Three Characteristics Make IgAN Easy To Develop Into Kidney Failure

When it comes to kidney disease, everyone will think that it has a very famous nickname: "the silent killer".

 

 

 

 

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Indeed, insidious onset can be said to be the biggest feature of chronic kidney disease, and because of this, many kidney friends miss the best time for treatment and embark on the road of lifelong treatment for kidney disease.

 

However, if you want to ask which type of kidney disease is the best at hiding, many people will vote for IgA nephropathy, and compared with other types of kidney disease, it seems to be more likely to develop into kidney failure. Why is this? It is mainly related to its three characteristics:

01 Young people are prone to IgA

When it comes to kidney disease, most people think that the patients must be mainly the elderly. Unless it is due to genetics, it is difficult for young people to have kidney problems, but this is not the case. IgA nephropathy is a kidney disease that likes to target young people. Types of.

 

According to epidemiological observations, most patients with IgA nephropathy are young and middle-aged males aged 20 to 30. Although young people's awareness of health care has become stronger and stronger, there must still be some people around us who do not I have the habit of having annual physical examinations, and I don’t want to go to the hospital when I feel unwell. I feel that there are too many people in the hospital and the queue is too troublesome. This can easily delay the timing of treatment and aggravate kidney damage.

02 No obvious edema

Edema is one of the most typical symptoms of kidney disease patients, but many kidney friends do not have obvious symptoms of edema until the end stage, and most patients with IgA nephropathy are also like this.

 

However, in the early or even middle stage of kidney disease, although many patients do not have obvious edema, kidney damage has already occurred. At this time, the sooner they receive treatment, the faster the disease can be controlled and the kidney function can be prevented from continuing to decline.

 

However, some kidney friends do not have a deep understanding of kidney disease and have only heard of edema, foamy urine, etc. When they find that they have no edema or the symptoms of edema are very mild, they tend to mistakenly think that their condition is not serious, and even think that they have recovered, in the face of treatment is no longer active, it is easy to develop into kidney failure.

 

Edema is also a typical symptom of kidney disease, but most patients with kidney disease do not have obvious edema. why?

 

Edema is mostly caused by urine protein. Such as nephrotic syndrome, if the urine protein is more than 3.5g, it belongs to severe proteinuria: it often causes severe edema. But in fact, patients with severe proteinuria only account for about 1/3 of kidney disease. The remaining 2/3 of patients have only mild to moderate proteinuria, the urine protein is less than 3.5g, the edema is not too obvious, and the patients often do not feel any abnormality. In 2/3 of patients, urinary protein and edema are inconspicuous, but they can still lead to kidney failure and uremia: that's why kidney disease is named "silent killer". Most of these 2/3 patients belong to IgA nephropathy: the title of the silent killer is mainly earned by it.

03 Urinary protein is not high

The presence of urinary protein in the urine is a very serious hazard to the kidneys. It will increase the burden of glomerular reabsorption, leading to glomerulosclerosis and renal tubular atrophy. Once the glomeruli and renal tubules are almost damaged The kidneys can hardly perform their due functions anymore, so the main purpose of many kidney disease treatments is to reduce urine protein.

 

However, clinically, patients with severe proteinuria only account for about one-third, and the remaining patients do not have particularly high proteinuria, and most of the remaining patients are patients with IgA nephropathy.

 

For kidney friends with the same degree of kidney damage but different disease types, the urine protein of IgA nephropathy patients is mostly less than that of other kidney diseases. In other words, if everyone's urine protein level is the same, IgA nephropathy is more serious than other kidney diseases.

 

Therefore, you must not think that your kidneys are healthier just because your urine protein is a few "+" less than others. It may be too late to rush to treat when the urine protein rises. I wait until I have obvious symptoms before I realize that I may have kidney disease. Generally, I am helpless. If IgA kidney friends do not want to fall into renal failure all at once, they must actively receive treatment and remain vigilant against the above three characteristics. , to prolong the survival time of your kidneys.

04 Summary: Is IgA nephropathy serious?

Patients with IgA nephropathy do not look serious or look like normal people, and their urine protein is not too much.

However, follow-up data show that among patients with IgA nephropathy diagnosed by renal biopsy, 20% of IgA nephropathy patients progress to uremia every 10 years, and eventually about half of the patients lose their renal function during their lifetime.

 

The decline in renal function of IgA nephropathy is described in textbooks as "gradual progress", which is often understood by patients as "slow progress". But you must know that the kidneys are often not afraid of fast progress, but slow progress.

 

Rapidly progressing nephropathy, such as malignant hypertensive nephropathy, post-infectious nephropathy, etc., has a rapid onset and rapid recovery. Even the notorious lupus nephropathy can recover after a rapid decline in renal function.

However, kidney disease that progresses slowly has a lot of "inertia", and it takes more effort to reverse kidney function.

 

For example, kidney disease that progresses rapidly is like an F1 racing car. Although the speed is fast, the steering wheel is also more sensitive, and it is easy to brake or turn around. Kidney disease that progresses slowly is like a 10,000-ton giant ship. Although it is slow, once it sets off, every step it takes is very calm and solid.

 

This has led to IgA, a kidney disease that progresses slowly, and has become the number one cause of uremia in my country.

 

IgA nephropathy possesses the qualities of a qualified killer: unassuming, unobtrusive, unobtrusive, silently sharpening the knife every day, with decades of perseverance and perseverance, methodically and gradually killing kidney function.

 

This kind of ruthless style of concealment comes from the battlefield position of IgA nephropathy: away from blood vessels.

The lesion site of nephrotic syndrome is the blood vessel wall of the kidney. After the blood vessel wall is destroyed, a large amount of protein in the blood will flow out. However, the place where IgA nephropathy invades is outside the blood vessel wall, in the mesangial area of the kidney: attacking here will seldom affect urine protein, but it can also damage kidney function.

In other words:

IgA nephropathy is more afraid of proteinuria than another nephropathy. With the same severity, IgA nephropathy has less urinary protein than another nephropathy. That is to say: at the same urine protein level, IgA nephropathy is more serious than another nephropathy.

The onset of IgA nephropathy is mainly for young people, and the survival time of the kidneys for 10 or 20 years is not enough. Therefore, remind IgA nephropathy, and patients diagnosed with chronic nephritis or nephritic syndrome (most people's pathology is IgA)

Even if there are no symptoms, it is a hidden murderous intent. As long as you are under 70 years old, you must reduce the urine protein to less than 0.5g (less than 0.3g is safer) to ensure that kidney failure does not occur in your lifetime. There is no specific drug for IgA nephropathy, and comprehensive treatment is often required: traditional Chinese medicine, Prix/sartan drugs, hormones, leflunomide, tripterygium glycosides, mycophenolate mofetil, etc. No single drug can stop this "big ship" on its own (not all of these drugs are used), and it needs to be superimposed on multiple targets according to the specific condition of the patient to block its progression to uremia.

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for more information:Ali.ma@wecistanche.com