Mesangial proliferative glomerulonephritis

Introduction to mesangial proliferative glomerulonephritis Mesangial proliferative glomerulonephritis (MsPGN) is a pathologically diagnosed nephritis according to light microscopy. It is a group of diffuse mesangial cell proliferation and varying degrees of mesangial matrix. The main feature of glomerular disease. The disease is more common in older children and young adults. The incidence of children is more common in 3 to 15 years old, with an average age of 8 years. The average age of onset of adults is 25 years. The incidence of men is slightly more than that of women. This group of diseases is less common in primary glomerulopathy, and is one of the few proliferative nephritis in nephrotic syndrome. The clinical manifestations of various pathological types are basically similar. Regardless of the clinical manifestations of the disease, almost all proteinuria and hematuria are present, proteinuria is non-selective, and hematuria is often microscopic persistent hematuria, with 10%. ~20% of patients often have paroxysmal gross hematuria after respiratory infection, which is a glomerular hematuria of severe and diverse urinary red blood cell malformation. basic knowledge The proportion of illness: 0.0025% Susceptible people: no special people Mode of infection: non-infectious Complications: renal vein thrombosis, renal failure

The cause of mesangial proliferative glomerulonephritis

Immune complex disease (30%):

There are three subtypes of mixed cryoglobulinemia in secondary membrane proliferative nephritis. Cryoglobulinemia is a single-part globulin, usually a myeloma protein. Usually, the single-plant peak IgM globulin binds IgG, also known as anti-IgG wind factor, while the type III is a multi-plant peak immunoglobulin. Type II and III cryoglobulinemia is prone to kidney damage. Its pathological features are hyperplasia of mesangial cells, leukocyte, especially mononuclear cell infiltration, and thickening of glomerular basement membrane. About 1/3 of the cases have small and medium arteritis, and there are microthrombus formation in the capillaries. The etiology and pathogenesis of MPGN are not well defined. Type I MPGN is considered to be an immune complex disease caused by repeated deposition of relatively large insoluble immune complexes. Immune complexes are also present in the serum of patients with type II MPGN, cryoglobulin, complement abnormalities, and serum C3 continue to decrease. Both suggest the role of immune complexes in type II MPGN.

Autoantibody disease (30%):

C3 nephritis factor (C3NeF) can be detected in the serum of MPGN patients. C3NeF is an autoantibody of C3bBb convertase, which enhances the action of C3bBb, resulting in continuous activation of the complement bypass, resulting in persistent hypocomplementemia and basement membrane degeneration. Therefore, complement metabolism disorder is the central link. In addition, 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.

Genetics (20%):

The disease may be related to heredity, and HLA-B7 is common in patients with type II MPGN. Most type I MPGN patients have a specific B cell alloantigen.

Mesangial proliferative glomerulonephritis prevention

Start with your own health, usually avoid fatigue, reasonable diet, scientific exercise, enhance physical fitness, improve the body's immunity, to prevent disease. For patients with and with complications, active and effective prevention and treatment should be carried out for primary disease and complications. Once an infection is found, antibiotics that are sensitive, potent, and non-neotoxic to pathogenic bacteria should be selected in a timely manner. Those with a clear infection should be removed as soon as possible to prevent the progressive development of renal insufficiency.

Mesangial proliferative glomerulonephritis complications Complications, renal vein thrombosis, renal failure

Infection

Mesangial proliferative glomerulonephritis manifests as nephrotic syndrome, a large number of protein loss, malnutrition, immune dysfunction and the use of glucocorticoid treatment can reduce the body's resistance, induce infectious diseases, and clinical signs are often not Obviously, although there are many antibiotics to choose from, if the treatment is not timely or incomplete, it is still easy to cause recurrence of nephrotic syndrome and worsening of the disease, and even lead to death of the patient.

2. Thrombosis, embolism

Increased blood viscosity due to blood concentration (effective blood volume reduction) and hyperlipidemia; large loss of protein and increased compensatory synthetic protein in the liver can cause imbalance in body coagulation, anticoagulation and fibrinolysis systems. In addition, platelet hyperfunction in nephrotic syndrome, combined with the use of diuretics and glucocorticoids, can increase hypercoagulable state, prone to thrombosis, 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. Complications of thrombosis and embolism 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 and induce pre-renal azotemia. Acute renal failure can occur in a small number of cases. Due to the intraluminal hypertension, the glomerular filtration rate is indirectly reduced, leading to acute renal renal failure. Common in patients over the age of 50, there are no obvious incentives, manifested as oliguria or no urine, expansion of diuretic is invalid. Renal biopsy pathological examination showed that glomerular lesions were mild, renal interstitial diffuse severe edema, renal tubules were normal or a few cells were degenerated, necrotic, and there were a large number of protein casts in the renal tubules.

Mesangial proliferative glomerular nephritis symptoms common symptoms low back pain with renal area snoring hematuria with proteinuria chronic renal insufficiency hematuria

This group of diseases is less common in primary glomerulopathy, and is one of the few proliferative nephritis in nephrotic syndrome. The clinical manifestations of various pathological types are basically similar. Regardless of the clinical manifestations of the disease, almost all proteinuria and hematuria are present, proteinuria is non-selective, and hematuria is often microscopic persistent hematuria, with 10%. ~20% of patients often have paroxysmal gross hematuria after respiratory infection, which is a glomerular hematuria of severe and diverse urinary red blood cell malformation. About one-third of patients are associated with hypertension, and the degree of hypertension is generally mild, but there are also cases, especially type II patients, which may have severe hypertension, and high-dose hormonal therapy may also induce hypertensive crisis. At least half of the patients have acute or chronic renal insufficiency, and renal insufficiency at the onset of the disease often indicates a poor prognosis. Patients often have more severe positive cells of pigmented anemia after onset, manifested as pale, shortness of breath, fatigue, and the degree of anemia is not proportional to the degree of renal dysfunction.

Examination of mesangial proliferative glomerulonephritis

Laboratory inspection:

1. Urine examination: There are often obvious abnormalities. Microscopic examination shows glomerular hematuria. The red blood cells in the urine are pleomorphic. The incidence of hematuria accounts for 70% to 90%, often under the microscope. Urine protein is often non-selective. Macromolecular proteins such as C3 and 2 macroglobulin can be found in the urine.

2. Blood examination: Most of the early renal function was normal, and a small number of glomerular filtration rate decreased. Serum IgG levels were slightly decreased, and in very few cases, C4 levels were reduced, and in some cases, blood IgM or IgG circulating immune complexes were positive. Serum IgA levels were not high, complement C3 was normal, anti-streptavidin "O" titers were generally normal, and antinuclear antibodies and rheumatoid factor were negative.

Diagnosis and differentiation of mesangial proliferative glomerulonephritis

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. With the increasing prevalence of hepatitis C-associated MPGN and HIV-associated MPGNC, patients with seemingly primary MPGN must have a corresponding serological examination. Common diseases that need to be identified are:

1. Diabetic nephropathy: MPGN nodular lesions occur in most glomeruli, while diabetic nephropathy has relatively few granules with nodular lesions, and can be identified by immunopathology.

2. Amyloidosis nephropathy HE, Congo red staining and electron microscopy can be identified.

3. Light chain nephritis: It is difficult to identify MPGN under light microscope, and immunopathology can be clearly distinguished.

4. Lupus nephritis: Chronic hypocomplementemia 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 have IgG, IgM, IgA, C3, C4, C1q in the glomerulus. Deposition, that is, "full house" performance, and MPGN is rare in the presence of multiple immunoglobulins and complement deposition.

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