IgA nephropathy (also known as IgA nephritis, IgAN, Berger's disease and synpharyngitic glomerulonephritis) is a form of glomerulonephritis (inflammation of the glomeruli of the kidney). This should not be confused with Buerger's disease, an unrelated condition.
IgA nephropathy is the most common glomerulonephritis throughout the world [1] Primary IgA nephropathy is characterized by deposition of the IgA antibody in the glomerulus. There are other diseases associated with glomerular IgA deposits, the most common being Henoch-Schönlein purpura (HSP), which is considered by many to be a systemic form of IgA nephropathy. HSP presents with a characteristic purpuric skin rash, arthritis, and abdominal pain and occurs more commonly in young adults (16-35 yrs old). HSP is associated with a more benign prognosis than IgA nephropathy. In IgA nephropathy there is a slow progression to chronic renal failure in 25-30% of cases during a period of 20 years.
But what are the Prognosis of IgA Nephropathy?
IgA Nephropathy is a rapidly progressive disease, so we should pay much attention to it. We have studied the mechanism of its progression with the most advance theory of renal fibrosis so as to interfere in the therapeutic measures. Clinical indexes of delaying and reversing the prognosis of IgA Nephropathy include proteinuria, level of hematuria, Hpertension and level of creatinine. Therefore we try to adopt a method combining TCM (Traditional Chinese Medicine) with western medicine to reduce these indexes to an ideal level.
Pathological indexes that influence the prognosis are also important. Pathological changes of IgA Nephropathy involve the glomeruli, renal rubules, renal interstitium and renal blood vessel and show great variety in degree and complexity. Pathological changes by renal biopsy are related to the clinical manifestations of the time and they are dynamic and developing with time. Reversibility and irreversibility are relatively spoken.
The following three aspects have certain influence on prognosis of IgA Nephropathy.
1. Pathological changes of the glomeruli: global sclerosis of the glomeruli is a recognized index of a poor prognosis. Proliferation of mesangial cells and matrix as well as deposition of IgA in mesangial area can remit and disappear after treatment, so they don’t have much influence on long-term prognosis. While periodic glomerulosclerosis, glomeruli-capsule adhesion, crescent formation and deposition of immune complex along the capillary loop are all indexes of a poor prognosis but it is without certainty on the basis of a multiplicity. It reminds us that the above changes are still reversible and should be treated positively instead of giving up.
2. Pathological changes of the tubule-interstitium: interstitial fibrosis and tubular atrophy are the index of a poor diagnosis, while infiltration of the interstitial inflammatory cells can be reduced or disappear after positive treatment and doesn’t have much influence on the prognosis.
3. Pathological changes of the tubules: with aggravating of the changes, reduction of blood capillary around the tubules also has direct influence on the prognosis.
2011年11月26日星期六
Live A Better Life with Diabetes
Everyone hope have a better life. But We all know that Diabetes is a lifelong disease and it can really threaten your life if you don’t take good care of it.
Then what should you do to better care for yourselves?
From a research which shows that Diabetes does shorten people’s lifespan we can know that what we should do includes the following aspects:
If you don’t have Diabetes, do what you can to prevent Diabetes. Know more about the risk factors of Diabetes and try to avoid them by developing a good living habit. For example, the most well known risk factors of Diabetes include obesity, less physical exercise, or unhealthy lifestyle. To avoid getting Diabetes, you should try to lose weight if you are overweight and do regular physical exercise, eat healthy and balanced diet and so on. These are all helpful in reducing your risk of getting Diabetes.
If you have Diabetes, the most important thing for you is to maintain tight control of blood sugar. The premise for this is to have a close monitoring of your condition. Pay regular visit to your doctor and know the specific condition of yourself. You can take important measures to reduce your risk of further health problems.
Change your eating habit to a healthier mode. Choose a diet that helps you to lose excess weight. Your diet also should be high in whole grains and fiber and low in saturated fat. Also, limit your intake of concentrated sweets, cholesterol and total calories. It may be helpful to meet with a nutritionist.
Exercise regularly. This is both good for you to lose weight and also helpful in building up your body resistance. You need to keep this as a part of your daily life and not just do it when you think of it.
Have regular eye and foot checkups. Diabetes may easily cause many complications, most of which are related to a bad blood sugar control. The problems can involve your eyes and your feet, so it is necessary for you to have regular examination of your eyes and your feet. In addition, you should try to protect them from being influenced by factors like infection or injury.
Apart from keeping your blood sugar at normal range, you should also pay attention to your blood pressure as well as cholesterol. Sometimes when there is anything abnormal, you may need to take more medicines under the guidance of your doctor.
Talk to your doctor about whether you should take low-dose aspirin to prevent blood clots and an ACE inhibitor to protect your kidneys.
Then what should you do to better care for yourselves?
From a research which shows that Diabetes does shorten people’s lifespan we can know that what we should do includes the following aspects:
If you don’t have Diabetes, do what you can to prevent Diabetes. Know more about the risk factors of Diabetes and try to avoid them by developing a good living habit. For example, the most well known risk factors of Diabetes include obesity, less physical exercise, or unhealthy lifestyle. To avoid getting Diabetes, you should try to lose weight if you are overweight and do regular physical exercise, eat healthy and balanced diet and so on. These are all helpful in reducing your risk of getting Diabetes.
If you have Diabetes, the most important thing for you is to maintain tight control of blood sugar. The premise for this is to have a close monitoring of your condition. Pay regular visit to your doctor and know the specific condition of yourself. You can take important measures to reduce your risk of further health problems.
Change your eating habit to a healthier mode. Choose a diet that helps you to lose excess weight. Your diet also should be high in whole grains and fiber and low in saturated fat. Also, limit your intake of concentrated sweets, cholesterol and total calories. It may be helpful to meet with a nutritionist.
Exercise regularly. This is both good for you to lose weight and also helpful in building up your body resistance. You need to keep this as a part of your daily life and not just do it when you think of it.
Have regular eye and foot checkups. Diabetes may easily cause many complications, most of which are related to a bad blood sugar control. The problems can involve your eyes and your feet, so it is necessary for you to have regular examination of your eyes and your feet. In addition, you should try to protect them from being influenced by factors like infection or injury.
Apart from keeping your blood sugar at normal range, you should also pay attention to your blood pressure as well as cholesterol. Sometimes when there is anything abnormal, you may need to take more medicines under the guidance of your doctor.
Talk to your doctor about whether you should take low-dose aspirin to prevent blood clots and an ACE inhibitor to protect your kidneys.
2011年11月11日星期五
Chronic Kidney Disease Overview
The kidneys are a pair of bean-shaped organs that lie on either side of the spine in the lower middle of the back. Each kidney weighs about ¼ pound and contains approximately one million filtering units called nephrons. Each nephron is made of a glomerulus and a tubule. The glomerulus is a miniature filtering or sieving device while the tubule is a tiny tube like structure attached to the glomerulus.
The kidneys are connected to the urinary bladder by tubes called ureters. Urine is stored in the urinary bladder until the bladder is emptied by urinating. The bladder is connected to the outside of the body by another tube like structure called the urethra.
The main function of the kidneys is to remove waste products and excess water from the blood. The kidneys process about 200 liters of blood every day and produce about two liters of urine. The waste products are generated from normal metabolic processes including the breakdown of active tissues, ingested foods, and other substances. The kidneys allow consumption of a variety of foods, drugs, vitamins and supplements, additives, and excess fluids without worry that toxic by-products will build up to harmful levels. The kidney also plays a major role in regulating levels of various minerals such as calcium, sodium, and potassium in the blood.
As the first step in filtration, blood is delivered into the glomeruli by microscopic leaky blood vessels called capillaries. Here, blood is filtered of waste products and fluid while red blood cells, proteins, and large molecules are retained in the capillaries. In addition to wastes, some useful substances are also filtered out. The filtrate collects in a sac called Bowman's capsule.
The tubules are the next step in the filtration process. The tubules are lined with highly functional cells which process the filtrate, reabsorbing water and chemicals useful to the body while secreting some additional waste products into the tubule.
The kidneys also produce certain hormones that have important functions in the body, including the following:
Active form of vitamin D (calcitriol or 1,25 dihydroxy-vitamin D), which regulates absorption of calcium and phosphorus from foods, promoting formation of strong bone.
Erythropoietin (EPO), which stimulates the bone marrow to produce red blood cells.
Renin, which regulates blood volume and blood pressure.
Chronic kidney disease
Chronic kidney disease occurs when one suffers from gradual and usually permanent loss of kidney function over time. This happens gradually, usually months to years. Chronic kidney disease is divided into five stages of increasing severity (see Table 1 below). The term "renal" refers to the kidney, so another name for kidney failure is "renal failure." Mild kidney disease is often called renal insufficiency.
With loss of kidney function, there is an accumulation of water; waste; and toxic substances, in the body, that are normally excreted by the kidney. Loss of kidney function also causes other problems such as anemia, high blood pressure, acidosis (excessive acidity of body fluids), disorders of cholesterol and fatty acids, and bone disease.
Stage 5 chronic kidney disease is also referred to as kidney failure, end-stage kidney disease, or end-stage renal disease, wherein there is total or near-total loss of kidney function. There is dangerous accumulation of water, waste, and toxic substances, and most individuals in this stage of kidney disease need dialysis or transplantation to stay alive.
Unlike chronic kidney disease, acute kidney failure develops rapidly, over days or weeks.
Acute kidney failure usually develops in response to a disorder that directly affects the kidney, its blood supply, or urine flow from it.
Acute kidney failure is often reversible, with complete recovery of kidney function.
Some patients are left with residual damage and can have a progressive decline in kidney function in the future.
Others may develop irreversible kidney failure after an acute injury and remain dialysis-dependent.
The kidneys are connected to the urinary bladder by tubes called ureters. Urine is stored in the urinary bladder until the bladder is emptied by urinating. The bladder is connected to the outside of the body by another tube like structure called the urethra.
The main function of the kidneys is to remove waste products and excess water from the blood. The kidneys process about 200 liters of blood every day and produce about two liters of urine. The waste products are generated from normal metabolic processes including the breakdown of active tissues, ingested foods, and other substances. The kidneys allow consumption of a variety of foods, drugs, vitamins and supplements, additives, and excess fluids without worry that toxic by-products will build up to harmful levels. The kidney also plays a major role in regulating levels of various minerals such as calcium, sodium, and potassium in the blood.
As the first step in filtration, blood is delivered into the glomeruli by microscopic leaky blood vessels called capillaries. Here, blood is filtered of waste products and fluid while red blood cells, proteins, and large molecules are retained in the capillaries. In addition to wastes, some useful substances are also filtered out. The filtrate collects in a sac called Bowman's capsule.
The tubules are the next step in the filtration process. The tubules are lined with highly functional cells which process the filtrate, reabsorbing water and chemicals useful to the body while secreting some additional waste products into the tubule.
The kidneys also produce certain hormones that have important functions in the body, including the following:
Active form of vitamin D (calcitriol or 1,25 dihydroxy-vitamin D), which regulates absorption of calcium and phosphorus from foods, promoting formation of strong bone.
Erythropoietin (EPO), which stimulates the bone marrow to produce red blood cells.
Renin, which regulates blood volume and blood pressure.
Chronic kidney disease
Chronic kidney disease occurs when one suffers from gradual and usually permanent loss of kidney function over time. This happens gradually, usually months to years. Chronic kidney disease is divided into five stages of increasing severity (see Table 1 below). The term "renal" refers to the kidney, so another name for kidney failure is "renal failure." Mild kidney disease is often called renal insufficiency.
With loss of kidney function, there is an accumulation of water; waste; and toxic substances, in the body, that are normally excreted by the kidney. Loss of kidney function also causes other problems such as anemia, high blood pressure, acidosis (excessive acidity of body fluids), disorders of cholesterol and fatty acids, and bone disease.
Stage 5 chronic kidney disease is also referred to as kidney failure, end-stage kidney disease, or end-stage renal disease, wherein there is total or near-total loss of kidney function. There is dangerous accumulation of water, waste, and toxic substances, and most individuals in this stage of kidney disease need dialysis or transplantation to stay alive.
Unlike chronic kidney disease, acute kidney failure develops rapidly, over days or weeks.
Acute kidney failure usually develops in response to a disorder that directly affects the kidney, its blood supply, or urine flow from it.
Acute kidney failure is often reversible, with complete recovery of kidney function.
Some patients are left with residual damage and can have a progressive decline in kidney function in the future.
Others may develop irreversible kidney failure after an acute injury and remain dialysis-dependent.
What causes kidney failure?
Examples of prerenal causes of kidney failure are:
- hypovolemia (low blood volume) due to blood loss;
- dehydration from loss of body fluid (for example, vomiting, diarrhea, sweating, fever);
- poor intake of fluids;
- medication, for example, diuretics ("water pills") may cause excessive water loss; and
- abnormal blood flow to and from the kidney due to obstruction of the renal artery or vein.
- Sepsis: The body's immune system is overwhelmed from infection and causes inflammation and shutdown of the kidneys. This usually does not occur with urinary tract infections.
- Medications: Some medications are toxic to the kidney, includingnonsteroidal anti-inflammatory drugs like ibuprofen and naproxen. Others potentially toxic medications include antibiotics like aminoglycosides [gentamicin (Garamycin), tobramycin], lithium(Eskalith, Lithobid), iodine-containing medications such as those injected for radiology dye studies.
- Rhabdomyolysis: This is a situation in which there is significant muscle breakdown in the body, and the damaged muscle fibers clog the filtering system of the kidneys. this can occur because of trauma, crush injuries, and burns. Some medications used to treat high cholesterolcan cause rhabdomyolysis.
- Multiple myeloma
- Acute glomerulonephritis or inflammation of the glomeruli, the filtering system of the kidneys. Many diseases can cause this inflammation including systemic lupus erythematosus, Wegener's granulomatosis, and Goodpasture syndrome.
- Obstruction of the bladder or the ureters can cause back pressure because the kidneys continue to produce urine, but the obstruction acts like a dam, and urine backs up into the kidneys. When the pressure increases high enough, the kidneys are damaged and shut down.
- Prostatic hypertrophy or prostate cancer may block the urethra and prevents the bladder from emptying.
- Tumors in the abdomen that surround and obstruct the ureters.
- Kidney stones. Usually, kidney stones affect only one kidney and do not cause kidney failure. However, if there is only one kidney present, a kidney stone may cause the lone kidney to fail
2011年10月22日星期六
What are Nephrotic syndrome
Nephrotic syndrome is a nonspecific disorder in which the kidneys are damaged, causing them to leak large amounts of protein (proteinuria at least 3.5 grams per day per 1.73m2 body surface area) from the blood into the urine.
Kidneys affected by nephrotic syndrome have small pores in the podocytes, large enough to permit proteinuria (and subsequently hypoalbuminemia, because some of the protein albumin has gone from the blood to the urine) but not large enough to allow cells through (hence no hematuria). By contrast, in nephritic syndrome, RBCs pass through the pores, causing hematuria.
According to NephCure, most often, Nephrotic Syndrome is defined by its primary diseases that attack the kidney’s filtering system. Some of these cases are idiopathic.
Signs and symptoms
It is characterized by proteinuria (>3.5g/day), hypoalbuminemia, hyperlipidemia and edema which is generalized & also known as anasarca or dropsy. Common among 2–6 years old boys. The edema begins in the face. Lipiduria (lipids in urine) can also occur, but is not essential for the diagnosis of nephrotic syndrome. Hyponatremia also occurs with a low fractional sodium excretion.
Hyperlipidemia is caused by two factors:
1 The most common sign is excess fluid in the body due to the serum hypoalbuminemia. Lower serum oncotic pressure causes fluid to accumulate in the interstitial tissues. Sodium and water retention aggravate the edema. This may take several forms:
3 Anemia (iron resistant microcytic hypochromic type) maybe present due to transferrin loss.
4 Dyspnea maybe present due to pleural effusion or due to diaphragmatic compression with ascites.
5 Erythrocyte sedimentation rate is increased due to increased fibrinogen & other plasma contents.
6 Some patients may notice foamy or frothy urine, due to a lowering of the surface tension by the severe proteinuria. Actual urinary complaints such as hematuria or oliguria are uncommon, though these are seen commonly in nephritic syndrome.
7 May have features of the underlying cause, such as the rash associated with systemic lupus erythematosus, or the neuropathy associated with diabetes.
8 Examination should also exclude other causes of gross edema—especially the cardiovascular and hepatic system.
Kidneys affected by nephrotic syndrome have small pores in the podocytes, large enough to permit proteinuria (and subsequently hypoalbuminemia, because some of the protein albumin has gone from the blood to the urine) but not large enough to allow cells through (hence no hematuria). By contrast, in nephritic syndrome, RBCs pass through the pores, causing hematuria.
According to NephCure, most often, Nephrotic Syndrome is defined by its primary diseases that attack the kidney’s filtering system. Some of these cases are idiopathic.
Signs and symptoms
It is characterized by proteinuria (>3.5g/day), hypoalbuminemia, hyperlipidemia and edema which is generalized & also known as anasarca or dropsy. Common among 2–6 years old boys. The edema begins in the face. Lipiduria (lipids in urine) can also occur, but is not essential for the diagnosis of nephrotic syndrome. Hyponatremia also occurs with a low fractional sodium excretion.
Hyperlipidemia is caused by two factors:
- Hypoproteinemia stimulates protein synthesis in the liver, resulting in the overproduction of lipoproteins.
- Lipid catabolism is decreased due to lower levels of lipoprotein lipase, the main enzyme involved in lipoprotein breakdown.
1 The most common sign is excess fluid in the body due to the serum hypoalbuminemia. Lower serum oncotic pressure causes fluid to accumulate in the interstitial tissues. Sodium and water retention aggravate the edema. This may take several forms:
- Puffiness around the eyes, characteristically in the morning.
- Pitting edema over the legs.
- Fluid in the pleural cavity causing pleural effusion. More commonly associated with excess fluid is pulmonary edema.
- Fluid in the peritoneal cavity causing ascites.
- Generalized edema throughout the body known as anasarca.
3 Anemia (iron resistant microcytic hypochromic type) maybe present due to transferrin loss.
4 Dyspnea maybe present due to pleural effusion or due to diaphragmatic compression with ascites.
5 Erythrocyte sedimentation rate is increased due to increased fibrinogen & other plasma contents.
6 Some patients may notice foamy or frothy urine, due to a lowering of the surface tension by the severe proteinuria. Actual urinary complaints such as hematuria or oliguria are uncommon, though these are seen commonly in nephritic syndrome.
7 May have features of the underlying cause, such as the rash associated with systemic lupus erythematosus, or the neuropathy associated with diabetes.
8 Examination should also exclude other causes of gross edema—especially the cardiovascular and hepatic system.
Polycystic Kidney Disease
Polycystic Kidney Disease (PKD or PCKD, also known as polycystic kidney syndrome) is a cystic genetic disorder of the kidneys.There are two types of PKD: Autosomal Dominant Polycystic Kidney Disease (ADPKD) and the less-common Autosomal Recessive Polycystic Kidney Disease (ARPKD).
It occurs in humans and some other animals. PKD is characterized by the presence of multiple cysts (hence, "polycystic") typically in both kidneys; however 17% of cases initially present with observable disease in one kidney, with most cases progressing to bilateral disease in adulthood.The cysts are numerous and are fluid-filled, resulting in massive enlargement of the kidneys. The disease can also damage the liver, pancreas and, in some rare cases, the heart and brain. The two major forms of polycystic kidney disease are distinguished by their patterns of inheritance.
Polycystic Kidney Disease is the most common life-threatening genetic disease, affecting an estimated 12.5 million people worldwide.[citation needed] In half of the people with Polycystic Kidney Disease, there is no family history of the disease. In these cases, the gene coding for the disease occurs out of a spontaneous genetic mutation without either parent being a carrier of the gene.
What are type of Polycystic Kidney Disease?
Autosomal dominant
ADPKD is the most common of all the hereditary cystic kidney diseases with an incidence of 1 to 2:1,000 live births.Studies show that 10% of end-stage renal disease (ESRD) patients being treated with hemodialysis in Europe and the U.S. were initially diagnosed and treated for ADPKD.ADPKD does not appear to demonstrate a preference for any particular ethnicity.
ADPKD is characterized by progressive cyst development and bilaterally enlarged kidneys with multiple cysts. There are three genetic mutations in the PKD-1, PKD-2, and PKD3 gene with similar phenotypical presentations. Gene PKD-1 is located on chromosome 16 and codes for a protein involved in regulation of cell cycle and intracellular calcium transport in epithelial cells, and is responsible for 85% of the cases of ADPKD. A group of voltage-linked calcium channels are coded for by PKD-2 on chromosome 4. PKD3 recently appeared in research papers as a postulated 3rd gene. At this time, PKD3 has not been proven.Fewer than 10% of cases of ADPKD appear in non-ADPKD families.
Cyst formation begins in utero from any point along the nephron, although fewer than 5% of nephrons are thought to be involved. As the cysts accumulate fluid, they enlarge, separate entirely from the nephron, compress the neighboring renal parenchyma, and progressively compromise renal function.
Under the function of gene defect, epithelial cells of renal tubule turn into epithelial cells of cyst wall after phenotype change, and begin to have the function of secreting cyst fluid, which leads to continuous cysts enlargement.
Autosomal Recessive
Studies show that the incidence of ARPKD is 1:20,000 live births and is typically identified in the first few weeks after birth. Unfortunately, resulting hypoplasia results in a 30% death rate in neonates with ARPKD.In ARPKD kidneys retain their shape but are larger than the normal anatomical range with dilated collecting ducts from the medulla to the cortex.
It occurs in humans and some other animals. PKD is characterized by the presence of multiple cysts (hence, "polycystic") typically in both kidneys; however 17% of cases initially present with observable disease in one kidney, with most cases progressing to bilateral disease in adulthood.The cysts are numerous and are fluid-filled, resulting in massive enlargement of the kidneys. The disease can also damage the liver, pancreas and, in some rare cases, the heart and brain. The two major forms of polycystic kidney disease are distinguished by their patterns of inheritance.
Polycystic Kidney Disease is the most common life-threatening genetic disease, affecting an estimated 12.5 million people worldwide.[citation needed] In half of the people with Polycystic Kidney Disease, there is no family history of the disease. In these cases, the gene coding for the disease occurs out of a spontaneous genetic mutation without either parent being a carrier of the gene.
What are type of Polycystic Kidney Disease?
Autosomal dominant
ADPKD is the most common of all the hereditary cystic kidney diseases with an incidence of 1 to 2:1,000 live births.Studies show that 10% of end-stage renal disease (ESRD) patients being treated with hemodialysis in Europe and the U.S. were initially diagnosed and treated for ADPKD.ADPKD does not appear to demonstrate a preference for any particular ethnicity.
ADPKD is characterized by progressive cyst development and bilaterally enlarged kidneys with multiple cysts. There are three genetic mutations in the PKD-1, PKD-2, and PKD3 gene with similar phenotypical presentations. Gene PKD-1 is located on chromosome 16 and codes for a protein involved in regulation of cell cycle and intracellular calcium transport in epithelial cells, and is responsible for 85% of the cases of ADPKD. A group of voltage-linked calcium channels are coded for by PKD-2 on chromosome 4. PKD3 recently appeared in research papers as a postulated 3rd gene. At this time, PKD3 has not been proven.Fewer than 10% of cases of ADPKD appear in non-ADPKD families.
Cyst formation begins in utero from any point along the nephron, although fewer than 5% of nephrons are thought to be involved. As the cysts accumulate fluid, they enlarge, separate entirely from the nephron, compress the neighboring renal parenchyma, and progressively compromise renal function.
Under the function of gene defect, epithelial cells of renal tubule turn into epithelial cells of cyst wall after phenotype change, and begin to have the function of secreting cyst fluid, which leads to continuous cysts enlargement.
Autosomal Recessive
Studies show that the incidence of ARPKD is 1:20,000 live births and is typically identified in the first few weeks after birth. Unfortunately, resulting hypoplasia results in a 30% death rate in neonates with ARPKD.In ARPKD kidneys retain their shape but are larger than the normal anatomical range with dilated collecting ducts from the medulla to the cortex.
2011年10月18日星期二
Treatment for Protein and Blood in Urine.
Proteinuria means the presence of an excess of serum proteins in the urine. The protein in the urine often causes the urine to become foamy, although foamy urine may also be caused by bilirubin in the urine (bilirubinuria), retrograde ejaculation, pneumaturia (air bubbles in the urine) due to a fistula, or drugs such as pyridium.
Treatment for Protein and Blood in Urine.
Some patients with chronic kidney disease will have continuous protein and blood in urine. They are worried that it may develop into Uremia stage, so they search for treatment all around. When the protein and blood in urine had been effective treated and reduced, but after catching a cold, fever or overwork, it will appear again. Patients with IgA Nephropathy often circles like this.
Why there is protein and blood in urine?
Blood in urine is actually abnormal increase of red blood cells in urine. There is no red blood cells or little red blood cells in the urine of healthy people. If there are often red blood cells in urine, or red blood cells are over 3/HPF in microscopic test, it can be called hematuria. Renal hematuria comes from the kidneys. It is caused by the structure changes of red blood cells in urine.
Protein in urine is really a headache for patients with chronic kidney disease. The amount of protein in urine is not only related to the degree of kidney damage, but also an important index judging the progressing of the illness condition. There is only extremely trace protein in urine for healthy people and the urinalysis shows urine protein negative. However, if the kidney damage leads to changes of glomerular function and the permeability of glomerular basement membrane increases, the protein in filtrated urine will increase, which is over the reabsorption ability of the tubules thus causing protein in urine.
What’s the treatment for protein and blood in urine?
According to the above analysis, we know that the main cause of leakage of protein and red blood cells is the damage to glomerular filtrating membrane. In the past, we treated only the primary disease and did little to repair the membrane. Therefore, even the protein and blood in urine will disappear for a while, the root cause has not been solved and the glomerular filtrating membrane has not been damaged. After the effect of the medicine or due to the inducing factors, protein and blood in urine will reappear.
Micronized Chinese medicine has higher activity. While giving full play of the effect of traditional Chinese medicine, it can relink the broken molecular chains of Chinese medicine and produce new function. It can act on the damaged glomerular basement membrane, remove the immune complex and damaged tissues deposited on the basement membrane and repair it. This is to repair the cells with pathological changes, activate the DNA replication in the damaged cells, promote the change of renal structure and recover the renal function. Therefore, after repairing the root cause of the pathological changes will thoroughly disappear and the protein and blood in urine will gradually decrease and disappear. The symptoms disappear with the root cause, so it is not easy to relapse after stopping the medicine.
In treating protein and blood in urine caused by kidney disease, the key point is treating the root cause, that is repairing the damaged basement membrane.
Treatment for Protein and Blood in Urine.
Some patients with chronic kidney disease will have continuous protein and blood in urine. They are worried that it may develop into Uremia stage, so they search for treatment all around. When the protein and blood in urine had been effective treated and reduced, but after catching a cold, fever or overwork, it will appear again. Patients with IgA Nephropathy often circles like this.
Why there is protein and blood in urine?
Blood in urine is actually abnormal increase of red blood cells in urine. There is no red blood cells or little red blood cells in the urine of healthy people. If there are often red blood cells in urine, or red blood cells are over 3/HPF in microscopic test, it can be called hematuria. Renal hematuria comes from the kidneys. It is caused by the structure changes of red blood cells in urine.
Protein in urine is really a headache for patients with chronic kidney disease. The amount of protein in urine is not only related to the degree of kidney damage, but also an important index judging the progressing of the illness condition. There is only extremely trace protein in urine for healthy people and the urinalysis shows urine protein negative. However, if the kidney damage leads to changes of glomerular function and the permeability of glomerular basement membrane increases, the protein in filtrated urine will increase, which is over the reabsorption ability of the tubules thus causing protein in urine.
What’s the treatment for protein and blood in urine?
According to the above analysis, we know that the main cause of leakage of protein and red blood cells is the damage to glomerular filtrating membrane. In the past, we treated only the primary disease and did little to repair the membrane. Therefore, even the protein and blood in urine will disappear for a while, the root cause has not been solved and the glomerular filtrating membrane has not been damaged. After the effect of the medicine or due to the inducing factors, protein and blood in urine will reappear.
Micronized Chinese medicine has higher activity. While giving full play of the effect of traditional Chinese medicine, it can relink the broken molecular chains of Chinese medicine and produce new function. It can act on the damaged glomerular basement membrane, remove the immune complex and damaged tissues deposited on the basement membrane and repair it. This is to repair the cells with pathological changes, activate the DNA replication in the damaged cells, promote the change of renal structure and recover the renal function. Therefore, after repairing the root cause of the pathological changes will thoroughly disappear and the protein and blood in urine will gradually decrease and disappear. The symptoms disappear with the root cause, so it is not easy to relapse after stopping the medicine.
In treating protein and blood in urine caused by kidney disease, the key point is treating the root cause, that is repairing the damaged basement membrane.
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