IgA nephropathy introduce

IgA nephropathy introduce

IgA nephropathy (IgA nephropathy) is 1968 by Berger first described, also known as Berger disease, is a special type of glomerulonephritis, mostly in children and young people, often before the onset of upper respiratory tract infection, its clinical manifestations Diversity, hematuria is the most common, can be accompanied by varying degrees of proteinuria, severe illness can also occur when the blood pressure and serum creatinine increased. IgA nephropathy must be diagnosed by renal biopsy, pathological changes characterized by mesangial proliferation and mesangial area markedly filled with IgA deposition characterized by a group of glomerular diseases. IgA nephropathy can be pided into primary and secondary two types, which are often secondary to cirrhosis, intestinal diseases, arthritis, herpes dermatitis and other diseases. It is also characterized by significant IgA deposition in the glomerular mesangial area.

IgA nephropathy is a common glomerular disease worldwide. In Asia and the Pacific, IgA nephropathy is the most common primary glomerular disease, accounting for 30-40% of patients with renal biopsy. IgA nephropathy in China is the most common chronic glomerulonephritis, accounting for 40% of primary glomerular disease to 47.2%. And the data show a nearly 10-year trend. Peking University First Hospital, Department of Nephrology data show that IgA nephropathy accounted for the proportion of all primary glomerular disease close to 60%. IgA nephropathy is not only common, but also one of the most common primary glomerular diseases leading to end-stage renal disease. It is found that patients with more than 20 years, about 20% to 30%, or even 20% to 50% End stage renal disease.

So far, the exact pathogenesis of IgA nephropathy has not been elucidated, a variety of factors involved in the occurrence and progress of the disease. IgA1 molecules (ie, immunoglobulins deposited in the glomerular mesangial area) are synthesized, released and persisted in peripheral blood, binding to mesangial cells, and deposition, as well as triggering inflammatory responses that are specific for IgA nephropathy Pathogenesis, and subsequent inflammatory response caused by glomerular cell hyperplasia, glomerular sclerosis, tubule atrophy and renal interstitial fibrosis is a common pathway for all glomerular disease progression.

IgA nephropathy can occur in the following clinical manifestations:

1. onset of naked eye hematuria: more common in children. Its gross hematuria in the upper respiratory tract infection (tonsillitis, etc.) occurred after the interval of more than 24 to 72 hours. Gross hematuria can be sustained for several hours to several days, and then to a continuous microscopic hematuria, some patients can disappear urine hematuria.

2. microscopic hematuria and asymptomatic proteinuria: This is the main clinical manifestations of children and adolescents with IgA nephropathy, often found in physical examination, can be expressed as a simple microscopic hematuria, or microscopic hematuria with a small amount of proteinuria.

3. Proteinuria: mild proteinuria, urine protein quantitative generally <1g / 24h, a small number of patients may be a lot of proteinuria and even nephrotic syndrome.

4. Other: some patients with IgA nephropathy may occur nephrotic syndrome, rapid nephritis syndrome, renal failure, a few can appear waist and / or abdominal pain with hematuria.

The following conditions may be considered for the diagnosis of IgA nephropathy:

1. upper respiratory tract infection after the gross hematuria or microscopic hematuria (glomerular origin, deformed red blood cells) or asymptomatic proteinuria; 2. serum IgA may be increased; 3. renal biopsy immunopathology check the glomerular Mesangial area can be seen in the granular IgA-based immunofluorescence; 4. In addition to streptococcal infection after acute glomerulonephritis, non-IgA mesangial proliferative glomerulonephritis, thin basement membrane nephropathy, lupus nephritis, purpura nephritis, cirrhosis And renal damage to alcoholic liver disease. But confirmed IgA nephropathy must have renal biopsy immunopathological examination.

????Special attention is to note that IgA nephropathy in the early general only proteinuria, occult blood and other urine abnormalities, physical symptoms are not obvious, if not urine or blood pressure measurement can not be found in the disease. But with the kidney damage inherent cells continue to increase, the scope of the gradual expansion of the late there will be renal anemia, renal hypertension, nausea and vomiting, etc., and this time and then clear diagnosis is often more difficult, renal function deterioration will be very rapid. Our daily work often encountered such cases, many years ago physical examination had found high blood pressure or urine abnormalities, but because there is no significant physical discomfort did not carry out further diagnosis and treatment, and many years later when there are obvious symptoms and then visit Found to have reached the stage of advanced uremia of nephropathy. Therefore, attention to physical examination, especially young people attach importance to the necessary physical examination, and physical examination must be routine urine examination is very important.

There is no cure for IgA nephropathy at present, and there is often a need to intervene from multiple levels, including:

1. To avoid infection, to prevent the invasion of the antigen, often involved in the eradication of surgical pathogens such as resection of the usual infection of the tonsils; 2. Active control of blood pressure, first choice renin angiotensin inhibitor or renin angiotensin receptor blockers ; 3 If the above treatment is not good, you can consider the use of hormones and other immunosuppressive drugs; 4. Clear immune complex; 5. Repair glomerular injury; 6. Traditional Chinese medicine.

????In addition IgA nephropathy is a long-term chronic disease, in general, will exist for life, so the treatment of IgA nephropathy need to adhere to, not because of a period of time normal test that has been cured, ignoring the future inspection, so often in a few years later To check the disease has been progress to the late stage, a serious impact on the quality of life of patients.

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