The Largest Number Of Patients With Kidney Disease! How Is Difficult Nephrotic Syndrome Diagnosed And Treated?

Now, whether in clinical work or consultation on WeChat, I have encountered more and more membranous nephropathy. Most of them are anxious and confused: I have been treated for so long and I can’t cure my disease, and I am full of proteinuria, what should I do?

Click to bioflavonoids tablets for kidney disease

Indeed, in the current clinical work of nephropathy, membranous nephropathy has become a very big challenge for two reasons:

First, the number of surges

In recent years, the number of patients with membranous nephropathy has increased by an average of 13% per year, which is twice as fast as the GDP growth rate of our country in recent years.

The etiology of this disease is related to many factors, such as heavy metals, excess nutrition, infection, tumor, nephrotoxic drugs, etc. In recent years, many new patients are due to air pollution (PM2.5). In many areas, such as our Hebei, the number of membranous nephropathies has surpassed that of IgA nephropathy, becoming the number one glomerular disease.

Second, it is not easy to treat

Membranous nephropathy is not particularly serious kidney disease, but it is indeed not easy to treat. Experts and scholars in the field of nephropathy call ependymal nephropathy "grinding nephropathy", which is grinding nephropathy because its remission is very slow and the progress is very slow.

Urinary protein is usually relieved after 3 months of treatment, and complete remission may take several years; the progress is also very slow, and it often takes ten, or twenty years or more to progress to uremia, which highlights this “slow” problem in chronic kidney disease. "Character.

In addition, the final outcome of membranous nephropathy has a very strange "one-third phenomenon":

1/3 of membranous nephropathy will resolve spontaneously without treatment;

1/3 of membranous nephropathy, only active treatment can stabilize the disease;

One-third of membranous nephropathy continues to progress despite treatment (the meaning of treatment is to slow progression).

Some people argue that since some membranous nephropathy can be cured without treatment, it should not be treated. But here's the thing: you don't know if you're part of the 1/3 that will heal yourself. After giving up treatment for a period of time, it is found that there is no self-healing, and the kidney function has deteriorated. This is a tragedy.

Therefore, membranous nephropathy still needs treatment. However, we still found some self-healing laws, which is to mention an indicator that shocked the nephrology community in 2009 - "anti-phospholipase A2 receptor antibody" - which has been brilliant in recent years. Had to mention this blood test.

A brilliant anti-phospholipase A2 receptor antibody

A series of studies have found that:

Phospholipase A2 receptor is the most important antigen in membranous nephropathy (accounting for 80%), and some patients with nephropathy can use this indicator to replace renal biopsy and urine protein test. Patients with lower antibody titers (below 100) have higher rates of spontaneous remission and are relatively easy to treat. On the other hand, patients with higher antibody titers (above 100) are more difficult to self-heal, have lower treatment remission rates, a longer time to remission, and a higher risk of renal failure. Phospholipase A2 receptor antibody can almost replace the urine protein test, and it can reflect the changes of the condition more timely and accurately than the urine protein.

Membranous nephropathy, what is a membrane? It is the wall of the capillaries in the kidneys. The walls of the blood vessels are first attacked by the immune system, and after a period of time, the lesions appear and the urine protein leaks from the blood vessels. If the anti-phospholipase A2 receptor antibody is relieved, it is in immunological remission, and the urine protein will be relieved after a period of time. Conversely, if the antibody increases, the urine protein will also increase over time (relapse). In general, changes in antibodies are 3 months earlier than changes in urine protein.

In 3 months, many treatment opportunities can be seized, and many ineffective treatments can be avoided. Due to the discovery of an anti-phospholipase A2 receptor antibody, a timely and accurate indicator, not only may it be possible to diagnose membranous nephropathy without renal puncture, but membranous nephropathy may also take off the hat of "chronic child" in the future. It is recommended that major hospitals actively carry out the test of anti-phospholipase A2 receptor antibody, which is of great significance to the diagnosis and treatment of the nephrotic syndrome.

Next, let's talk about the treatment of membranous nephropathy.

How is membranous nephropathy treated?

First, to risk stratify membranous nephropathy:

1. Low risk:

Diagnosis: Patients with normal renal function and urine protein less than 3.5g.

Treatment: conventional treatment

2. Medium risk:

Diagnosis: Patients with normal renal function, and after 6 months of pril/sartan treatment, the urine protein is still higher than 4g and the decrease is not more than 50%. or anti-phospholipase A2 receptor antibody less than 50 RU/ml

Treatment: conventional treatment or conventional treatment + immunotherapy: rituximab, cyclosporine, tacrolimus.

3. High risk:

Diagnosis: renal function has declined or urine protein is 8g for more than 6 months or anti-phospholipase A2 receptor antibody is higher than 150 RU/ml

Treatment: conventional treatment + immunotherapy: rituximab, cyclophosphamide, "cyclosporine/tacrolimus + rituximab"

4. Very high risk:

Diagnosis: Life-threatening complications of nephrotic syndrome or rapid deterioration of renal function

Treatment: Cyclophosphamide, we can see that the treatment method for membranous nephropathy depends on the risk of progression.

For patients with membranous nephropathy with a relatively low risk of progression, conventional treatment is sufficient, including basic treatment of chronic kidney disease: Prixil/sartan, glisten, traditional Chinese medicine, and symptomatic and supportive treatment: diuretic, antihypertensive, anticoagulation, etc.

For membranous nephropathy with a high risk of progression (high proteinuria, high antibody, decreased renal function), immunotherapy should be added on the basis of conventional treatment.

Of particular concern are patients with high-risk membranous nephropathy.

For high-risk, immunotherapy can choose one of the four immunosuppressants, rituximab, cyclophosphamide, tacrolimus, and cyclosporine. Cyclophosphamide is cheap and the most commonly used in the past, but due to its large side effects (gonadal toxicity and tumor risk), it has been used less and less now, and hormones are also used in small doses. During treatment, it is necessary to dynamically observe the changes of anti-phospholipase A2 receptor antibodies. Decreased antibodies indicate improvement (urinary protein will be reduced); if anti-phospholipase A2 receptor antibodies are found to be elevated, a second immunosuppressant should be added. When adding a second immunosuppressant, it is not recommended to add tacrolimus and cyclosporine, but to add rituximab, or add cyclophosphamide.

In short, to deal with membranous nephropathy, we must do 3 points:

1. Psychological preparation for protracted combat;

2. Dynamic observation of anti-phospholipase A2 receptor antibody;

3. Treatment and adjustment for risk classification.

Finally, I wish my friends with membranous nephropathy to regain their health!

for more information:ali.ma@wecistanche.com