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显示标签为“glomeruli”的博文。显示所有博文

2014年9月17日星期三

A variety of systemic diseases are associated with IgA nephropathy

 IgA nephropathy
A variety of systemic diseases are associated with IgA nephropathy such as liver failure, celiac disease, rheumatoid arthritis, Reiter's disease, ankylosing spondylitis and HIV. Diagnosis of IgA Nephropathy and a search for any associated disease occasionally reveals such an underlying serious systemic disease. Occasionally, there are simultaneous symptoms of Henoch-Schönlein purpura; see below for more details on the association. Some HLA alleles have been suspected along with complement phenotypes as being genetic factors.

In IgA Nephropathy [IgAN], unknown agents cause the glomeruli to become — and to stay — inflamed. IgAN is the world’s most common glomerulonephritis [inflammation of the glomeruli], but its pathogenesis [how the disease develops] is not known. IgAN is considered to be an immune-complex mediated disorder (or immunologically mediated disorder), which means that immune complexes may not be the direct cause of the disease but they help bring about the end result, which is widespread inflammation of the kidneys.

What happens in IgAN is essentially a vicious cycle: inflammatory chemicals increase the permeability of the glomerular capillary wall, and that increased porosity enhances the absorption of other chemicals that stimulate cellular growth and, ultimately, structural damage. These changes take time because our kidneys have a lot of excess capacity built into them. The damage is, however, slowly progressive and, in the case of sclerosis [scarring], irreversible.

We do not know what antigen is responsible for triggering IgAN, nor do we know whether IgAN results from defects in the body’s creation or elimination of immune complexes. There is evidence that immunoglobulin A is overproduced in the bone marrow of IgAN patients; some patients also show decreased capacity to remove immune complexes from their systems.

Who is likely to get IgA nephropathy?

The condition is three times as common in males as females -but this difference is unexplained. It also seems to be more common in some parts of the world – especially Japan, Singapore and other countries in the Pacific Rim. It is more common in Southern Europe compared to Northern Europe. We do not know the reasons for these geographical differences.

It can be diagnosed at any age but most commonly in children and young adults who are likely to have the typical story of episodes of visible haematuria. Older people are less likely to have visible haematuria; they are more likely to have protein as well as blood in the urine at the time of diagnosis and to have hypertension and other evidence of more advanced kidney damage. We presume that these older people have in fact had IgA nephropathy for many years but because they never had visible haematuria or a routine urine test, it was not diagnosed until a much later stage.

Does IgA nephropathy affect any part of the body other than the kidneys?

No, it does not, but there is a condition called Henoch-Schönlein purpura (often shortened to HSP) which is related to IgA nephropathy. HSP gets its odd name from the two German doctors who originally described it over a hundred years ago. We now know that the kidney problem in HSP is very similar to IgA nephropathy; but patients with HSP also get a skin rash and may have aches and pains in their joints and attacks of abdominal pain. IgA is found in the skin as well as in the kidneys in HSP. The skin, joint and abdominal effects of HSP often go away in a few weeks or months, but the kidney problem can stay much longer, and may eventually cause kidney failure. HSP can occur at any age but is commonest in young children.

A proper diet can double the curative effect, but a bad diet may make your disease worse. So pay attention to the foods you eat, if you need any help in making the diet plan or cure your disease, you can email us. Our email: sjzkidneyhospital@hotmail.com

2014年9月13日星期六

Causes of Glomerulosclerosis

Kidney disease
Damaged glomeruli can't perform their job adequately. As a result, large amounts of protein from the blood leak into the urine rather than remaining in the bloodstream. This leads to a condition called proteinuria.

Causes of Glomerulosclerosis
Focal segmental glomerulosclerosis (FSGS) is a kidney disease that can lead to glomerulosclerosis. In FSGS, the scarring occurs only in some of the glomeruli. And only part of the individual glomeruli is damaged.

Untreated, it can lead to kidney failure. In some cases, kidney failure can occur despite treatment.

FSGS most frequently occurs without a cause. In such cases it is called idiopathic or primary FSGS. Sometimes, though, FSGS does have a known cause, and these can include:

HIV infection
Obesity
Sickle cell disease
Birth defects of the kidneys
Heroin or other drug use
Genetic causes (in rare cases)
Besides FSGS, glomerulosclerosis can be caused by these diseases:

Diabetes
Lupus
HIV infection
Sickle cell disease
Conditions that damage the kidneys can also lead to glomerulosclerosis. These include:

Glomerulonephritis, which causes the glomeruli to become inflamed.
Reflux nephropathy, in which urine flows back into the kidney.
Chemicals and medicines that harm the kidneys can also cause glomerulosclerosis.

Symptoms of Glomerulosclerosis
At first, there are no obvious signs of glomerulosclerosis. Over time, symptoms can develop. These include:

Swelling. Because of fluid retention, you may have swelling in various parts of the body, including:

Hands
Feet
Legs
Abdomen
Around the eyes
The swelling may be painful. It may also cause rapid weight gain.

Changes in urine. You may have foamy or bubbly urine, caused by proteinuria.

Often, glomerulosclerosis is discovered during a routine checkup. Tests during a checkup can reveal an abnormally high protein content in the urine (proteinuria). Or they may show a low level of protein in the blood (hypoproteinemia).

Symptoms that often accompany glomerulosclerosis include:

High blood pressure
High cholesterol
In glomerulosclerosis patients, high blood pressure can be difficult to control.

Diagnosis of Glomerulosclerosis
The only way you can be certain of an accurate diagnosis of glomerulosclerosis is to get a kidney biopsy. That's because the symptoms of glomerulosclerosis can also occur in many other conditions.

In a kidney biopsy, your doctor removes a very small amount of kidney tissue. The tissue is examined for signs of scarring.

Diagnosing glomerulosclerosis may require multiple biopsies. That's because the scarring does not occur throughout the kidney. So your doctor may have to look at samples from several different parts of the kidney until an affected area is found.

And we also have many other unique therapies. We will adopt the best systemic therapy which is most suitable to the patient's kidney condition. If you need any help in curing your disease, you can leave messages or email to us. Our email: sjzkidneyhospital@hotmail.com

2014年8月23日星期六

Causes chronic nephritis

Chronic glomerulonephritis is the advanced stage of a group of kidney disorders, resulting in inflammation and slowly worsening destruction of internal kidney structures

Chronic glomerulonephritis occurs when there is slow, progressive destruction of the glomeruli of the kidney, with progressive loss of kidney function. In some cases, the cause is found to be a specific attack to the body's immune system, but in most cases, the cause is unknown. Iit is generally thought that a still-unidentified abnormality of the immune system is to blame.

Damage to the glomeruli affects the kidney's ability to filter fluids and wastes properly. This leads to blood and protein in the urine.
This condition may develop after survival of the acute phase of rapidly progressive glomerulonephritis. In about one-quarter of people with chronic glomerulonephritis there is no prior history of kidney disease, and the disorder first appears as chronic kidney failure.

Glomerulonephritis is among the leading causes of chronic kidney failure and end stage kidney disease. Causes include:

Because symptoms develop gradually, the disorder may be discovered when there is an abnormal urinalysis during a routine physical or during an examination for another, unrelated disorder. It may be discovered as a cause of high blood pressure that is difficult to control.

Laboratory tests may reveal anemia or show signs of reduced kidney functioning, including azotemia. Later, signs of chronic kidney failure may be apparent, including edema .

Treatment varies depending on the cause of the disorder, and the type and severity of symptoms. The primary treatment goal is control of symptoms. High blood pressure may be difficult to control, and it is generally the most important aspect of treatment. Various medications may be used to attempt to control high blood pressure.
Corticosteroids, immunosuppressives, or other medications may be used to treat some of the causes of chronic glomerulonephritis.

Treatment for chronic nephritis depends on the type and cause of the condition. It aims at reducing inflammation, relieving the symptoms and repairing the damaged kidney tissues, as well as improving kidney function. Based on the aim, here are several treatment options are suggested.

Chinese Herbal Medicine. It uses specific herbs which help repair the damaged kidney tissues and improve kidney function. In addition, patients usually get the additional effects for the symptoms, because Chinese herbal medicine offers holistic effects.

Immunotherapy. It is a biological therapy which helps use the immune system to control the inflammation on kidneys. This helps delay the progression of Nephritis.

Diet Management

Eating habits and diet management show a very important role which patients can not ignore. Patients with chronic nephritis are suggested to take a low-phosphorus, low-protein diet.

Patients should ensure adequate carbohydrates, in patients with chronic nephritis due to limit protein intake, heat is supplied primarily by carbohydrates, dietary carbohydrate should increase to meet the needs of the body heat.

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