Treatment measures for IgA nephritis, what to do with IGA nephropathy? Is there a good treatment

To date, there is no satisfactory solution for this disease. The use of adrenocorticosteroids with or without immunosuppressants in patients with progressive renal insufficiency has been inconsistent. Recent data suggest that alternate-day adrenocorticosteroids are beneficial in improving proteinuria in patients with proteinuria greater than 1 g day.

Minimal change nephropathy with IgA deposition may relieve proteinuria. The combination of cyclophosphamide, dipyridine, and huaforin reduced proteinuria with no effect on glomerular filtration rate; Concomitant use of cyclosporine A also reduces proteinuria but also decreases creatinine clearance. The efficacy of phenytoin, antiplatelet drugs, cromolyn disodium and diphenylhydantoin is uncertain.

Urokinase has been reported to protect glomerular filtration rate, but it is far from conclusive. In patients with tonsillitis, tonsillectomy may be beneficial; Antibiotic prophylaxis and **infection may be helpful in some patients presenting with acute nephritic syndrome and acute renal failure. A smaller series of observations using fish oil preparations reduced proteinuria and increased glomerular filtration rate.

During severe IgA nephropathy (glomerular filtration rate decreases by 2 4 mL min per month), intravenous infusion of high-dose immunoglobulin can stop the decline in glomerular filtration rate and improve hematuria and proteinuria, but it is often ** after discontinuation of the drug**. In cases of hypertension and severe proteinuria, convertase inhibitors can slow the rate of decline in glomerular filtration rate and reduce proteinuria, so in severe IgA nephropathy, convertase inhibitors are the antihypertensive drugs of choice. It is unclear whether switching inhibitors are effective in normotensive patients.

Patients with end-stage IgA nephropathy undergo kidney transplantation, and the transplanted kidney develops IgA deposition in the mesangial area soon after; If the donor has subclinical IgA nephropathy, IgA deposits in the donor mesangial area often disappear rapidly after implantation in non-IgA nephropathy uremia. Progressive renal failure does not necessarily occur with IgA nephropathy in a transplanted kidney, but immunosuppression**, including cyclosporine A, administered after kidney transplantation, does not prevent its progression. For cadaveric kidney transplantation, the 1-year and 3-year survival rates of transplanted kidney can be 87% and 77%, but the survival rate of individual IgA kidney transplant patients with anti-HLA antigen antibodies can reach 100% at 2 years, and it is reasonable to assume that these anti-HLA antigen antibodies play a beneficial role in increasing the survival rate of transplanted kidneys.

Hello, according to the specific type and degree of nephritis, the general acute is very easy**, protein and hematuria within 1 can be traditional Chinese medicine**, creatinine is high, protein 2, red blood cells 2 or more need Western medicine**, protein 3 or more is recommended to be hospitalized, the possibility of puncture and hormone drugs is not ruled out.

Traditional methods**IgA nephropathy: conventional western medicine, kidney transplantation: use hormones, immunosuppressants**, temporarily relieve symptoms, *** large, treat the symptoms but not the root cause.

After kidney transplantation in patients with IgA nephropathy, IgA deposition in the mesangial region occurs soon after the transplanted kidney. Neither Western medicine nor kidney transplantation can lead to IgA nephropathy. Traditional Chinese medicine, home remedies**:

Traditional Chinese medicine is difficult to swallow, and long-term use hurts the spleen and stomach; It is a three-part poison that increases the burden of kidney detoxification; Superstitious Chinese herbal remedies aggravate kidney damage.

Another way - to create a new way of "meridian administration".

Through the national patent "Kidney Care Instrument", the non-toxic active ingredients of the drug are introduced into the kidneys to avoid the toxins of oral drugs from entering the blood and prevent the production of drug toxins.

There is no special method for this disease, and different measures are adopted clinically according to the different manifestations and course of the disease, with the aim of protecting kidney function and slowing down the progression of the disease. According to the clinical classification**IgA nephropathy is as follows:

1.Isolated microscopic hematuria.

No special ** is required, regular follow-up is required.

2.Reverse ** is the gross hematuria type.

For lesion removal such as tonsillectomy, triptyre** (tripterygium wilfordii, emodin, acei arb) can be used depending on the amount of proteinuria.

3.Abnormal urine test type.

Triptylene** (Tripterygium wilfordii polyglycosides, emodin, acei arb).

4.Vasculitic type.

1) MMF** regimen: Methylprednisolone intravenous infusion pulse** for three days, followed by prednisone, reduced by 5 mg daily to 10 mg daily every 2 weeks, and then maintained at this dose. MMF was started on 2 days, increased according to the blood concentration, and used for 6 months, maintained at a daily dose, and the total course of treatment was 2 years.

2) Cyclophosphamide (CTX)** regimen: methylprednisolone and MMF** regimen. CTX Shock**, once a month for 6 months, and every 3 months thereafter. The total dose is maintained with azathioprine after the end of **, and the total course of treatment is 2 years.

5.Massive proteinuria (with minimal lesions).

Prednisone regular**.

6.Massive proteinuria.

Low-protein diet with tripterygium wilfordii polyglycosides, emodin, acei arb drugs**.

7.Hypertensive type.

If you choose to use antihypertensive drugs such as acei ARB, CCB, and diuretics, you can use tripterygium wilfordii polyglycoside tablets together.