IgA Nephropathy, also known as Berger's disease, is a kind of primary glomerular nephritis characterized by deposition of IgA or IgA antibodies in glomerular mesangial areas. Common clinical manifestations mainly includes frequent or recurrent hematuria and protein in urine. Severe high blood pressure is also seen in some cases. If not treated properly, the disease will develop into chronic kidney failure.Back top
IgA Nephropathy is generally accepted as a glomerular disease caused by the deposition of immune complex. Its occurrence is associated with the following factors:
1.Immune system disorders. IgA nephropathy is mainly caused by the deposition of Polymer IgA in the glomeruli and this indicates disorders of the IgA immune system.
2.Bone morrow disorders. The IgA depositing in the kidneys is bone marrow-derived.
3. Abnormal cellular inflammatory factors. The IgA1 in the mesangial areas will cause the mesangial cells to secrete inflammatory factors and cause extreme inflammatory reaction resulting in damages of renal structure and renal function.Back top
Typical pathological change in IgA Nephropathy is the deposition of IgA in glomerular mesangium, C3, IgG and IgM deposition can also be detected in most patients.
IgA nephropathy can be divided into 5 stages according to the severity of mesangial proliferation, cresent and tubulointerstitium changes.
Level I: Most glomeruli are normal; occasional moderate mesangial broadening with or without cell proliferation; the tubulointerstitium is normal.
Level II: Focal glomerular proliferation and sclerosis(50%), cresent is rarely seen; the tubulointerstitium is normal.
Level III: Diffuse glomerular filtration; more cresents; interstitial edema, cell infiltration is occasionally seen and tubular atrophy is rare.
Level IV: Severe diffuse mesangial proliferation with focal or total glomerular sclerosis; cresents (<45%); tubular atrophy, interstitial infiltration and interstitial foam cells can be occasionally seen.
Level V: cresents is more than 45%, the tubulointerstitium changes are similar with level VI, but more serious.Back top
1. Combine exertion and rest. Have moderate and regulate exercise to build up physical strength and avoid over-tiredness.
2. Avoid any contact with medicines and drugs that have renal toxicity and ask for the doctors' advices before taking medicines.
3.Develop good life habits. Limit the intake of alcohol, tobacco and avoid too frequent sexual intercourse.Back top
1. Immune tests: serum IgA increase is seen in 50% patients. 37-75% patients have specific circulating immune complexes.
2. Proteinuria: those with protein in urine<1g/24h belong to minimal or mesangial proliferative proliferation.
3. Kidney function test: creatinine of 1.5mg/dl indicates progress of the illness condition. Pathology type is above Level Ⅲ when GFR<20ml/min.
4. Hematuria (blood in urine): red blood cells in urine present different shapes, which indicates the blood comes from renal glomeruli.Back top
1. Recurrent hematuria (30-40%)
Usually occurs hours or 1-2 days after upper respiratory tract infections.
Many have no other symptoms. Some cases can be easily misdiagnosed as acute bladder inflammation due to urinary discomforts.
Seen in 80-90% children and youngsters; and 30-40% adults.
Seen in LevelⅡ～Ⅲ
2. Chronic nephritis.
High blood pressure is commonly seen.
Kidney function is likely to decline.
Pathological type LevelⅡ～Ⅳ
3. Heavy proteinuria or Nephrotic syndrome
Most have high blood pressure
Some have symptoms of Nephrotic syndrome-proteinuria, swelling and hypoproteinemia. Microscope indicates Minimal change and moderate diffuse proliferative nephritis.
4. Malignant hypertension:
Uncontrolled high blood pressure.
Often combined with renal insufficiency.
Protein urine+-+++, microscopic hematuria is sometimes detected.
5. Acute Nephritis syndrome.
Kidney function deteriorates continuously. Persistent reducing urine output.
Protein in urine+-++
Most have high blood pressure and anemia
Pathology often indicates cresent nephritis. Lee Level IV～V.Back top
Traditionally there is no special treatment for IgA nephropathy, different treatments will be used according to different clinical types, severity of the illness condition and duration of the disease. The purpose is to protect kidney functions and slow down the illness progress. Conventional treatments mainly include tripterygium wilfordii, emodin, ACEI (Angiotensin-Converting Enzyme Inhibitors), methylprednisolone, prednisone, cyclophosphamide, diuretics. For those that have repeated tonsil inflammation, tonsil excision can help reduce hematuria and proteinuria and have long term protection of renal functions.
As symptomatic treatments, they are very effective at relieving symptoms and discomforts, however they can not solve the deposition of IgA and there will be more deposition, that is why IgA is easy to relapse and the kidney functions will continue to deteriorate.
Since IgA Nephropathy is an auto-immune disease, the key point is to regulate the disorders and imbalances of the immune system and enhance immunity.
1. Immune diagnosis. Only if we make everything clear of the disease can we treat it targeted and effectively. Though patients are all diagnosed with IgA Nephropathy, the antibodies level and amount and position of different kinds of toxins vary from person to person. We should also know the severity degree of glomerular and tubular damages. Therefore, some tests have to be done for guiding the treatment. Tests of beta 2 microglobin, Cystatin C, homocysteine and retinol binding protein are necessary.
2. Immune blockage . According to scientific diagnosis, the dose and duration of medicines will be very accurate. Scientific use of immunosuppressants will bring the abnormal immune inflammatory reactions in the kidneys well under control so as to prevent further damages to the renal cells and tissues.
3. Immune tolerance. As the disease often relapses, we have to assess the disease condition before inflammation in the kidneys becomes serious again. Giving small dose of immunosuppressants regularly can prevent the relapse of the disease. This is to let our body accept the fact that there is immune complex in the kidneys and the antibodies will stop attacking them temporarily.
4. Immune regulation. The immune complex cannot always stay in our kidneys, so we have to remove it out sooner or later. Micro-Chinese medicine can invigorate blood circulation and remove blood stasis thus increasing the blood flow in the kidneys. The special material in the Chinese medicine will combine with the immune complex and take it out of body through blood circulation.
5. Immune protection. For the damaged and remaining inherent cells and tissues, we have to repair them and recover the kidney function. Glucocorticoid and oral intake of Chinese medicines will play key roles in this step. Active materials in micro-Chinese medicine can regulate the immune system and recover the self renewal ability of the body.
6. Immune clearance. Actually this step runs through the above five steps. Immune adsorption can effectively remove the toxic things in the body and control the disease in a short time so that we can strive more time for repairing the kidneys. Only by controlling the continuous progress of the disease can we repair the kidneys well.Back top
1.The diet for IgA nephropathy patients should be light and easy to be digested and try to avoid sea products, beef, mutton, spicy and excitant foods such as alcohol, spiced aniseed, parsley,coffee, etc.
2.Have more fresh vegetables and fruits and moderate water ; avoid all cordial, tonic, and foods that are easy to cause excessive internal heat such as hot pepper, litchi, chocolate, etc especially those that suffer from stasis syndrome like bosom frowsty, abdominal distension, etc.
3.In case of severe edema, patients should have no salt and limit the intake of protein and water; if the edema is not so serious, patients can have low-salt diet and if there is no edema, patients need not control water and protein. Patients that have microscopic hematuria should drink more water and eat more foods that have cooling effects such as apple, sugar, black sesame, edible fungus, etc.Back top
There are about 20% to 50% patients will develop into end stage renal disease and the factors affecting the prognosis include gender, the age of onset, severity of hematuria, proteinuria and hypertension. The prognosis is good in case of positive response to glucocorticoids.Back top
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