Pięć rozwijające Etapy policystycznych choroby nerek (PKD)

Wielotorbielowatość nerek jest genetyczną nerek, które charakteryzuje się skupisk wypełnionych płynem pęcherzyków po obu stronach w nerkach. Torbiele mogą się powiększyć w okresach czasu, w procesie tym pacjenci mogą doświadczyć krwiomocz, białkomocz, wysokie ciśnienie krwi, itp. Początek PKD jest zwykle na swoich 30-tych. Rozwijające etapy PKD jest wyjaśnione w tym fragmencie, tak aby pomóc Ci zrozumieć chorobę lepiej.
Istnieje pięć klinicznych rozwijających etapy policystycznych choroby nerek:
1. Okres Emergence To rodzaj choroby genetycznej, więc pacjenci mieli torbiele, kiedy się urodził, jak torbiele były małe, więc trudno być sprawdzone przed 20 lat.
2. Okres wzrostu. Torbiele wzrośnie szybko, gdy pacjenci są 30-40 lat, a w niektórych krajach zachodnich nie ma żadnych sposobów radzenia sobie z nimi, a oni myślą, że torbiele nie muszą być traktowane, jednak agresywne leczenie jest bardzo ważne, celem leczenia jest utrzymać torbiel z uprawy lub opóźnić jej prędkość rośnie, aby przedłużyć życie pacjentów za pomocą Micro-medycyny chińskiej, może promować krążenie krwi i usuwanie krwi stasis.
3. Swelling.When pacjenci są ponad 40 lat, torbiele stanie się większy, gdy torbiel jest więcej niż 4 cm więcej kliniczne objawy pojawią się, takie jak bóle pleców, białkomoczem wysoki poziom kreatyniny, podwyższone ciśnienie krwi, hematuresis itp. Ten etap jest krytyczny, jeżeli może być dobrze traktowani pacjenci nerek można odzyskać także może to spowodować niewydolność nerek szybko.
4. Burst etap. czy torbiel rośnie w jakimś przyczyny zewnętrznej będzie wybuchać, co może spowodować zakażenie i ichorrhemia oraz ostra niewydolność nerek.
5. Mocznica. Pacjenci mają do wyboru dializy lub przeszczepu nerki w celu ochrony ich czynność nerek co gorsza ich czynność nerek nie można odzyskać.
Jeśli nie można PKD traktowano dobrze terminowo, to będzie dostać niewydolność nerek szybko. Dzienna opieka pielęgniarska i prawidłowe leczenie choroby jest niezbędna, aby spowolnić pogarszanie się choroby.

Jak diagnozować choroby policystycznych nerek

Przed dokonaniem diagnozy policystycznych choroby nerek, lekarze zazwyczaj zadać szereg pytań, takich jak jakie są obecne objawy i Masz PKD historię. Ponadto, pacjenci są proszeni o wykonanie fizycznego egzamin i kilka testów związanych z nerkami, w tym USG, rezonans magnetyczny (MRI), skomputeryzowany teomography Scan (TK) i badania genetyczne.
Policystycznych objawy choroby nerek pomóc lekarze mają ogólnej diagnozy na temat tej choroby. PKD przynosi im różne objawy w innym etapie, więc ucząc ich objawów, lekarze będą mieć ogólną wiedzę na temat ich obecnego stanu choroby.
Diagnozowanie choroby policystycznych nerek przez jej objawów
W ogóle, PKD pacjenci cierpią żadnych objawów na samym początku. PKD jest chorobą dziedziczną, czyli większości chorych rodzą się z PKD genu. PKD gen leży w 16. chromosomie komórki nabłonka kanalików nerkowych. Przed torbiele w PKD pojawiają się i uszkodzenie tkanki nerek, chorzy zazwyczaj nie czuję nic innego i mogą żyć tak swobodnie, jak im się podoba. W takim przypadku, nie może mieć żadnych uszkodzeń nerek lub po prostu łagodne uszkodzenia nerek.
Ponieważ coraz więcej cysty pojawiają się w nerkach, PKD pacjenci będą cierpieć różne objawy, takie jak bóle pleców, moczu krwi, moczu spienionej, wysokie ciśnienie krwi, wzrost nerek i niedokrwistość i tak dalej. Występowanie tych objawów wskazuje sprecyzowane poważne uszkodzenia nerek.
Podobnie jest z wieloma innymi chorobami nerek powiązanych, takich jak nefropatia cukrzycowa, nefropatia IgA i nefropatią nadciśnienie, choroby policystycznych nerek będzie również z pewnością rozwinie się niewydolność nerek, które muszą być traktowane z dializy lub przeszczepu nerki. Aby uniknąć takiej złe konsekwencje, zatrzymując cyst ze rozszerzającej jest kluczowy punkt.
Chociaż objawy policystycznych choroby nerek pozwala uzyskać o stanie choroby, dokładne rozpoznanie potrzeb PKD być na absis medycznych testów.
Testy medyczne zdiagnozować choroby policystycznych nerek
Ultradźwięki: Jako pierwszy wybór dla diagnozowania choroby policystycznych nerek, USG działa przekazując fal dźwiękowych przez ciało, aby stworzyć obraz nerek i cysty w nerkach. Ponadto, może on wykrywać torbieli nerek płodu.
Rezonans magnetyczny (MRI): Podobnie z USG, rezonans magnetyczny może być również stosowany do wykrywania torbieli w nerkach. Ale to jest rzadziej stosowana w diagnostyce choroby policystycznych nerek w porównaniu z USG.
Komputerowy Teomography Scan (TK): CT scan umożliwia lekarzom zobaczyć przekrojowe obrazy nerki, więc jest to także bardzo ważny test do diagnozowania Polycytic choroby nerek.
Badanie genetyczne: W odróżnieniu od powyższych testów, test genetyczny jest bardziej zaawansowany z możliwości, że wykrywając obecność mutacji PKD autosomalna dominująca przed torbiele rozwoju. Osoba, która wie o PKD mutacji genów może być w stanie zapobiec tej chorobie poprzez regulowanie diety i kontroli ciśnienia tętniczego.
General diagnoza o policystycznych choroby nerek pozwala nam ogólną wiedzę o naszym stanie choroby, ale dokładna diagnoza pozwala nam podjąć odpowiednie środki w celu zwalczania choroby policystycznych nerek. Dlatego z tej perspektywy, dokładna diagnoza o policystycznych choroby nerek jest bardziej korzystne.

Pięć rozwijające Etapy policystycznych choroby nerek (PKD)

Wielotorbielowatość nerek jest genetyczną nerek, które charakteryzuje się skupisk wypełnionych płynem pęcherzyków po obu stronach w nerkach. Torbiele mogą się powiększyć w okresach czasu, w procesie tym pacjenci mogą doświadczyć krwiomocz, białkomocz, wysokie ciśnienie krwi, itp. Początek PKD jest zwykle na swoich 30-tych. Rozwijające etapy PKD jest wyjaśnione w tym fragmencie, tak aby pomóc Ci zrozumieć chorobę lepiej.
Istnieje pięć klinicznych rozwijających etapy policystycznych choroby nerek:
1. Okres Emergence To rodzaj choroby genetycznej, więc pacjenci mieli torbiele, kiedy się urodził, jak torbiele były małe, więc trudno być sprawdzone przed 20 lat.
2. Okres wzrostu. Torbiele wzrośnie szybko, gdy pacjenci są 30-40 lat, a w niektórych krajach zachodnich nie ma żadnych sposobów radzenia sobie z nimi, a oni myślą, że torbiele nie muszą być traktowane, jednak agresywne leczenie jest bardzo ważne, celem leczenia jest utrzymać torbiel z uprawy lub opóźnić jej prędkość rośnie, aby przedłużyć życie pacjentów za pomocą Micro-medycyny chińskiej, może promować krążenie krwi i usuwanie krwi stasis.
3. Swelling.When pacjenci są ponad 40 lat, torbiele stanie się większy, gdy torbiel jest więcej niż 4 cm więcej kliniczne objawy pojawią się, takie jak bóle pleców, białkomoczem wysoki poziom kreatyniny, podwyższone ciśnienie krwi, hematuresis itp. Ten etap jest krytyczny, jeżeli może być dobrze traktowani pacjenci nerek można odzyskać także może to spowodować niewydolność nerek szybko.
4. Burst etap. czy torbiel rośnie w jakimś przyczyny zewnętrznej będzie wybuchać, co może spowodować zakażenie i ichorrhemia oraz ostra niewydolność nerek.
5. Mocznica. Pacjenci mają do wyboru dializy lub przeszczepu nerki w celu ochrony ich czynność nerek co gorsza ich czynność nerek nie można odzyskać.
Jeśli nie można PKD traktowano dobrze terminowo, to będzie dostać niewydolność nerek szybko. Dzienna opieka pielęgniarska i prawidłowe leczenie choroby jest niezbędna, aby spowolnić pogarszanie się choroby.

Diet for People with IgA Nephropathy

IgA nephropathy is a type of kidney disease.
IgA nephropathy is a kidney disorder that occurs when IgA-a protein that helps the body fight infections-settles in the kidneys. After many years, the IgA deposits may cause the kidneys to leak blood and sometimes protein in the urine.

Who is at risk for IgA nephropathy?
IgA nephropathy can occur at any age, even in childhood. More men are affected than women. Although found all over the world, IgA nephropathy is more common among Caucasians and Asians. It is one of the most common diseases of the kidney, other than those caused by diabetes or high blood pressure.

Diet for People with IgA Nephropathy
Low protein diet because protein rich foods will make the person glomeruli to function without rest thus making the kidney pressure higher.
Medical professionals recommend the patient with IgA Nephropathy to be a vegetarian. To prevent or slow the progression of kidney damage.
Diet that has low salts as well as controlling fluid intake of the person is also part of the treatment to reduce the swelling that the person is experiencing.
These foods should be avoided by the patient:
Stimulating foods such as seafood, beef and spicy foods.
Foods that stimulate the internal heat of the body like chocolate and hot pepper.
Food that is high in potassium like banana, potato and tomato.
Patients that has a high uric acid should avoid foods like fish, shrimp, and crab.

FISH OIL SUPPLEMENTS IN KIDNEY DISEASE

Ever since James Donadio, MD, published his 1999 paper about the benefits of fish oil for patients with IgA nephropathy, patients with all types of chronic kidney disease have sought more information. Donadio's paper suggested that fish oil retarded the progression of IgA nephropathy, a disease that can end in renal failure. Writing from the Mayo Clinic, Donadio's work had a blush of credibility that other claims lack. While the jury is still out, many nephrologists suggest that patients with chronic immunologically mediated kidney diseases take fish oil.
Warning
Never confuse fish oil with cod liver oil. While fish oil may be beneficial, cod liver oil can be toxic because it contains high concentrations of vitamin A. This is particularly problematic for patients with kidney damage. Packages of fish oil and cod liver oil are labeled very differently. Fish oil containers never include the phrase "cod liver oil." Kidney patients should steer clear of cod liver oil until they consult their nephrologists.
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Conflicting Results
After Donadio's paper appeared, studies in everything from rats to transplant patients examined the possible benefit of supplementation with fish oil. While many of these results look promising, studies are often small and the results are not conclusive. However, many nephrologists believe that supplementation with fish oil has no dangers, so they recommend fish oil to their patients.
Omega-3 Fatty Acids
Fish oil contains a mixture of omega-3 fatty acids. With respect to kidney disease, the important omega-3s are eicosapentanoic acid and docosahexanoic acid, which are abbreviated EPA and DHA, respectively. Although standard dosages of fish oil have never been established, many people look to the Donadio paper for guidance. Donadio's 1994 Mayo Clinic trial report involves dosing patients with 1.8 g of EPA and 1.4 g of DHA. While the EPA and DHA content of different fish oil brands varies, many patients find that 6 g of fish oil twice a day had the necessary amounts of these fatty acids.
Contra-Indications
The Foundation for IgA Nephropathy notes that fish oil can increase the anti-platelet activity of aspirin, ibuprofen and other non-steroid anti-inflammatory drugs. While you should always discuss taking any drug or supplement with your nephrologist, this is doubly important if you take aspirin regularly. Your nephrologist may be able to adjust doses so that you get the maximum possible benefit with the least possible risk

WHAT CAUSES PROTEIN IN IgA Nephropathy?

Several conditions can cause protein in your kidneys. According to the National Institute of Diabetes and Digestive and Kidney Diseases, or NIDDK, when blood passes through healthy kidneys, the kidneys filter out waste products and leave things that your body needs, such as proteins, in your blood. Most proteins are too large to pass through your kidneys' filters and into your urine. However, certain diseases, called glomerular diseases, can attack the tiny blood vessels, or glomeruli, in your kidneys, causing protein to accumulate in your kidneys and, eventually, your urine.
IgA Nephropathy
IgA nephropathy can cause protein in your kidneys and urine. The NIDDK states IgA nephropathy, also known as Berger's disease, is a kidney disorder that develops when IgA -- a protein that helps your body ward off infections -- settles in your kidneys. Over time, the IgA deposits can cause your kidneys to leak blood and protein into your urine. IgA nephropathy can occur at any age, reports the NIDDK, even in childhood. Men are more commonly affected than women, and IgA nephropathy is more likely to occur in caucasians and Asians. Along with kidney problems caused by diabetes and elevated blood pressure, IgA nephropathy is one of the most common kidney diseases. According to MayoClinic.com, common signs and symptoms associated with IgA nephropathy include protein in your kidneys and urine, cola- or tea-colored urine, flank pain, foamy-appearing urine, swelling in your hands and feet, high blood pressure and low-grade fever.

Iga nephropathy Lifestyle and home remedies

IgA nephropathy (nuh-FROP-uh-the) is a common kidney disease that occurs when an antibody called immunoglobulin A (IgA) lodges in your kidneys. This hampers your kidneys' ability to filter waste, excess water and electrolytes from your blood. Over time, IgA nephropathy — also called Berger's disease — can lead to blood and protein in your urine, high blood pressure, and swollen hands and feet.


In 1968, French nephrologist Dr. Jean Berger first described immunoglobulin A (IgA) nephropathy. Sometimes referred to as Berger’s disease, IgA nephropathy is a kidney disease that causes the kidneysto become inflamed. At first the disease was believed to be of little threat. But after more and more researchers looked into IgA nephropathy, it turned out that as many as 50 percent of the cases progressed to end stage renal disease (ESRD), or kidney failure, according to the IgA Nephropathy Support Network. After diabetes and high blood pressure, IgA nephropathy is the third leading cause of chronic kidney disease in the United States.
Immunoglobulin A is an antibody. Antibodies are produced when there is a virus, bacterium or toxin, threatening your body. Normally, these antibodies will help fight the thing that is invading your body. For reasons that are unknown, IgA can get into the kidney, causing inflammation. IgA can eventually lead to blood and protein in the urine, high blood pressure, swollen hands and feet and other signs of chronic kidney disease.


Some steps you can take on your own that may help keep your kidneys healthier include:

Some steps you can take on your own that may help keep your kidneys healthier include:
Switch to a low-salt diet. Keeping your blood pressure levels near normal may help slow kidney damage from IgA nephropathy. Your doctor may recommend changes in your diet — such as limiting your salt intake — to help manage your blood pressure. A low-salt diet can also help minimize fluid retention and swelling.
Eat less protein. Reducing the amount of protein you eat and taking steps to decrease your cholesterol levels may help slow the progression of IgA nephropathy and protect your kidneys.
Monitor your blood pressure levels at home. Write down each reading and bring this record with you to your doctor's appointments.

Note iga nephropathy treatment

iga nephropathy treatment considerations? IgA nephropathy in the name, people feel very puzzled, because patients do not know that fact, IgA is an immune protein, once its produce alienation, will be a lot of precipitation in the kidney area, resulting in kidney damage. This problem in the medical profession, there has been no conclusion However, some of the principles for the treatment of IgA nephropathy patients can understand. The following experts from our hospital as we explain:
Treatment for the cause of clear immune complexes, adjust the body is the key.
The cause of IgA nephropathy is caused by a variety of reasons, the innate immune cells of the kidney of variation and kidney count. Should take the following measures:
Try to clear immune complexes, and to prevent the immune complexes to continue deposition. In the meantime, try to make the patient's body from the upper respiratory system infection distress factors.
Second, for the treatment of the disease process, improve their immune system is the key.
Off kidney fibrosis process is of great significance for the effective control of IgA nephropathy. Lies in improving repair inherent cells, blocking the process of renal fibrosis have lost their own immunity. Only own immune system has been improved, the immune system will not have too much alienation reaction.
Third, for the treatment of symptoms, regulate the body balance is the key.
IgA in patients with clinical symptoms, mostly associated with water, electrolyte and acid-base balance; otherwise can be expressed as the amount of symptoms of nephrotic syndrome. For the treatment of the symptoms can be improved within the environment of disorder, regulate renal imbalance and improve the quality of life of patients with IgA nephropathy.
Iga nephropathy treatment considerations detailed explain, preferably by TCM systemic conditioning our hospital nephrology experts, after years of clinical practice, long combination of Chinese and Western medicine, the creation of a 3D live kidney therapy three-dimensional living renal therapy, balance the body's yin and yang to the greatest degree, stimulate the remaining functions of the kidneys.

iga nephropathy should be how care

iga nephropathy should be how to care? iga nephropathy has been plagued by people as a disease, has numerous iga nephropathy patients still suffer torture. Here biological immune treatment center experts for our simple answer.
IgA nephropathy is immune pathological diagnosis is not a single disease, but a total of
With the immune pathological features (IgA or IgA main immunoglobulin with C3 was granular deposition in the mesangial) is a group of diseases, the pathological mesangial hyperplasia. The typical clinical manifestations of asymptomatic hematuria, some accompanied by back pain and abdominal pain. The principle of treatment is rest, anti-inflammatory and symptomatic treatment. Common care issues: ① pain; ② lack of knowledge.
Pain
Relevant factors
Due to the small blood vessels in the kidney swelling stretch the capsule of the kidney and renal.
Mainly
The kidneys District dull pain, hematuria, particularly at night, and some patients with abdominal pain significantly compared with other glomerular diseases.
【Care goals]
The pain is relieved or disappeared.
Master methods of pain relief.
【Care measures]
The nature of the pain, location, intensity, duration, etc. were observed.
To explain the causes of pain.
To help patients change position to relieve pain.
Local hot or treatments.
Patients listening to music, talking with people to distraction to relieve pain.
Prescribed for analgesic efficacy and side effects.
Key evaluation
Patient pain is alleviated.
Lack of knowledge
Relevant factors
Patient feels very light or no symptoms, easily overlooked.
Unwilling to accept a kidney biopsy surgery.
Mainly
Not trust that renal biopsy surgery research needs.
【Care goals]
Patients understand the process of the development of this disease.
With the necessary diagnostic measures - Renal biopsy surgery.
【Care measures]
For the disease knowledge missionaries, provide written materials and the introduction of the latest developments at home and abroad.
Explain early diagnosis: the need for renal biopsy and preoperative and postoperative considerations.
Isolated hematuria, whether with or without proteinuria should be maintenance-based, do not fatigue, anti-cold, time to cure the infected lesions, drugs caution renal damage.
Chronic tonsillitis, acute phase after tonsillectomy can reduce kidney damage.
Regularly check blood pressure, urine and renal function.
Key evaluation
The level of awareness of the disease.
With the diagnosis and treatment of the case.
iga kidney disease should be how care? the above biological immune treatment center experts made answer. If you still care iga nephropathy do not know, you can consult our online experts, hospital online experts for your detailed answers. I wish you a speedy recovery of the body.

iga nephropathy is caused by what

iga nephropathy is one of the more serious kidney disease, this disease is due to what causes it? Let us follow the biological immune therapy center experts to look at iga nephropathy is due to what causes.
(A) causes
The cause is not very clear, with a variety of factors. Most scholars believe that this disease is to contain IgA circulating immune complexes deposited in the kidney and disease. Complex antigen may be infected with respiratory or gastrointestinal mucosa viruses, bacteria, or food ingredients.
(B) in the pathogenesis
. Pathogenesis of renal tissue of IgA, C3, and (or) IgA, IgG deposition, IgA nephropathy is an immune complex glomerulonephritis, the incidence of IgA immune disorders are closely related, the present study has depth to IgA molecular structure level.
(1) the structure and characteristics of immunoglobulin A: IgA is an important immune globulin, accounting for 15.2% of the total serum immunoglobulin, 80% of serum IgA in the form of the monomer four chain monomer The inter-connected by disulfide bonds and the stability of the J chain. By α heavy chain different antigenic IgA is divided into two serotypes, i.e., IgA1 and IgA2.
IgA1 is the main subtype in the serum, accounting for 80% ~ 90%, IgA2, only 10% to 20%. IgA1 hinge region is 1 times longer than IgA2 IgA2 can be divided into the the IgA2m (1) and the IgA2m (2), although the concentration in serum IgA2 only IgA1 1/4, but the secretion of fluid equal to the 1gA2 concentration IgA1. Structure IgA2m (1) alpha chain and light chain disulfide bonds, connected to rely on non-covalent bonds, but between the light chain and α chain disulfide bonds connected.
Another form of IgA called secretory IgA (SIgA) exist in the outer secretions, such as saliva, tears, intestinal secretions and colostrum. Secretory IgA and serotype different, it is a dimeric molecule with a J chain, and the other outer secretory component (SC), composition (IgA) 2-J-SC complexes. Serotype is (IgA) 2-J composition.
J chain consists of 137 amino acids, molecular weight of 1500, is an acidic glycoprotein containing 8 cysteine ​​residues, six with intra-chain disulfide bond formation, and the two with the connection of the α chain. 18 additional amino acid residues of the C-terminus of the known α chain, J chain is connected through the first two cysteine ​​residues with an α-chain with the C-terminus of the α chain. Both of which are produced by plasma cells, and secretion would be connected together.
SC is synthesized by the epithelial cells in the mucosal tissue or endocrine body, connected through one of the two monomer IgA disulfide colleagues SIgA, SC is from 549 to 558 amino acids of the polypeptide chain, a molecular weight of about 7 Wan, glycosyl content of up to 20%. 5 homologous region in its polypeptide chain, each of the homologous region from the 104,114 amino acids, these homologous regions in the three-dimensional structure similar to and Ig. It has been known that is connected to the α-chain in the Fc region, but the precise positioning is not yet clear. The SIgA configuration may add up to the Y-shaped arrangement: ① a heap; ② The end of the end of the arrangement, the two IgA Fc α connected double Y-shaped structure.
Local tissue plasmacytomas (IgA) 2-J through the: ① with epithelial cell surface of the substrate side of the SC combination formed IgA-J-SC, and transferred to the top surface of a vesicle and secreted; ② (IgA) 2-J lymphatic vessels into the blood circulation, SC combined with the surface of the liver cells and clear, then turn to enter the biliary vesicle mechanism of liver cells, and eventually into the intestines.
The serum IgA terminal connected to each other may be formed to open at the end of polymer, and an obvious feature is a poly body size heterogeneity, the serum IgA 20% of polymer present in the form, and the sedimentation coefficient of 10s 13s, 15s ranging addition IgA Ease of a tendency to form a complex with other proteins, which are vulnerable due to the α-chain of the amino acid residues in the formation of intermolecular disulfide bonds. IgA molecular structure of these characteristics is important in IgA nephropathy.
(2) IgA deposition in the mesangial area: IgA nephropathy, IgA deposition and glomerular pathological changes parallel. Associated with mesangial proliferative mesangial IgA deposition, deposition on the capillary accompanied by changes of the vascular endothelial.
IgA deposition caused by pathological factors: ① antigen from the mucous membrane into the body and stimulate IgA immune system, the antigen component of a wide range of microorganisms, Food (ovalbumin, bovine serum albumin, casein), etc.. ② IgA immune response abnormalities lead to high molecular weight poly-IgA formation. (3) antigen-binding poly-IgA by electrostatic (λ chain), receptor (Fear) or connected to the fiber to protein binding and deposition in the kidneys, it has been found that the serum IgA-fibronectin complex is characterized IgA nephropathy. ④ Other IgA clearance mechanisms (such as liver) damage or saturation.
Existing studies show that the deposition in the glomeruli of the IgA IgA nephropathy is mainly poly λ-IgA1, the average IgA nephropathy patients, serum IgA1, poly-IgA, λ-IgA1 water visible increased. B cells in patients with reduced end link of galactose, β-1, 3 galactosyl transferase (β-1, 3GT) defects, resulting in O-glycosylation of IgA1 hinge region, this change may affect IgA1 and oligonucleotide on the sialic acid in the liver cell receptor (ASGPR) binding affect the clearance of IgA, but also increase the combined deposition and kidney tissue.
Harpel by in situ hybridization study found that of IgA nephropathy intestinal mucosa express an essential component of the synthesis of poly-IgA J chain mRNA levels decreased, while the bone marrow is increased. In addition tonsil PIgA1 also increased. The due production of tonsil PIgA is far lower than the mucosa and bone marrow, it is deposited in the kidney tissue PIgAl mainly derived from bone marrow rather than tonsils and mucosal.
(3) IgA nephropathy immune abnormalities: IgA nephropathy humoral and cellular immune extensive research shows that patients with IgA nephropathy immune abnormalities, including:
① autoantibodies: Fornesier, has been found in the serum of kidney patients have antibodies for kidney mesangial cell cytoplasm macromolecular components. In addition to antibodies against the basement membrane Ⅰ, Ⅱ type III collagen fibers laminin, Gliadin ingredients. IgA anti-neutrophil cytoplasmic antibodies (IgA-ANCA) is also found in the blood of some patients. IgA nephropathy received renal allograft re-appear in the transplanted kidney the IgA nephropathy pathological changes by as much as 40% to 50%, these data are autoantibodies play an important role in the pathogenesis of IgA nephropathy.
② cellular immunity: studies have shown that the cellular immune function disorders are IgA nephropathy play an important role in the pathogenesis. IgA specific inhibition of the decline in the activity of T cells resulting in B lymphocytes increased synthesis of IgA. T helper cell (Th) of activity in IgA nephropathy increased activity of Th / Ts increased. IgA specific receptor of T cells referred to as a the Tα cell, Talpha cells increase the role of IgA production. It was found that IgA nephropathy, especially for patients with gross hematuria Tα increased significantly, Tα helper cells resulted in significantly increased IgA synthesis increased.
③ cell factor and inflammation of the media: many cytokines involved in the regulation of the immune system, including lymphokines White mediated hormone (interleukin, of IL), tumor necrosis factor, a polypeptide growth factor, these cytokines for the exercise of normal immune function from the important role in the abnormal circumstances will cause the offset of the cytokine network, thereby generating immune injury. Mesangial cell proliferation, cytokine and inflammatory mediators (complement components MAC, IL-1, MCP-1, reactive oxygen species, etc.) play an important role.
④ immune genetic: there are family members has suffering from IgA nephropathy reported, suggesting that genetic factors important role in IgA nephropathy. IgA nephropathy associated HLA antigen sites also reports vary, Europe and the United States Bw35, Japan and China DR4 common, also reported in northern China Han DRWl2 most common, in addition to B12, DR1 and IL-RN.2 bit gene, ACED / D genotype reported.
These sediments have diagnostic value. I, III, type IV collagen and laminin, fibronectin in IgA nephropathy glomerular capillary loop expression increased significantly, I type III collagen expression in mesangial area also increased significantly, the majority of patients with tubular basement IV also increased the expression of collagen type. And accompanied by large lumpy electron dense deposits.
iga nephropathy is caused by what? These are the biological immune treatment center experts to make the answer for this problem. If your browser process what can not understand the local hospital online experts, experts can consult for your answers carefully.