What Are the Common Causes of Kidney Scarring?

Renal fibrosis is a pathophysiological change. It is a gradual process in which the function of the kidneys changes from health to injury, to damage, until loss of function.

Kidney fibrosis concept

Kidney diagram Renal fibrosis is a pathophysiological change. It is a gradual process in which the function of the kidneys changes from health to injury, to damage, until loss of function. The kidneys are stimulated by various pathogenic factors such as trauma, infection, inflammation, blood circulation disorders, and immune responses, and their inherent cells are damaged. A large amount of collagen deposition and accumulation develops in the later stage, causing the renal parenchyma to gradually harden and form scars until the kidney Complete loss of organ function. The process of fibrosis and sclerosis inherent in the kidney is also the process of renal fibrosis. Renal fibrosis is characterized by abnormal deposition of extracellular matrix (ECM).

Stages of renal fibrosis disease

Primary inflammatory response

This period is the stage of inflammatory response after kidney tissues are damaged by various pathogenic causes. In this period, except for the abnormal urine test, there is no discomfort, which is also called asymptomatic period. Because the filtering function of the glomerulus is highly compensatory, the renal function may not be affected or slightly damaged at this time, but the pathological damage after the inflammation in the kidney is severe, and some patients have already developed glomerulosclerosis. The appearance of clinical symptoms is lagging. If the standard treatment in this period. If vascular dilatation, anti-inflammatory, anticoagulation, antithrombotic, and degradation treatments are used, the condition can be completely reversed and even healed. If there is no standard treatment or missed treatment time, the pathological damage inside the kidney will gradually increase, and the disease will rapidly progress to the fibrosis and scar formation stage, which will bring great difficulty to the treatment, and it will have more difficulties and less chances of reversal. .

Secondary fibrosis

This stage is that the formation of renal fibrosis has spread to the whole kidney tissue. The inflammation damage after fibrosis has broken through the healthy nephrons and affected the renal function. The disease has entered the decompensation stage or renal failure stage. If you continue to standardize treatment during this period, continue to expand blood vessels, anti-inflammatory, anticoagulation, and focus on the degradation of fibrous tissue. As long as these four blocking treatment measures are in place, the disease may be reversed and stay away from dialysis. Effective prevention and control of susceptible factors, failure to control diet or inadequate treatment, if some reversible factors miss the favorable treatment opportunity, the disease will soon enter the scar formation phase-end stage of uremia.

Tertiary scar formation

Once renal fibrous tissue develops into scar tissue, it is never possible to reverse it. If the patient still has more than 1,000 ml of urine output, it means that there is still residual renal function to maintain urine output. As long as the minimization of traditional Chinese medicine multi-target treatment can protect the current residual nephrons and prevent the renal function from continuing to deteriorate, It is hoped that the dialysis time will be gradually extended or gradually get rid of dialysis.

In order to facilitate understanding, the process of kidney fibrosis formation is simplified into two phases. The first is the reversible phase, that is, the inflammatory reaction phase and the pre-fibrosis phase. If the treatment is standardized in time, the fibrotic pathological damage can be completely cured. The second is the irreversible phase, which is the period of scar formation. Once the functional nephron becomes scar tissue, it is irreversible. ^[1]

Renal Fibrosis Disease Relationship

Due to various pathogenic causes, the kidney's intrinsic cells are damaged, and a series of inflammatory mediators are released. The inflammatory response appears and the cell activity increases. The initial stage of the onset of this kidney disease is the nephritis stage; as the degree of cell damage increases, The cell phenotype is transformed, the cells begin to harden, and the function begins to lose. When the degree of loss is less than 50%, that is, when the total number of cell sclerosis is not more than half, this is the early stage of renal fibrosis. At this stage, due to the strong compensatory capacity of the kidney, there are still no changes in clinical indicators, and creatinine and urea nitrogen have not exceeded the healthy range, but at this time renal fibrosis is approaching the intermediate stage. As kidney fibrosis continues to develop, dysfunctional sclerotic cells gradually increase, and there are fewer and fewer healthy nephrons. When the healthy nephron (also known as the remaining nephron) is less than 20%, it enters the period of renal failure, and some symptoms of uremia such as acidosis begin to appear. At this time, we call it the matrix synthesis phase of renal fibrosis. When 90% of the kidney cells have been fibrotic, that is, the residual nephron is less than 10%, the patient will have severe symptoms of metabolic acidosis, and a series of worsening symptoms will appear in the heart and brain. Entered into end stage renal failure (ESRF), the stage of uremia. The degree of renal fibrosis at this time is called the post-matrix synthesis phase. During this period, the remaining nephrons have entered the sclerosis phase, and the cells have entered the sclerosis process, also known as the stromal autonomous generation phase. At this time, the synthesis of extracellular matrix does not rely on external factors to promote it, but instead generates and self-values.

Renal fibrosis It can be seen that if chronic nephritis is not effectively controlled, it will lead to the initiation of renal fibrosis. If the process of renal fibrosis cannot be blocked, it will lead to the gradual loss of renal function and then reach the stage of uremia. Therefore, uremia is the ultimate manifestation of enlarged renal fibrosis. Whether it is preuremic or treatment of uremia, it must start by blocking the process of renal fibrosis.

Renal fibrosis

The microscopic manifestation of renal fibrosis is fibrosis of renal intrinsic cells, and in essence, renal intrinsic cells necrosis due to damage. According to the degree of damage to the kidney's intrinsic cells, and whether it can be repaired, we divide the process of renal fibrosis into two stages.

The first stage: the reversible stage of fibrosis formation and progress

Pathogenic factors such as drug poisoning, hypertension, diabetes, persistent colds, and infections can cause damage to the kidney's inherent cells. After the cells are damaged, some cytokines are released, such as IL-1 and tumor necrosis factor (TNFa). These cytokines will attract a series of inflammatory cells in the blood (such as white blood cells, lymphocytes, platelets, monocytes-macrophages, etc.) to infiltrate into the mesangial area, blood vessel area, and renal interstitial area, and release a series of inflammation. Sexual mediators cause an inflammatory response, which in turn promotes the phenotypic transformation of the kidney's intrinsic cells. At this time, the function of the kidney's inherent cells has changed, and a series of nephrotoxic cytokines and growth factors have begun to be released, such as: TGF-B, PDGF, Bfgf, EGF, etc. These factors can cause fibroblast proliferation in the renal interstitial And differentiate and transform into myofibroblasts.

Under the continuous stimulation of cytokines and growth factors, fibroblasts continue to activate and proliferate, and synthesize extracellular matrix (ECM) components (first synthesize and secrete fibronectin to form a scaffold structure, and then continue to synthesize collagen , , IV, V components). During this period, the kidney's intrinsic cells, such as mesangial cells, glomerular epithelial cells, and renal tubular epithelial cells, can also be transformed into myofibroblasts. Although the structure and function of the kidney have changed, the damaged cells can still perform part of their original functions. The damaged cells can be reversed to normal cells by treatment, and the original functions can be restored. In fact, blocking the conversion of damaged cells into myofibroblasts is a key step in blocking renal fibrosis. As long as the native cells are not transformed into myofibroblasts, the process of fibrosis is blocked. Therefore, we call this stage the reversible stage of fibrosis formation and progression. Treatment at this stage is of great significance for the rehabilitation of renal disease and the reversal of renal failure, and both doctors and patients should pay great attention to it.

The second stage: the scar formation stage

When the intrinsic cells are transformed into myofibroblasts under the influence of inflammatory stimuli and cytokines and growth factors, the process of renal fibrosis reaches the stage of scar formation. Through the research of cell transformation, it was found that once the normal inherent cells are transformed into myofibroblasts, they no longer rely on the inflammatory mediators and cytokines in the primary disease to undergo transformation, but instead increase their value independently, continue to secrete and synthesize easily. Degraded collagen types I and III cause abnormal synthesis of the extracellular matrix (ECM) and decrease the degradation rate. This imbalance in the rate of synthesis and degradation promotes the formation of a large number of fibrous tissues, causing abnormal accumulation and deposition of extracellular matrix, and eventually leading to glomerular sclerosis, renal tubules, renal interstitial and renal vascular fibrosis, and the formation of persistent scars. During the period of kidney scar formation, the number of effective functional nephrons gradually disappears, and renal failure progresses progressively. This period is clinically referred to as the end stage of renal failure, also known as the uremia stage. During this period, although it is possible to prevent the process of renal fibrosis, it is difficult to repair the kidney tissue that has become scarred.

Mechanism of renal fibrosis

The primary and secondary causes of kidney disease, through the damage to the kidney, activate the activity of capillary endothelial cells in the glomerulus and attract the infiltration of inflammatory cells in the blood, while releasing the nephrotoxic inflammatory mediators, causing Intrarenal inflammatory response. another

Pathological map (2 photos)

In addition, under the action of a series of nephrotoxic factors, the original functional cells of the kidney were damaged and the phenotype changed, and the inherent cells after the phenotypic change secreted a series of nephrotoxic cytokines and growth factors. These nephrotoxic cytokines and growth factors in turn activate fibroblasts in the renal mesenchyme to transform into myofibroblasts. Myofibroblasts are the key cells that cause fibrosis in the kidney. The collagen fibers they secrete are not easily degraded, which leads to the accumulation and deposition of a large amount of extracellular matrix collagen, which destroys the kidney tissue structure. Eventually, scar tissue is formed. Renal function also showed a progressive decline, leading to the destruction of all or most of the nephrons and the complete or almost complete loss of function. Clinically manifests as end-stage renal failure (uremia)

Causes of renal fibrosis

First, streptococcal infections such as the throat and tonsils

No one will associate this type of infection with kidney disease, and it is for this reason that it leaves the soil for the infection to survive. Due to a moment of inattention, repeated infections must be cured immediately, antibiotics must be taken thoroughly, and they should not be abandoned halfway, otherwise streptococcus is easily infected.

Once streptococcal infection, the self-regulation mechanism in the body becomes dysfunctional. Cause the virus to spread to the kidneys, cause glomerular damage, start the process of renal fibrosis, and induce kidney disease.

Second, long-term use of drugs that cause kidney damage

Analgesics damage the kidney. It is strictly forbidden to use commonly available painkillers, analgesics and general analgesics (injections or oral) without a doctor's prescription. If you want to use them for a long time, please discuss with your kidney specialist for long-term use of painkillers. Serious damage to the kidneys. Without a doctor's prescription, taking medicines in a disorderly way, and obstructing kidney function, many people often buy their own medicines (antibiotics) when they are ill. If they take too much antibiotics, they will impede the function of the kidneys. Especially diuretics cannot be taken privately.

Third, bad habits

Overeating is harmful to the health of the kidneys. The human body eats a large amount of food (animal and plant proteins), and the last metabolizing organisms (waste), uric acid and urea nitrogen, etc., must be ruled out by the kidneys. Therefore, excessive food (overeating, overeating) Will increase the burden on the kidneys.

Moderate (full) drinking water does not hold back urine. Urine is prone to multiply bacteria in the bladder for too long. Bacteria are likely to infect the renal pelvis through the ureter, causing renal tubular fibrosis. If the process of renal fibrosis is not controlled in time, it may even cause acute renal failure.

4. Ignore hypertension

Due to long-term hypertension, the microvasculature of the kidney will be constantly destroyed. Once the microvasculature is damaged, the function of vascular endothelial cells will be disturbed, causing an inflammatory reaction. The kidney is made up of 2 million renal corpuscles (microvessels). If high blood pressure is not effectively controlled, the number and degree of microvascular damage will increase, and the degree of renal fibrosis will naturally increase.

But many hypertensive patients have the wrong idea that they are healthy and that high blood pressure is fine. And kidney disease often quietly rises in people's negligence.

In addition to the above factors leading to kidney disease, diabetes, colds and other factors are also factors that are vulnerable to kidneys. Many people will ask, how should we protect the kidneys? Faced with this problem, chief physician Chen Zhenyuan, a nephrologist at Shijiazhuang Nephropathy Hospital, pointed out that almost half of the kidney patients' kidney damage is carried out unknowingly, so when the body feels uncomfortable, it is likely that it has reached the end of kidney disease-must not No more dialysis. Therefore, to protect the kidney, you need to start by caring for healthy kidneys in daily life!

For example, it is strictly forbidden to use analgesics to damage the kidneys without a doctor's prescription; do not overeating; drink plenty of water without holding back urine; the throat tonsil glands must be cured when streptococcal infection occurs, "take antibiotics thoroughly and not waste them"

Renal fibrosis collateral process

(A) treatment principles

1. Dilate the renal arteries and digestive tract arteries, increase the blood flow perfusion of the kidneys and the whole body;

2.Improve microcirculation disorders, increase oxygen supply and enhance metabolism;

3. Relieve the disorder of the internal environment caused by hypoxia;

4. Reduce symptoms of poisoning. ^[2]

(B) common clinical manifestations

1. After dilation of renal arteries at all levels of the kidney, due to the increase of the effective perfusion of the glomerulus, the internal pressure of the glomerulus is reduced, and the state of high filtration of the glomerulus is also reduced.

This will inevitably delay and control the progress of glomerulosclerosis, so the following clinical manifestations can be seen:

(1) The amount of urine begins to increase, the color of urine becomes darker, and the smell becomes stronger;

(2) Urinary creatinine begins to increase gradually, and kidneys begin to detoxify;

(3) Urine protein leaks and occult blood gradually decreases;

(4) Puffiness begins to subside.

2. After the peripheral blood vessels are dilated, due to the increase of the effective circulating blood volume throughout the body, it will inevitably improve the skin microcirculation disorder and relieve the symptoms of poisoning caused by renal failure.

(1) Symptoms of general weakness gradually ease;

(2) The face and palms become rosy;

(3) Began to sweat;

(4) Symptoms of itching of the skin are gradually reduced;

(5) The symptoms of blood pressure are gradually stabilized, and can even be reduced to normal. The antihypertensive drugs used consistently can be gradually reduced, and some patients can stop using antihypertensive drugs without rebound.

3. After the blood vessels of the digestive tract are dilated, the blood perfusion volume of the digestive tract is increased, and the microcirculation disturbance of the digestive tract caused by renal failure is improved. At this time, the edema of the mucosa of the digestive tract begins to subside, the secretion of digestive juice begins to increase, and the intestinal detoxification function Began to increase, specifically the following clinical manifestations: (1) the ammonia taste in the mouth began to disappear;

(2) Appetite begins to increase;

(3) The symptoms of uremic gastritis are relieved, and the symptoms of nausea and vomiting disappear;

(4) Improved digestive tract function, increased intestinal detoxification function, smooth stool, etc.