Mesangial proliferative glomerulonephritis is caused by what

(A) causes
Membranoproliferative glomerulonephritis according to their clinical and laboratorycharacteristics are divided into primary and secondary glomerular disease.
Primary membranoproliferative glomerulonephritis of unknown etiology, is generally believed that type Ⅰ immune complex disease; type II immune complexes andautoantibodies in disease, may be related to heredity.
Secondary mixed cryoglobulinemia, membranoproliferative glomerulonephritis, there arethree kinds of subtypes. Type Ⅰ cryoglobulinemia monoclonal peaks globulin, usually amyeloma protein. Type Ⅱ usually a combination of IgG monoclonal peak of IgM globulin, also known as anti-IgG rheumatoid factor, and type Ⅲ is a multi-strain peakimmunoglobulin. Type Ⅱ and Ⅲ cryoglobulinemia prone to kidney damage. Itspathological features proliferated mesangial cells, white blood cells especiallymononuclear cell infiltration, glomerular basement membrane thickening of the double-track phenomenon. About 1/3 cases of small and medium-sized arteritis, capillarymicrothrombosis. The etiology and pathogenesis of MPGN is not very clear. Type ⅠMPGN immune complex disease, repeatedly sustained by the relatively large insolubleimmune complex deposition. Patients with type II MPGN serum immune complexes,cryoglobulin, complement abnormalities, sustained reductions in serum C3. Promptimmune complexes in the type of MPGN II. Can be detected in patients with type II MPGNserum C3 nephritis factor (C3NeF), C3NeF, C3bBb converting enzyme autoantibodies,C3bBb role to strengthen, leading to sustained activation of the complement bypass, resulting in the degeneration of sustained hypocomplementemia and basement membrane. Complement metabolic disorder as the central link.
In addition, the type II MPGN kidney transplantation often relapse may be due to materialdeposition can cause abnormal glycoproteins in the basement membrane nephritis inserum.
The disease may be related to inheritance, type II MPGN often in patients with HLA-B7.Most of type Ⅰ MPGN patients with a special B-cell alloantigen.

What is a membranous nephropathy

What is membranous nephropathy, a? Believe that a lot of friends do not quite understand, membranous nephropathy is kidney disease a membranous nephropathy isdivided into several phases, each phase has its own features, here we come tounderstand.
What is membranous nephropathy, a? Believe that a lot of friends do not quite understand, membranous nephropathy is kidney disease a membranous nephropathy isdivided into several phases, each phase has its own features, here we come tounderstand. In the understanding of the what is a membranous nephropathy,membranous nephropathy, membranous nephropathy, we briefly introduced the generalwas nephrotic syndrome (proteinuria, hypoalbuminemia, hyperlipidemia, high degree ofedema) or asymptomatic proteinuria. Membranous nephropathy, pathological changesare generally glomerular capillary loops, immune complexes in the epithelial cell calmcharacterized, followed by basement membrane thickening and deformation, the generalnon-proliferation of mesangial, endothelial or epithelial cells or cells infiltration.Immunofluorescence IgG and C3 showed diffuse and uniform granules along thebasement membrane distribution, rare IgM and IgA calm. Membranous nephropathy inseveral specific pathological changes as follows: ① accompanied by more pronouncedmesangial proliferation and mesangial matrix expansion; ② accompanied by interstitiallesions; ③ of the disease associated with glomerular progressive, segmentalhyalinization sclerosis, accompanied by interstitial fibrosis; ④ of the disease can be transformed into a crescent body nephritis type Ⅰ; ⑤ The occasional disease withmesangial IgA dominant immune pathological changes, namely, overlappingmembranous nephropathy and IgA nephropathy performance. A membranous nephropathy, membranous nephropathy, a number of pathological variant is lighter, onlymesangial proliferation, mesangial matrix increase, and the absence of interstitial,glomerular stage of hyalinization as well as the crescent, you renal biopsy puncture reportfully proved consistent with a membranous nephropathy.

Membranous nephropathy etiology

The exact cause of this disease is not yet clear, Clinical according to their causes can be divided into primary MN and secondary MN two categories. The former is of unknown etiology, the latter because it often accompanied by autoimmune diseases such as systemic lupus erythematosus, the incidence of hepatitis B and C, is now generally believed that the disease exist autoimmune abnormalities. Secondary causes of membranous nephropathy caused by:
An autoimmune disease systemic lupus erythematosus, rheumatoid arthritis, diabetes, Hashimoto's thyroiditis, Graves disease, mixed connective tissue disease, Sjogren syndrome, primary biliary cirrhosis, ankylosing spondylitis and acute infectious polyneuritis.
(2) infected with hepatitis B, hepatitis C, syphilis, leprosy, filariasis, schistosomiasis and malaria.
Drugs and toxic organic gold, mercury, D-penicillamine, captopril and probenecid.
Tumors of lung cancer, colon cancer, breast cancer and lymphoma.
Sarcoidosis, graft recurrence of sickle cell disease and angiolymphoid hyperplasia (Kimura disease). 75% of membranous nephropathy can not find the above reasons, that is, belonging to idiopathic membranous nephropathy.

Asymptomatic glomerulonephritis, also known as asymptomatic hematuria or proteinuria ((and)asymptomatic hematuria and / or proteinuria), patients with no edema, hypertension and renal damage, only showed glomerular hematuriaor proteinuria (and) a group ofglomerular disease. Acute infection after glomerular nephritis, referred to as acute nephritis, is a clinical syndrome characterized by acute onset, hematuria, proteinuria, hypertension, edema, oliguria, renal damage, also known as acute nephritis syndrome.Its onset is often infection, streptococcal infection is immune complex type nephritis.

Asymptomatic glomerulonephritis also known as asymptomatic hematuria or proteinuria (and),but only a group of glomerular proteinuria and (or) hematuria of glomerular kidneydisease. The patients had no edema, hypertension, renal damage. This group of diseases caused by a variety of pathological types of primary glomerular disease, thepathological changes of more than a lighter. Hematuria performance IgA nephropathy.

Clinical manifestations of membranous glomerulonephritis

Idiopathic membranous nephropathy can occur at any age, more common in adults, average age 35 years old, male to female ratio of about 1.5 to 2:1. Insidious onset, a small number of precursor infection after the onset. The first symptom of 15% to 20% of asymptomatic proteinuria, 80% with nephrotic syndrome, non-selective proteinuria.Microscopic hematuria in adults about 60% of children with gross hematuria, but rarely see the red tube. Early blood pressure more than normal, with about 50 percent of the progression of high blood pressure, relax and disappear with kidney disease. In the early days, the renal function is normal. 80% have varying degrees of edema, severe chest, ascites, and other body cavity effusions, the mechanism is multifactorial. There are two serious complications of idiopathic membranous nephropathy: ① high coagulation disorder and renal vein thrombosis: increased levels of blood coagulation factor due to nephrotic syndrome, enhanced platelet adhesion and cohesion, antithrombin Ⅲ Kangxian plasmin activity increased, resulting from high-blood clotting disorder.Dexamethasone can promote coagulation. This disease is about 50% of the incidence of renal vein thrombosis, no obvious symptoms, but the nephrotic syndrome increase the more common chronic form. Acute type can show the sudden appearance of low back pain, often more severe, accompanied by the kidney area, hit pain, hematuria, often gross hematuria, white blood cells in urine, a sudden increase in proteinuria, hypertension and acute renal dysfunction, bilateral renal vein thrombosis even oliguria and acute renal failure, the kidneys were increased. Chronic type of renal tubular dysfunction in performance such as: renal glucosuria, amino acids, urine, and renal tubular acidosis. In addition, it may be complicated by pulmonary embolism. Can also occur such as: brain, heart, legs, and extra-renal thrombosis. Clear diagnosis of the need for renal vein or renal artery angiography, radioactive renography and CT are also helpful in the diagnosis. ② combined anti-GBM crescentic glomerulonephritis: the basement membrane damage, membrane antigen exposure or release can lead to the formation of anti-basement membrane antibodies. May be detected in the serum anti-basement membrane antibodies, anti-neutrophil antibodies (ANCA). Therefore, if medically stable patients with rapid renal dysfunction and rapidly progressive glomerulonephritis-like performance, should be highly alert to the possibility of complications.

Symptoms of chronic glomerulonephritis

Chronic nephritis is diverse etiology, pathological and clinical manifestations similar to a group of glomerular diseases, they are common manifestations of edema, hypertensionand urinary abnormalities.
Edema: (1) in the whole course of the disease, most patients with varying degrees ofedema. Edema can be can be light weight, light in only the morning from the chronic nephritis edema found in the performance of the bed, around the eyes, facial swelling, or in the afternoon of both lower extremities ankle edema. Patients with severe, generalized edema. However, there are a very small number of patients throughout the course of the disease do not always appear edema, is often easily overlooked.
(2) high blood pressure: some patients are hypertension symptoms to hospital for treatment, doctors want them to laboratory urine, chronic nephritis caused by high blood pressure. For patients with chronic nephritis, the incidence of hypertension is one sooner or later, their blood pressure can be continuous, intermittent, and diastolic blood pressure (higher than 12.7kPa) is characterized by high blood pressure there are greatindividual differences in the degree of light only 18.7-21.3/12.7-13.3kPa, severe casescan even be more than 26.7/14.7kPa.
(3) urinary abnormalities: abnormal urine is almost a must in patients with chronic nephritis, including urine output changes and microscopic abnormalities. Edema in patients with decreased urine output, and the more severe edema, decreased urine output, the more obvious, and no edema in patients with normal urine majority. Whenpatients with kidney serious damage, urine concentration - dilution of functional disorder, but also increased nocturia and urine specific gravity decreased. The urine of patients with chronic nephritis put under the microscope, you can find almost all of the patients had proteinuria, urinary protein content ranging from (±) to (). Urine can see the levelranging from red blood cells, white blood cells, granular casts, transparent tube. Whenthe acute attack, may have significant hematuria, or even gross hematuria. In addition,patients with chronic nephritis also dizziness, insomnia, anorexia Shenpi fatigue,impatience, and varying degrees of anemia and other clinical symptoms.

Concrete manifestation of acute and chronic nephritis symptoms

Concrete manifestation of the symptoms of acute and chronic nephritis, a lot of people heard of this disease, but specific to the disease what the performance is not clear, which makes many people sick without knowing it, until the discovery condition is very serious? because they missed the best time for treatment to regret it.
Mainly acute and chronic nephritis symptoms: The disease before the onset of more than a history of scarlet fever, tonsillitis, streptococcal infection, 7 to 21 days after infection onset. Three major characteristics of the symptoms of acute and chronic nephritis
Edema: eyelid edema, a few days later the development of the lower limb and body swelling disappear after 2 to 4 weeks.
2, hematuria: the majority of the dark brown or brown. About two weeks after the disappearance of gross hematuria, microscopic examination of hematuria sustainable for several months.
Hypertension: the majority of mild to moderate blood pressure increases, the performance of headache, dizziness, vomiting, usually last for two weeks, then gradually decreased. In addition, it can also be associated with mild anemia, fatigue and low back pain. In the treatment, such as early detection, and complete bed rest, careful treatment, the prognosis is good.
Expert tips can also refer to the laboratory screening and diagnosis of acute and chronic nephritis symptoms
Urinary protein excretion daily 0.5 ~ 2g/m2; any urine protein / creatinine ratio may be <2 (normal 0.1 to 0.3). Urine contains a shaped red blood cells, white blood cells and renal tubular cells, casts, including red blood cell casts and hemoglobin tube characteristic, the more common white blood cell casts and granular casts (protein droplets).
Anti-pathogenic infectious agent antibody titers are usually 1 to 2 weeks rose. Antibody increase against streptococcal antigen products can be measured: the antistreptolysin prime-O (ASO) is upper respiratory tract infection the best instructions, and pyoderma anti-hyaluronidase and anti-DNase B. usually reduce the disease activity of C3 and C4.Return to normal complement levels in 80% of the PSGN cases 6 to 8 weeks, in fact, one case of mesangial proliferative glomerulonephritis (MPGN) is so. Cryoglobulinemia is often persist for several months, and circulating immune complexes can only be detected within a few weeks.
Tubular function is often due to changes in the disorder of interstitial inflammation, leading to decreased ability to concentrate urine and acid secretion capacity, solute exchange impairment of the renal unit. Has some intrinsic glomerular hypertrophy and the ability of tubular function defects is usually occurs before the GFR was significantly reduced. With the gradual progress of glomerular dysfunction, total filtration area was significantly reduced decline in GFR, azotemia appear. GFR can be cleared from the serum creatinine concentration or urine creatinine, estimated rate of GFR is usually returned to normal in 1 to 3 months, proteinuria may last 6 to 12 months, microscopic hematuria for several years. Short-term changes in the urinary sediment of mild upper respiratory tract infection could happen again.
Before the onset of 1 to 6 weeks of this syndrome, there is a history of streptococcal infection, sore throat, impetigo or culture confirmed and the increase can be helpful in the diagnosis of anti-streptococcal antibody titer. Red tube in any glomerulonephritis are visible, but when and clinical manifestations associated, strongly suggestive of acute nephritic syndrome. The ultrasound can help differentiate the acute disease (kidney volume is usually normal or slightly larger) and chronic diseases increased (decreased renal size).
The above symptoms on acute and chronic nephritis, specific to each person will have a gap.