits different degrees of expansion due to cell proliferation and increased matrix. It usually affects almost all the leaflets uniformly, which can cause the lobular structure of the capillary plexus to protrude. Therefore, this lesion is called lobular glomerulonephritis in the early stage. There is a causal or sequential relationship between lobulated and non-lobulated lesions. It is still inconclusive. The mesangial area is obviously dilated to form a nodular shape, and the middle part of the nodule may have a sclerotic foci, which is hardened or diabetic with glomerulus. The lesions of the chain deposition disease are similar, but the results of immunofluorescence and electron microscopy can easily distinguish the disease from other diseases. Another obvious but not specific manifestation is the thickening of the glomerular basement membrane. Appropriate staining (such as silver staining or periodic acid Schiff acid staining) can be easily seen as double or multi-layered due to the proliferation of mesangial cells and their matrix extension and insertion. Between the endothelial cells and the endothelial cells, the interstitial space is formed, that is, the inserted mesangium forms a pseudo basement membrane instead of the generally considered basement membrane division. Occasionally, eosinophilic deposits can be seen in the subendothelial area, and a few patients may have new Moon body, but rarely involving more than 50% of glomeruli, like other nephritis, such as a large number of crescents suggest poor prognosis, advanced patients often have interstitial fibrosis, tubule atrophy and interstitial mononuclear inflammatory cells Infiltration, "transparent thrombosis" appears in the capillary lumen, suggesting that the lesion may be secondary to cryoglobulinemia or systemic lupus erythematosus. "Transparent thrombosis" is not a true thrombus, but an immune complex filled with capillary lumen. .

Under the renal biopsy light microscope, MPGN can be divided into 5 subtypes: 1 lobulated type: capillary vasospasm is obviously lobulated, mainly cell proliferation, and can also be accompanied by different degrees of hardening, 2 classic type ( Double-track type): The basement membrane is diffusely thickened due to the insertion of the mesentery, and there is a double-track, lobulated atypical, 3-mixed type: mesenteric insertion and lobulation are not typical, but under the epithelium of the basement membrane, There are immune complex deposition in the subcutaneous and mesangial areas, mesangial cell proliferation and stromal hyperplasia, and the basement membrane is obviously hypertrophic. This type is very similar to the diffuse hyperplasia of lupus nephritis. Some people call it mixed membrane and hyperplasia. Glomerulonephritis, 4 focal types: MPGN changes account for less than 50% of all glomeruli, 5 crescents: more than 50% of glomeruli appear crescent.

(2) Electron microscopy: The typical feature of ultrastructure is the extension and metaphase between mesangial cells and matrix in the basement membrane of glomerular capillaries and endothelial cells, with electron dense immune complex deposition, mesangial capillary kidney The name glomerulonephritis is derived from this change in mesangial and capillaries in type I lesions. New basement membrane material is formed around the subendothelial sediment and in the vicinity of the cytoplasm of mesangial cells. In areas where mesangial cell proliferation and mesangial matrix expansion, there is usually scattered dense deposits, and there may be many different types of electron dense deposits under the epithelium. When the amount is sufficient, it is similar to membranous nephropathy, some kidney pathologists call it. "Mixed membranous and proliferative glomerulonephritis", or Burkholder's "type III mesangial capillary glomerulonephritis", there are very few lesions with glomerular damage and type I light microscopy and immunity The fluorescence is similar, but the ultrastructure is characterized by irregular thickening of the glomerular basement membrane and a large number of sediments with different densities in the membrane. Such lesions are also classified as type III, and there may be between the mesangial matrix and the basement membrane. Single core Infiltration of cells or neutrophils, some of the renal biopsy tissue has a small to medium amount of extra-membranous deposits that are "hump", and the epithelial foot processes often disappear. The transparent thrombus under the light microscope is characterized by intravascular spheroidal compacts. When these structures or any other electron-dense deposits present a microtubular-like structure, suggesting that it may be cryoglobulinemia or immunological whisker-like nephropathy.

(3) Immunofluorescence: The characteristic change is that the complement, especially C3 and immunoglobulin, are in a granular or band-like distribution, which can show the contour of the periphery of the leaflet, which is related to the site of the deposition of the subendothelial immune complex observed by electron microscopy. Consistently, the morphology of sediments is usually not as symmetrical as membranous nephropathy, and the granules are not so obvious. The properdin and B factors are similarly distributed. The granular deposition of mesangial membranes may or may not be obvious. A few type I visible immune complexes Along the basement membrane of the tubule and/or the glomeruli outside the glomerulus, the composition of the deposited immune complex can vary widely and may reflect multiple causes of type I. Most patients deposit C3 more than any immune ball. The proteins are obvious, some are mainly IgG or IgM; there are very few IgA-based IgA nephropathy, which is considered to be mesangial capillary glomerulonephritis, and early contributing complement components such as C1q and C4 A little less than C3, a small number of patients can see a segmental granular distribution of Ig (especially IgM and IgG) in the capillary wall, occasionally in the mesangial area, a large number of immunoglobulins in the capillary lumen Complement deposition forms a globular structure, which is consistent with the transparent thrombus observed by light microscopy, suggesting that the lesion is secondary to systemic lupus erythematosus or cryoglobulinemia.

2. Type II membranous proliferative glomerulonephritis pathology and biopsy:

(1) Light microscopy: Type II changes in light microscopy are more variable than type I, not just changes in membrane proliferation, which is what some renal pathologists consider to be called dense deposits than type II mesangial capillary kidneys. Small ball nephritis is more accurate. In 1995, WH0 classified it as a secondary metabolic disease. In histology, it showed glomerular mesangial cells and stromal hyperplasia. When hyperplasia was obvious, it could form a distinct lobulated structure. Capillary wall thickening, some capillaries due to interstitial space, the capillary wall is double-orbital, these typical membrane proliferative changes are similar to type I, but some have obvious capillary wall thickening, cell proliferation is foci No or no cell proliferation, and some cells only have focal or diffuse hyperplasia, but there is no significant thickening of the capillary wall. The degree of mesangial changes is highly individual, mesangial cells and matrix. The increase can be very mild or severe. There are circular eosin deposits in the mesangial area with Masson's trichrome staining. Some may have subepithelial "hump"-like deposits, and the number of neutrophils in the capillary lumen is often Increase, a small number of crescent formation, interstitial may have leukocyte infiltration and fibrosis, therefore, type II light microscopic changes can be similar to other nephritis, the need to combine the results of electron microscopy and immunofluorescence to accurately determine, there are individual reports of this type The patient is not associated with mesangial hyperplastic changes and is therefore different from type I.

(2) Electron microscopy: Type II, also known as compact deposition disease, emphasizes that the diagnostic feature of this disease is the formation of discrete electron dense bands on the glomerular basement membrane, accompanied by mesangial or irregular compacts. Deposition, sometimes under the subendothelial and subepithelial deposits, some changes similar to the "hump" of glomerulonephritis after streptococcal infection, the basement membrane is significantly widened and has an extremely electronic dense structure, which has great diagnostic significance, but In each glomerulus, some capillary walls may not have the above lesions, and the dense structure may be fusiform, globular or sausage-like, and the boundary between the normal structure and the normal structure is clear, and the mesangial cells and the matrix often extend to the periphery. Interstitial, but not obvious type I, epithelial cell foot processes often disappear completely, many patients in the mesangial area often have round electron dense deposits, such as renal tubular basement membrane with electron dense deposits, it is highly suggestive of type II disease damage.

(3) Immunofluorescence: a large amount of C3 is linear or banded in the basement membrane of the glomerular capillary wall, and C3 is a discontinuous linear type, which can show the contours of the capillary wall, renal capsule and renal tubule. Membrane deposits are scattered needles or rings, and the ring shape is the result of staining only the outer side of the sediment. In addition, many capillary walls may have granular C3 deposits, and the linear capillary wall fluorescence The double-orbital shape is due to the deposition of C3 on both sides of the basement membrane. Other complement components are found in less than 50% of biopsy cases, and immunoglobulin deposition is rare.

3. Other types of mesangial capillary glomerulonephritis:

It is not yet certain whether they are variants of type I lesions or independent lesions. These types are almost always identified on the basis of electron microscopy. Burkholder proposed a type III lesion, which is characterized by a common pathology other than type I. In addition to the changes, there is a prominent subepithelial immune complex deposition, and the blood vessel wall is accompanied by isolated extramembranous deposits, which are isolated by the basement material protrusions (similar to the nail shape of the membranous glomerulonephritis basement membrane). Protrusion), some scholars believe that this type is a mixture of membranous and proliferative glomerulonephritis. In addition, in recent years, some scholars have reported various types of mutations, such as type IV, with basement membrane division. The layered features are characterized by subepithelial and subendothelial deposits, and the rest are not described here.

Diagnosis and differentiation of membrane proliferative glomerulonephritis

Diagnostic criteria

The main basis for the diagnosis of this disease is the pathological examination results. Electron microscopy and immunofluorescence can distinguish between type I and type II, persistent hypocomplementemia, persistent non-selective proteinuria (or nephrotic syndrome) with severe diversity. Malformed erythrocyte urine, anemia that is not proportional to the decline in renal function, often suggests that the disease occurs. C3 nephritis factor and blood complement C3 decrease simultaneously often suggest disease activity, and low C3emia is also seen in other secondary glomerulopathy such as: Active liver disease, leukemia, metastatic tumors, and immunoglobulinemia are not difficult to identify because of their primary disease characteristics.

Because MPGN often develops acutely after upper respiratory tract infection, it is characterized by acute nephritis syndrome. Even half of the patients have positive evidence of anti-O Streptococcus infection, so it should be differentiated from glomerulonephritis after streptococcal infection. Frequently, there is gross hematuria, and the level of blood complement often returns to normal within 2 months. The gross hematuria of this disease is rare in the first year after onset, while the persistent low-complementemia should be suspected of this disease, and after streptococcal infection. The pathology of nephritis often manifests as intraproliferative proliferative glomerulonephritis, which is not difficult to distinguish with pathological examination.

Type IV systemic lupus erythematosus active period, complement, especially C3 is often reduced, pathological examination sometimes has mesangial structure to the basement membrane and endothelium to form a metaphase, the lesions are extensive, immune complexes can be deposited in the glomerulus The site is somewhat confused with the disease type I, but attention can be made to the positive degree of C1q combined with other clinical manifestations and immunofluorescence and serum immunological examination.

Pathological examination of type I is markedly dilated in the mesangial area and may be manifested as a nodular sclerosis, similar to the light microscopy of diabetic glomerular sclerosis or light chain deposition disease, but the results of immunofluorescence and electron microscopy can easily It is distinguished from other diseases, and of course, combined with clinical manifestations, blood biochemistry and serum immunological examination are easier to identify.

Should be differentiated from other secondary mesangial capillary nephritis, such as hepatitis B associated nephritis, according to viral serology and kidney tissue hepatitis B virus antigen markers can be identified, cryoglobulinemia clinical and pathological are similar to the disease However, it is rare, and the former has a corresponding systemic manifestation. Pathology includes renal vasculitis and transparent thrombosis suggesting secondary lesions.

Differential diagnosis

Diagnosing MPGN requires the exclusion of all secondary factors, such as hepatitis B or hepatitis C, AIDS, other infections or connective tissue diseases. The diagnosis of MPGN is mainly through histopathological examination, along with hepatitis C-related MPGN, HIV-related MPGNC is becoming more and more popular, and patients with seemingly primary MPGN must have a corresponding serological examination. Common diseases that need to be identified are:

Diabetic nephropathy

The nodular lesions of MPGN appear in most glomeruli, while the small balls with nodular lesions in diabetic nephropathy are relatively few, and can be identified by immunopathology.

2. Amyloidosis nephropathy

HE, Congo red staining and electron microscopy can be completely identified.

3. Light chain nephritis

Under light microscopy and MPGN are difficult to identify, immunopathology can be clearly distinguished.

4. Lupus nephritis

Chronic hypo-complementemia should be differentiated from lupus nephritis. There are many types of pathological changes in lupus nephritis. For example, MPGN-like changes similar to type I and III can occur, but lupus nephritis can be found in the glomerulus. There are depositions of IgG, IgM, IgA, C3, C4, C1q, that is, "full hall bright" performance, while MPGN is rare in the presence of multiple immunoglobulins and complement deposition.

5. Allergic purpura nephritis

There may be pathological changes similar to MPGN, and the main points of differentiation are a large amount of IgA deposition on the mesangial area and capillary vasospasm of purpuric nephritis, and may also show skin purpura, joint pain and abdominal pain.

6. Post-infection nephritis

Post-infection nephritis and MPGN type I are sometimes difficult to identify, but the course of nephritis is generally shorter after infection, and occasionally nephritis can also develop into MPGN.

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