We should give full attention to secondary prevention of kidney disease

Secondary kidney disease is systemic disease caused kidney damage, including glomerular disease, renal tubular - j interstitial diseases and renal vascular disease, and many of them secondary to a high incidence of nephropathy against large, cause full attention.

With the increase in the incidence of diabetes, diabetic glomerulosclerosis (hereinafter referred to diabetic nephropathy) were also increasing. In Europe and the United States end-stage renal failure patients, the highest percentage of the disease, more than 30%. According to China’s 1999 preliminary statistics, in hemodialysis patients with the disease for the second place, accounting for 13.5% in peritoneal dialysis patients with the disease for the third place, accounting for about 12.0%. In recent years, prevention and treatment of diabetic nephropathy has been great progress. In the control of high blood sugar, the target target has been revised, more stringent requirements (should strive to be in control of fasting blood glucose 6.1 mmol / L, postprandial blood glucose of 8.0 mmol / L, HbA1c was 6.2%); On the other hand, treatment the continuous emergence of new diabetes, and high blood sugar control more effective. Practice shows that early blood glucose control standards will prevent diabetic nephropathy is an important measure. Diabetic nephropathy event that the moratorium should be focused on the progress of renal damage, in addition to effective control of high blood sugar, the early application of vascular

Tension-converting enzyme inhibitor (ACEI) or angiotensin receptor antagonist Ⅱ (ATlRA), the active treatment and the incidence of hypertension and hyperlipidemia, their control standards, Hypertension target had been revised are: negative urine protein Quantitative or <1.0 g / d, blood pressure should be down to 130/80 mmHg (1mmHg = 0.133kPa), urinary protein: 1.0 g / d, blood pressure should be down to 125/75 mmHg; on hyperlipidemia Jiangzhi target should strive to cholesterol drop of <4.5 mmol / L, triglyceride <1.5 mmol / L, LDL <2.5 mmol / L, high-density lipoprotein> 1.15 mmol / L, respectively. When a diabetic nephropathy

Henoch-Schonlein Purpura Nephritis outlined

Will be divided into two types:
Traditional Chinese and Western Medicine
Purpura Nephritis (anaphylatic purpura nephritis) refers to Henoch-Schonlein purpura caused kidney damage, the cause can be bacteria, viruses and parasites, and other infections caused by allergic, or for certain drugs, such as food allergies, or plant pollen, Huiyao, caused by cold stimulation. Clinical manifestations Purpura except for the skin, joint pain, abdominal pain, blood in the stool, mainly hematuria and proteinuria, occurred in more than one month after the skin purpura, or some at the same time and can see skin purpura, abdominal pain, and some Asymptomatic only the abnormal urine. If too much protein loss, nephrotic syndrome can be a performance, if hematuria and proteinuria long-term persistence can be associated with renal dysfunction, which leads to chronic renal failure. Henoch-Schonlein Purpura renal involvement led to a ratio of 20% to 100%, with men more than women.
Diagnostic Criteria
1. International Children’s Kidney Disease Research (1 sKDC) Pathologic classification
I: for small lesions.
II: for mesangial proliferative.
III: (a) focal and (b) of diffuse proliferative or hardening, crescent formation <50%.
IV: (a) focal and (b) of diffuse mesangial proliferative or hardening, crescent formation 50% to 75%.
V: (a) local and b (a) of diffuse mesangial proliferative or hardening, crescent formation> 75%.
VI: membrane of hyperplastic lesions.
2. The World Health Organization (WHO) histological grade
I would include: small lesions, small lesions with focal segmental notable focal proliferative glomerulonephritis mild.
II include: diffuse proliferative glomerulonephritis mild, diffuse proliferative glomerulonephritis with mild focal segmental significant.
III: including focal proliferative glomerulonephritis Medium, diffuse proliferative glomerulonephritis moderate.
IV include: diffuse proliferative glomerulonephritis severe, end-stage renal.

Acute nephritis easily confused with the diseases?

Early acute nephritis easily confused with the following diseases, should draw attention.

(1) fever proteinuria can occur at any febrile illness. During the heat can be detected in urine protein and type, but very few red blood cells, no edema and hypertension. Heat Forward, urine abnormal rapid recovery.

(2) any abnormal urinary infection caused by infections such as bacteria, viruses, particularly hepatitis B hemolytic streptococcus infection, about 1 / 3 of patients, there will be mild microscopic hematuria, a small amount of urine protein and the type, but no edema and hypertension, when infection control, urine inspection is back to normal.

(3) focal glomerulonephritis generally occurs during infection (acute nephritis occurred in about two weeks after infection); focal nephritis with hematuria and proteinuria very light; cure infection, check urine of patients to return to normal, good prognosis. And the only light acute nephritis urine changes, but no edema and hypertension similar.

(4) Movement abnormal urine after strenuous exercise (such as long-distance running, swimming, a quick march……) or over exertion, in the urine within a few hours there can be unusual - hematuria, proteinuria and type urine, but the rest 1-2 days (by less than 7 days) is back to normal. In the event of abnormal urine at the same time without edema and hypertension (individual may have temporarily hypertension).

(5) lupus nephritis systemic lupus erythematosus caused kidney damage, and sometimes similar performance acute nephritis, accompanied rashes, hair loss, photosensitivity, joint pain and heart, liver, lung, brain and other organs of lesions, and there are fever, leukopenia, laboratory SM antibodies or anti-DNA antibodies and anti-nuclear antibody positive.

(6) toxemia of pregnancy occurs late in pregnancy, patients edema, hypertension, proteinuria and possession of urine, can be serious in hypertensive encephalopathy, especially in the last month of pregnancy when the more obvious symptoms. However, the lack of hematuria is the main feature, and most of normal renal function, fundus that retinal artery spasm, bleeding, leakage and other changes, and after the vast majority of patients to return to normal.

(7) primary nephrotic syndrome of acute nephritis with nephrotic syndrome and nephrosis are easily confused. The latter proteinuria (≥ 3.5 g / day) and hypoproteinemia features without hematuria, the former hematuria, no more than hypoproteinemia, differential points for kidney inspection, the former capillaries diffuse proliferative nephritis, which can be a minor disease or other chronic pathological changes in glomerular damage.

(8) acute renal pelvis nephritis acute nephritis occurred if the urethra, bladder mucosa and kidney congestion and edema can cause bladder stimulation symptoms similar acute pyelonephritis. But pyelonephritis fever, hematuria, interleukin are more positive urine culture, effective antibiotic treatment, and no significant edema, hypertension, and other performance, nor red blood cells in urine tube.

acute pyelonephritis and chronic nephritis acute confusion.

Lost salt nephritis which clinical performance?

Salt nephritis is lost for various reasons tubular dysfunction caused by disease, in 1944 from Thorn reported for the first time, it is known as Thorn syndrome. It is a group of serious renal salt loss for some of the characteristics of the particular type of renal disease, found in most chronic pyelonephritis, followed by renal medullary cystic sexually transmitted diseases, such as polycystic kidney disease and renal calcification.

The disease is a prominent clinical manifestations of hyponatremia can lead to circulatory failure, fine-speed pulse, blood pressure decrease or postural hypotension, syncope, and peripheral vein collapse, patients accompanied water loss, poor skin elasticity, the eye Depression, myasthenia gravis, loss of appetite, nausea, vomiting, weight loss and severe muscle spasm, etc.. If not promptly added sodium, patients can LOCA, missing salt, a sharp decline in glomerular filtration rate from uremia and death. The disease hyponatremia, have lower blood chlorine, but slightly higher serum potassium, BUN may have varying degrees of increase, and often metabolic acidosis, sustained increase in urinary sodium and urine output in the aldosterone increase, it should be timely treatment to the hospital for an examination.

Taboos on chronic nephritis

Chronic nephritis is the short form of chronic glomerulonephritis, is a common kidney disease.

The disease is divided into three types of Chinese rule, such as the spleen deficiency, in addition to the performance of chronic nephritis, there dorsal cold Shiling, stool Xilan, fat tongue desalination dental India, Shen Fine veins; hepatorenal Yin, with Yanankousao, urine short yellow, red tongue, Moss small veins breakdown; blood shortage, there are anemia, dizziness or tinnitus hyperhidrosis, unable to sleep at less satisfied, the tongue desalination Shen, and other veins. Differentiation can be treated.

In addition to drug therapy, in the daily lives of taboos is also very important. Should pay attention to the following aspects:

1. Bogey high fat food

Chronic nephritis patients of hypertension and symptoms of anemia, hypertension and animal fats anemia is unfavorable factors, because fat can inhibit atherosclerosis and increase the hematopoietic function, it should not be too much of chronic nephritis patients consumption. But if there is no chronic nephritis fat intake of more weak machine, it can be used in their daily lives instead of vegetable oil, about 60 grams daily.

2. Salt restriction

Edema and blood volume, the relationship between sodium greatly. Every 1 g of salt can be brought about 110 ml of water, such as nephritis patients with excessive consumption of salt, and urinary function also damaged, and often will add edema symptoms, blood volume increases, resulting in heart failure, salt restriction and it must be given low-salt diet. Daily salt intake should be controlled in the 2-4 grams of the following to prevent the edema and increased blood volume increased accidents.

3. Restrictions Hanpiaoling high and high nitrogen content of food in order to reduce the burden of kidney and renal cell stimulation should be restricted food such as spinach, celery, small turnips, beans, soybean products, sardines and chicken soup, fish soup, meat soup. Hanpiaoling because these foods high in nitrogen and high in renal dysfunction, its metabolites or timely discharge of a negative impact on renal function.

4. Jiyong strong seasoning

Strong spices such as pepper, mustard, coffee guts, peppers and other adverse renal function should be Jishi. MSG because more water will be thirsty to drink water restrictions in the amount should also use less MSG.

5. Restrictions plant proteins

Protein intake should be as renal conditions. In oliguric patients with edema, hypertension and retention of nitrogen, the daily protein intake of 20 to 40 grams should be controlled in order to reduce the burden of kidney and avoid non-protein nitrogen accumulation in the body. Special plant protein contains a large number of fat-yin base, the middle of the kidney to increase metabolism, it is not appropriate to use dry beans and soybean products as a nutritional supplement. Beans and soybean products including soybeans, mung beans, broad beans, soy milk, tofu, etc..

6. Liquid volume restrictions

Chronic nephritis patients hypertension and edema, fluid intake should be restricted. Daily intake should be controlled in 1200-1500 ml, including beverages and dishes in the water 800 ml. If serious edema, or moving more to strictly control the water. In voiding the circumstances, may be appropriate to relax.

Early detection of chronic nephritis from uremia

Dear readers, when you see that the “uremia,” and these three words, and certainly one critically patients, and one troubled family, and “HD” and “transplant” This can be several afraid of the word, and the huge medical expenses linked. Indeed, uremia, which is primary or secondary various chronic kidney disease caused by renal failure, the simple word, the kidney is useless and can not work. Compared to other common diseases, the incidence of low uremia. In China, about 10,000 individuals in the year a person is a disease, but once the disease, the only means of treatment of patients “HD” and “transplant” requires a large amount of cost to the individual patient and the family has brought enormous economic and spiritual burden. At the same time, sick people concentrated in the young adults, many people are at the peak of their studies and career, became ill after the loss of the workforce, will give individuals, families, the loss of many of the community.

That we have to ask, can prevent uremia? The answer is yes. Prevention is possible, or that the delay of the onset of the disease is possible. So, how to prevent? The focus should be on prevention of a disease prevention, early detection that has occurred in all you or your family on the chronic kidney disease through diet, drugs and good living habits, such as secondary prevention measures to mitigate the process of kidney damage. In China, resulting in uremic disease is the most important primary renal disease, and in these diseases cause major diseases is uremia chronic glomerulonephritis (hereinafter referred to chronic glomerulonephritis).

Now, a lot of people on the existence of chronic nephritis understanding of the three errors. It is precisely these errors, and sometimes everyone off guard.

“Chronic nephritis, as a disease, there should be obvious signs and symptoms of performance” Indeed, any illness is a performance of the signs and symptoms, such as nausea and hepatitis, skin discolouration sclera; pneumonia have a cough, Nongtan. And chronic nephritis What performance? Four common performance edema, hypertension, proteinuria, hematuria. But in fact, sometimes these signs and symptoms were very mild, or that people do not easily found and think they have contracted the disease glomerulonephritis. First said edema, nephritis edema eyelid edema is generally to get up early morning after the most common. However, insufficient sleep in normal circumstances, will emerge in the morning to get up after eyelid edema, up activities will be dissipated. This daily experience very easy to patients and their families to reduce vigilance, the author has deep feelings about it. Before I get up there sometimes eyelid edema, but in general are working or studying in the lack of tension sleep under, and in sufficient sleep, there are very few such cases, I have no mind. The situation was later asked in the course of treatment in many patients, many of them also have similar experiences. Another symptom is hypertension. Indeed, part of hypertension in patients with chronic glomerulonephritis is the performance, but concentrated in the young age of onset, heart and vascular conditions are good, strong ability to compensate, many people are accidentally found themselves high blood pressure, and More people, especially young people, no dizziness, lightheadedness, heart palpitations feeling is not specifically to blood pressure, it has high blood pressure do not know. In addition, some patients with high blood pressure in the performance of the disease is advanced kidney function discompensation because it demonstrated. The other two signs hematuria, proteinuria, these terms more easily misunderstood, hematuria is blood in the urine is not? Proteinuria is not protein in the urine is? To say that not right. Say that because this is the fact that the wrong people is a reality in these two very little understanding of the state, is generally thought hematuria can be seen urinating blood, and proteinuria What is the status of the more obscure. In fact, people usually think of hematuria is gross hematuria, gross hematuria are usually not because most of the situation arising from chronic nephritis, but the other urinary system diseases, and chronic nephritis hematuria are mostly microscopic hematuria, it is necessary to know the laboratory . Proteinuria for those of us who experienced the disease, it is very familiar, in general is very turbid urine, and some larger bubble, but a longer time will not disappear. But in real life, very few people pay special attention to their own urine, especially for a lot of very good people living habits, hear a urinate End urine Chongdiao will not leave observe whether or not the bubble turbid. Some patients with chronic glomerulonephritis the signs and symptoms are very minor and hide, and they almost do not affect the daily lives of patients and work, but in reality, but in the development of illness.

” ‘Chronic’ are from the ‘acute’ conversion from the” this view is wrong. Chronic glomerulonephritis is a group of more than causes, from all kinds of bacteria, viruses, protozoa, such as infection or through immune mechanisms, and non-inflammatory mediators of immune mechanism caused the glomerular diseases, the majority of patients with streptococcal infection does not clear , According to statistics only 15% to 20% of patients from acute glomerulonephritis (hereinafter referred to acute nephritis) transformation from. Therefore, we identify this disease at the very puzzled, when in the disease ah? Not too acute nephritis ah? Here, many people with acute nephritis and chronic nephritis confused. In simple terms, the link between them, but not one-to-one contact, that is, not everyone will be acute nephritis patients to chronic nephritis, chronic nephritis is not every patient has acute nephritis this process. Should arouse people’s attention is that the etiology of chronic nephritis is a very complicated, many patients with occult onset can be no acute process.

“Young people will be suffering from chronic nephritis how” in the treatment of the disease process, many people said that how so young will be in this disease? In fact, the incidence of this disease uremia concentrated on young people, if we review history, many people may be suffering from a chronic nephritis, began the age of very light because a lot of people to check on uremic period is not clearly know in the end when suffering from the disease of chronic nephritis, and therefore is not very accurate statistical data suggest that chronic nephritis our age specific incidence. However, in order to draw attention to the chronic nephritis in any age can happen, and the majority of patients age of onset is very light, from the onset to develop uremia, if not for as long as possible a few years to more than 10 years.

Misprision of a chronic nephritis, with many people understanding on the deviation, although the “invisible killer” in a step by step erosion of the patient’s kidney, but has a strong compensatory renal function, even if the patients had been seriously ill entangled, but also without any symptoms, Like all humans, and on the surface. In fact, the compensatory and decompensated seems to be burst dam and the dam burst, the former all seem normal, what a disaster would have to come. If the “burst”, the remedial work done well, it is possible to avoid uremia, it can at least be delayed arrival.

Focal Glomerulosclerosis

Focal glomerulosclerosis (focal glomeruloscerosis) glomerular capillary loop is a focal segmental sclerosis or hyalinization, no significant proliferation of a class of glomerular capillary. Can be used as mesangial proliferative, mesangial IgM deposition and focal glomerulosclerosis, but the minimal change nephropathy steroid resistant chronic recurrent progress consequences. Also on the hormone invalid primary nephrotic syndrome early renal biopsy which is focal glomerulosclerosis. Therefore, whether the disease as an independent glomerular diseases are still controversial. However, a representative of kidney disease and other different types of clinical pathology, also as an independent disease, more common, and there is a growing trend.

[Treatment]

(A) General for the performance of a large number of proteinuria, edema, for low-salt diet, the proper use of diuretics. Hypoalbuminemia obviously, can be suitably used albumin. Hypertension obviously, limit sodium, diuretic invalid, and can be used antihypertensive drugs such as angiotensin-converting enzyme inhibitors, calcium antagonists, such as.

(B) hormones and other immunosuppressants

1. Hormone nephrotic syndrome to the main performance, in particular the original biopsy for minimal change, the development of focal segmental glomerular sclerosis, still preferred hormone, mostly favourable response, the adult dose prednisolone 0.5 ~ 1mg / (kg d), 6 to 8 weeks, and then gradually over the next day reduction therapy, in the course of more than a year. Pei, and other reports with prednisone treatment of primary focal glomerulosclerosis, the complete remission rate of 47%, and kidneys of these patients survived five years was significantly higher than that without remission (96% vs. 55%). Although information hormone plus the effect of cytotoxic drugs is not better than the hormone alone. But many scholars advocate hormone invalid, dependent and should be repeated attack-combined. Because of cytotoxic drug can significantly reduce the relapse rate and extended remission period. And reduce the amount of hormones, reducing their side effects. Multi-use cyclic monophosphate amines, intermittent intravenous medication, the dose <150 mg / kg. Benzene can also be oral acid nitrogen mustard. In recent years, also with cyclosporine A treatment of this disease, a certain effect recently, in the process of reducing or stopping easy to relapse. And the high prices and potential renal toxicity, it is not appropriate for the preferred drug.

(C) other treatment angiotensin-converting enzyme inhibitor can not only lower blood pressure, and can reduce urinary protein might be useful delay renal failure. In addition, the patients with nephrotic syndrome were not only of high blood coagulation, there intrarenal blood coagulation, balloon adhesion should be anticoagulant therapy such as: dipyridamole 25 ~ 75 mg / d, Flynn, 2.5 mg / d, reduce proteinuria and improve renal function.

[Etiology:

(A) The primary focal glomerulosclerosis unknown etiology.

(B) Secondary focal glomerulosclerosis

1. Glomerular diseases heroin-related nephropathy, tumor-associated nephropathy, diabetes, AIDS, hereditary nephritis, IgA nephropathy, and preeclampsia, such as Hodgkin's disease.

2. Tubular, mesenchymal and vascular disease reflux nephropathy, radioactive nephritis, analgesics and kidney, such as sickle-cell disease.

3. Other renal hypoplasia, obesity and the elderly and so on.

[Pathogenesis]

Is not yet clear. Most believe that the changes in glomerular hemodynamics or basement membrane damage and the ball overload membrane uptake of macromolecules substances glomerulosclerosis. Near myeloid human embryonic kidney unit in early, bulky, the filtration rate is higher, capillary pressure, hyperfiltration eventually lead to structural damage, kidney disease nearly myeloid units appeared early and severe damage. As can be segmental glomerular epithelial cell damage to the basement membrane barriers anion electrical damage, chronic overload proteinuria, continuing high filtration and high perfusion will lead glomerulosclerosis. Glomerular hypertrophy and foam cell formation in the formation and development of the disease is of great significance. In the 5 / 6 nephrectomy model, glomerular plasma flow and pressure were increased glomerular epithelial cells were damaged, hyperthyroidism residual renal units, resulting in transparent degeneration. Fogo, and so will be the primary focal glomerulosclerosis pathophysiology associated with the clinical and found that adults and children, the sick, the average glomerular area significantly larger than the same age tiny lesions. Repeat biopsy also confirmed that some of the initial performance for minimal change, which has obvious proliferative glomerulonephritis. In addition, in many patients with primary focal glomerulosclerosis glomerular shows that the foam cells, macrophages it is the group of features, as well as by circulating mononuclear cells or conversion from mesangial cells. Some cytokines and growth factors such as IL-1, TNF-α, IL-6, such as glomerular sclerosis in the lead in a certain role. There are animal experiments found that serum cholesterol levels and related sclerosis.

Immune damage has been participating in the occurrence of this disease and development, and immunopathological in that area glomerulosclerosis granular IgM and C3 deposition. Electron microscopy showed a large number of electronic sclerosis lesions dense deposit. And the disease in kidney transplantation easy to relapse.

[Pathological changes:

Diagnosis of the disease depends mainly on renal biopsy. Light microscopy of segmental glomerular some of the glass-like protein homogeneous material. Without hardening the relatively normal. Sclerosis lesions typical of the area that a large number of cell-free matrix and transparent-like substance. PAS staining positive. Capillaries collapse, foam cell formation and local epithelial cell proliferation, glomerular capsule with Paal adhesion Paper pulp at the junction of the ball was first involved. In the non-sclerosis, glomerular epithelial cell swelling, hyperplasia, in the cytoplasm that degeneration and PAS positive tablets larger droplet. Corresponding tubular atrophy and renal interstitial fibrosis, a focal distribution. Immunofluorescence inspection: ordinary visible in the hardened area IgM and C3 deposition. Electron microscope: a large sclerosis lesions dense deposit. Non-hardening District capillary loop epithelial cells showed extensive foot process integration and dissipated, severity, the epithelial cells from the membrane-based separation, loss.

[Clinical]

The disease can occur at any age, mainly to young people. Have shown for continuing non-selective proteinuria. Most typical cases of nephrotic syndrome onset, or about 50 percent of the primary nephrotic syndrome 5% to 20%. 50% to 60% of patients with hematuria. Hypertension and renal damage reports ranging from 10% to 50%, and clinical manifestations in particular the level of urinary protein and prognosis.

[Prognosis]

And a variety of related factors: ① urine protein levels: urinary protein> 10 g / 24 hours, the progress of the disease quickly, in the more than six years the loss of renal function in urinary protein 3 ~ 3.5 g/24h, 50% of 6 to 8 years of development 10% of end-stage uremia. <3g/24h, 10 years after renal function remained normal levels. ② nephropathy or mitigation - response to treatment: Where are rarely sensitive to hormones to the development of renal failure. Complete remission, end-stage renal failure incidence of 15%, did not complete remission for 85%. ③ age: Adult relatively good. There are reports of the disease nephrotic syndrome and the incidence of relapse rate, the adult and 55% respectively 15%, compared with 76% of children and 80 per cent. ④ race: Ingulli such as children with nephrotic syndrome study found that the incidence of blacks than whites, and rapid development. 78% of blacks 8.5 years for the development of end-stage uremia. At the same time only 33% of whites. ⑤ course and degree of hypertension: Where treatment has been referred to the latter part of the course, hypertension serious poor prognosis. ⑥ renal pathology: the degree of damage or a serious film, mesangial proliferative vascular damage and easy access to renal failure.

Hereditary Nephritis conducted for genetic diagnosis

First Hospital of Peking University, Professor Ding Jie leadership of the Group of Alport syndrome (a hereditary nephritis, or AS) in a gene from clinical diagnosis to a series of studies, for further study and identification of Chinese people AS clinical phenotypes characteristics and gene mutation characteristics, in-depth study of gene function, as well as related molecular pathogenesis of AS laid the foundation.

According to Professor Ding Jie, AS mainly as hematuria, and decreased kidney function, sensorineural deafness and eye abnormalities, and the prognosis is serious hereditary kidney disease, hereditary kidney disease are common types. Ever seen electron microscope regarded renal glomerular basement membrane-specific lesions, as a diagnosis of AS “gold standard”, but a relatively big trauma, especially for children with difficult to accept. Ding Jie Professor AS skin biopsy in the mutant gene product (type IV collagen α5 chain) for the expression of the clinical diagnosis of AS, the method is simple and reliable, and markedly increase the rate of diagnosis. Group also an innovative way to analyze fibroblast starting mR-NA gene mutation detection, and the detection rate (90.6%), the result is accurate, is relatively fast and inexpensive.

The series of studies in the international community first reported one case of AS with neurofibromatosis type I cases found and reported 18 new COL4A5 gene mutation identified gene mutation AS Chinese characteristics is the first time the Chinese people on two genes mutation (COL4A5 and COL4A6) AS patients and family, and confirmed with AS without esophageal leiomyoma and COL4A6 gene mutation position from the gene level revealed the organization on the basement membrane type IV collagen expression of all of the normal chain AS the molecular basis.

Hereditary Nephritis gene was found

Surname Zhou also can not think of how patients and their doctor, the doctor has told him to inform his brother together. The results, both brothers died of hereditary nephritis hospital. Kidney from Ruijin Hospital Medical Director Professor Chen Nan led the team, the first time from the nation’s largest group of home-nephritis disease found in human hereditary nephritis mutant gene, preliminary clinical testing results.

From 1997, Ruijin Hospital renal medicine to Professor Nan Chen, director of the research team mainly from kidney disease in a typical family of genes in the patient group of small sites, through 27 of the 531 family members investigation, and which Some patients undergo a genetic test and found that these patients are different from the normal gene sequencing. The outcome of further studies, the first time that the family of hereditary nephritis patients with the mutant gene, so as to look for genetic causes of nephritis a breakthrough.

The research results show that the use of new genetic testing technology, can be found early in the census nephritis patients, but also in the future prenatal diagnosis, early child know that the next generation of renal genetic defects, the home of the patients also found in the early not feeling the same symptoms of patients with glomerulonephritis.

Treatment of hepatitis B-related nephropathy

Hepatitis B can lead nephritis, hepatitis B virus antigen induced kidney damage caused by a series of symptoms of nephritis, or kidney, known as hepatitis B associated glomerulonephritis. Children than adult patients most were more men than women. Hepatitis B epidemic in the area, the high incidence of nephritis, and nephritis patients with hepatitis B virus-positive rate is significantly higher than healthy subjects.

Hepatitis B related nephritis onset variety, the more performance hepatitis not obvious, and many patients with renal disease as the first symptom. Nephritis and hepatitis incidence interval few months to several years, and see in the course of proteinuria, microscopic hematuria or gross hematuria, most of the patients blood pressure and renal function was normal. At the same time there sometimes liver and kidney damage, kidney typical performance may, in some patients hepatomegaly, abnormal liver function. The pathological nature of it is virtual heresy, features a hot and humid Stasis drug blues, liver, spleen, kidney disorders, there is virtual heresy love, strength inclusions, and healthy trends weak, cult poison in volts, of the pathological changes of potential deferred,

The treatment of hepatitis B associated glomerulonephritis to identify false and evil is the focus, and distinguish the wet, hot, drugs, and the primary and secondary stasis and folders. Committed liver hepatitis B virus, a blood-heat toxin; nephropathy is immune complex deposition in the glomerular basement membrane, a Chinese “Stasis swollen” area. Therefore, in the Diagnosis and Prescription At the same time, the appropriate electoral and Liangxue Huayu, Huoxue Quyu, Sanyu swelling, and other traditional Chinese medicine, to eliminate hepatitis B virus, the elimination of eggs often received unexpected results.