Patients with IgA nephropathy diet what needs attention? Many kidney patients
are very concerned about, understanding of patients in normal life, eating is
not very comprehensive, and patients to a good understanding of the diet of the
iga nephropathy, this is very helpful for the treatment of Experts to give you
to make explanations, I hope we can help.
1, the supply of protein
IgA nephropathy in the diet should be based on the degree of impairment of
renal function to determine the protein intake. Longer duration of renal damage
is not severe cases, the protein in the food you do not have strictly limited,
but should not exceed 1 gram per kilogram of body weight per day, high-quality
protein to achieve 50% or more.
2, the supply of energy
Because some patients limits the protein, the heat supply to the carbohydrate
and fat as the main source of energy supply, as the labor intensity. The rest,
adult daily supply of 30 to 35 kcal / kg body weight. And to meet the needs of
the patient's activities.
3, the control of sodium intake
Should be considered in patients with or without hypertension and edema were
treated with salt, no salt diet. Severe edema and hypertension, the amount of
sodium to control the less than 2 g / day, or even to give salt-free diet, is
generally appropriate to the low-salt. Also fasting other salty food and sugar
drinks and pungent foods.
4, limiting the intake of potassium
IgA in patients with oliguric (daily urine output of less than 1000 ml), then
high potassium foods such as kelp, seaweed, animal offal, bananas, citrus,
potatoes, tomatoes, squash, tea, soy sauce, MSG, etc. need to limit.
5, the intake of water
IgA nephropathy patients should drink plenty of water or drink. If there are
no special circumstances, such as disease doctor told him to let more than to
drink water and other, more important aspect of drinking water in IgA
nephropathy diet care, family members can also urge patients to drink plenty of
water. IgA nephropathy is the further development of renal insufficiency,
uremia, in addition to strictly limit the protein, but also strictly limit the
intake of water.
6, vitamin supplements
Any IgA patients in the daily diet should be given plenty of vitamins,
especially vitamin C, because long-term IgA nephritis patients may have anemia,
vitamin C can increase iron absorption and should supplement rich in vitamin B
and folic acid food, to correct anemia.
Patients with IgA nephropathy diet what needs attention? We should be the
diet of patients with IgA nephropathy need to pay attention to have a certain
understanding. Experts suggest that patients should reasonably arrange their own
diet, to promote the optimal therapeutic effect.
Learn more knowledge of kidney disease, early found early treatment, prevention of dialysis, improve the quality of life. http://www.nephritiscn.com
Showing posts with label IgA. Show all posts
Showing posts with label IgA. Show all posts
Wednesday, June 27, 2012
Thursday, May 17, 2012
IgA nephropathy is why permanently?
IgA nephropathy will be permanently Why? Why doctors symptomatic drugs
prescribed by that time well now committed? Study the root causes, treatment can
only see the appearance, not simply start taking medication, no hematuria, in
fact, general doctor of medicine western medicine tired hormone substances,
Western medicine is only symptomatic treatment, that Western medicine is just to
eliminate the hematuria did not repair the damaged kidney, so the drug is
stopped here there would hematuria.
Hematuria, the real reasons of IgA nephropathy: kidney consists of five intrinsic cells generated with IgA nephropathy is mesangial cells inherent in the kidney cells proliferation, it is also called the iga type mesangial cell hyperplasia.
Then, the blood in the urine of IgA nephropathy is how to generate? Susceptible populations of IgA nephropathy is defective mucosal immune function, when mucosal decreased immune function, very prone to upper respiratory tract infection or gastrointestinal infection, those antigens (inflammatory substances such as bacteria, viruses) enter the body and the body iga inflammatory response constitute the IgA immune complexes, leading to large amounts of immune complex deposition in glomerular mesangial cells District as pathogenic factors invade makes mesangial cell proliferation proliferation, inflammatory substances continue to stimulate mesangial cell dysfunction, and mesangial cell function is swallowed, the physiological function of macromolecules decreased, making the red blood cells leak more and more, and ultimately is occult blood in a single laboratory has been increasing.
IgA nephropathy hematuria how to treat? Of IgA nephropathy why permanently? Purely traditional treatment In order to eliminate blood in the urine, as in a short period of time will inhibit the development of the disease, however, the real onset of the reasons has not been eliminated, good scar is also pain, how to cure blood in the urine?
The emergence of blood in the urine of IgA nephropathy nephropathy due to invasion of external inflammatory substances cause damage, so in the course of treatment will be carried out anti-inflammatory, inhibiting inflammatory substances continue to be intrinsic cells of the kidney mesangial cell damage; external inflammatory substances into the human body with IgA antigen-antibody immune complexes, and then deposited in the glomerular mesangial area, kidney ischemia and hypoxia, and thus do the vasodilators to improve blood circulation and kidney ischemia hypoxic state to provide a good treatment for the repair of mesangial cells; inflammatory cells that would increase blood viscosity increased, the platelet hyperfunction, enhanced coagulation, resulting in the micro thrombosis composition, in order to prevent microthrombi composition, and thus to anticoagulant therapy, maintaining smooth blood to avoid the excessive deposition of immune complexes; inflammatory cells of IgA immune complex deposition led to an increase in mesangial cell proliferation, atrophy, and cell extracellular matrix, and therefore must extracellular matrix deposition degradation, so that it can be excreted with the urine. The above inter-related treatment, IgA nephropathy hematuria before it can be restored to normal.
IgA nephropathy why permanently? Overall the treatment of IgA nephropathy hematuria can not simply eliminate the hematuria, and should thus be treated, to repair damaged kidney mesangial cells, as will be made in the treatment of a multiplier effect, the other IgA due to immune dysfunction, kidney patients need time to prevent some of the invasion of bacteria, viruses, that is, to prevent colds and infections, I believe, IgA nephropathy will soon be recovered by treatment of science and daily life cautious.
Hematuria, the real reasons of IgA nephropathy: kidney consists of five intrinsic cells generated with IgA nephropathy is mesangial cells inherent in the kidney cells proliferation, it is also called the iga type mesangial cell hyperplasia.
Then, the blood in the urine of IgA nephropathy is how to generate? Susceptible populations of IgA nephropathy is defective mucosal immune function, when mucosal decreased immune function, very prone to upper respiratory tract infection or gastrointestinal infection, those antigens (inflammatory substances such as bacteria, viruses) enter the body and the body iga inflammatory response constitute the IgA immune complexes, leading to large amounts of immune complex deposition in glomerular mesangial cells District as pathogenic factors invade makes mesangial cell proliferation proliferation, inflammatory substances continue to stimulate mesangial cell dysfunction, and mesangial cell function is swallowed, the physiological function of macromolecules decreased, making the red blood cells leak more and more, and ultimately is occult blood in a single laboratory has been increasing.
IgA nephropathy hematuria how to treat? Of IgA nephropathy why permanently? Purely traditional treatment In order to eliminate blood in the urine, as in a short period of time will inhibit the development of the disease, however, the real onset of the reasons has not been eliminated, good scar is also pain, how to cure blood in the urine?
The emergence of blood in the urine of IgA nephropathy nephropathy due to invasion of external inflammatory substances cause damage, so in the course of treatment will be carried out anti-inflammatory, inhibiting inflammatory substances continue to be intrinsic cells of the kidney mesangial cell damage; external inflammatory substances into the human body with IgA antigen-antibody immune complexes, and then deposited in the glomerular mesangial area, kidney ischemia and hypoxia, and thus do the vasodilators to improve blood circulation and kidney ischemia hypoxic state to provide a good treatment for the repair of mesangial cells; inflammatory cells that would increase blood viscosity increased, the platelet hyperfunction, enhanced coagulation, resulting in the micro thrombosis composition, in order to prevent microthrombi composition, and thus to anticoagulant therapy, maintaining smooth blood to avoid the excessive deposition of immune complexes; inflammatory cells of IgA immune complex deposition led to an increase in mesangial cell proliferation, atrophy, and cell extracellular matrix, and therefore must extracellular matrix deposition degradation, so that it can be excreted with the urine. The above inter-related treatment, IgA nephropathy hematuria before it can be restored to normal.
IgA nephropathy why permanently? Overall the treatment of IgA nephropathy hematuria can not simply eliminate the hematuria, and should thus be treated, to repair damaged kidney mesangial cells, as will be made in the treatment of a multiplier effect, the other IgA due to immune dysfunction, kidney patients need time to prevent some of the invasion of bacteria, viruses, that is, to prevent colds and infections, I believe, IgA nephropathy will soon be recovered by treatment of science and daily life cautious.
Tuesday, April 10, 2012
IgA nephropathy Note
1.In the past the medical profession that the IGA nephropathy development
is slow, causing a paralysis of thought in recent years, the serious
consequences of the IGAnephropathy development, once the creatinine began to
increase, and soon will bedevelopment of uremia. So, regardless of severity
should seize the time for effective treatment, should lose no time.
2.The treatment of hematuria can not use hemostatic necessary to clear the the IGAsediment to heal. TCM and more use to stop bleeding prescription, the sight of blood to stop bleeding, headache medicine head rule France, although at that time to eliminatethe symptoms, but delay the best time for treatment.
3.If inappropriate medication, only a temporary solution, and will acceleratedeterioration, delay the timing of treatment, and ultimately become uremia, so the choice is very important.
2.The treatment of hematuria can not use hemostatic necessary to clear the the IGAsediment to heal. TCM and more use to stop bleeding prescription, the sight of blood to stop bleeding, headache medicine head rule France, although at that time to eliminatethe symptoms, but delay the best time for treatment.
3.If inappropriate medication, only a temporary solution, and will acceleratedeterioration, delay the timing of treatment, and ultimately become uremia, so the choice is very important.
IgA nephropathy etiology and pathogenesis
The etiology and pathogenesis of IgA nephropathy has not yet been fully
understood, is generally believed that IgA nephropathy is a glomerular disease
caused by immune complexes. TCM etiology and pathogenesis of IgA nephropathy
understanding can be summarized as:
, Pathogenic foreign attacks
Wind clip hot evil foreign attacks, the homes in the lung, downstream bladderwaterways negative, hot forged focus, can cause edema and hematuria.
Second, liver and kidney
Ferrite deficiency, or over-the troubles that liver and kidney yin deficiency, the raw heat,thermal injury Shenluotong hematuria.
Third, spleen and kidney Qi
Ferrite deficiency of qi, or overwork, injuries to the spleen and kidney, resulting inspleen and kidney Qi, Shengqing spleen, kidney failure to seal Tibet, proteinuria, the gas is not taken blood, hematuria.
In short, of IgA nephropathy total yin or qi deficiency-based wind cold, damp heat,blood stasis as the standard, Yin Chang, chief damp heat, qi deficiency with blood stasis.
, Pathogenic foreign attacks
Wind clip hot evil foreign attacks, the homes in the lung, downstream bladderwaterways negative, hot forged focus, can cause edema and hematuria.
Second, liver and kidney
Ferrite deficiency, or over-the troubles that liver and kidney yin deficiency, the raw heat,thermal injury Shenluotong hematuria.
Third, spleen and kidney Qi
Ferrite deficiency of qi, or overwork, injuries to the spleen and kidney, resulting inspleen and kidney Qi, Shengqing spleen, kidney failure to seal Tibet, proteinuria, the gas is not taken blood, hematuria.
In short, of IgA nephropathy total yin or qi deficiency-based wind cold, damp heat,blood stasis as the standard, Yin Chang, chief damp heat, qi deficiency with blood stasis.
Children with IgA nephropathy renal damage which several types?
IgA nephropathy (1gAGN) is a group associated with system disease, renal
biopsy immune pathology in glomerular mesangial granular deposition of IgA-based
disease.IgAGN for the pathological diagnosis of an immune name, clinical
glomerulonephritis with hematuria as the main manifestation, but also led to one
of the main end-stage renal failure. That the Department of an independent
clinical a pathological syndrome. Renal damage following types:
First, episodes of gross hematuria
Often in a variety of respiratory tract infections in 1-3d after gross hematuria, it is also known as pharyngitis synchronization hematuria, this common sense of acute chain glomerulonephritis. Deformability of urinary red cell morphology, suggestive of glomerular hematuria. I have seen homes in addition to gross hematuria, and in some cases accompanied by the waist and (or) severe abdominal pain, often misdiagnosed as urinary calculi, acute abdomen (appendicitis). Such abdominal pain mechanism may be associated with inflammatory lesions of small arteries in the ureter or gastrointestinal mucosa manifestations of systemic small vessel vasculitis lesions. In addition, the electron microscope shows submucosal small artery injury was fibrinoid necrosis, IgA, and C3, and fibrin deposition to support IgAGN gastrointestinal tract has also been compromised. Low back pain associated with urinary retention or temporary oliguria may be of small blood clots occur in the urinary tract caused by a temporary obstruction.
Second, the nephrotic syndrome
Individually or in some cases associated with hypertension, hematuria. If the histopathological glomerular sclerosis and renal vascular sclerosis poor prognosis.Shanghai Children's Hospital have reported 20 cases IgAGN, which manifested as nephrotic-type, 9 cases (47%), showing that this type of a certain proportion of children IgAGN.
Third, the nephritic syndrome
This type of performance with / without mild edema of asymptomatic microscopic hematuria, often misdiagnosed as the chain sense glomerulonephritis more common in urine screening examination and confirmed by biopsy.
Fourth, the simple proteinuria
Proteinuria as the first symptom in the pediatric majority showed mild or moderate proteinuria without edema and other symptoms of kidney damage.
Fifth, rapidly progressive glomerulonephritis
Rare. Continuous gross hematuria, proteinuria associated with heart, brain involvement, the abrupt deterioration of short-term renal function, renal biopsy widely (50% -100%) glomerular crescent form. Severe hematuria hemoglobin on renal tubular toxicity and tubular obstruction with acute tubular necrosis.
First, episodes of gross hematuria
Often in a variety of respiratory tract infections in 1-3d after gross hematuria, it is also known as pharyngitis synchronization hematuria, this common sense of acute chain glomerulonephritis. Deformability of urinary red cell morphology, suggestive of glomerular hematuria. I have seen homes in addition to gross hematuria, and in some cases accompanied by the waist and (or) severe abdominal pain, often misdiagnosed as urinary calculi, acute abdomen (appendicitis). Such abdominal pain mechanism may be associated with inflammatory lesions of small arteries in the ureter or gastrointestinal mucosa manifestations of systemic small vessel vasculitis lesions. In addition, the electron microscope shows submucosal small artery injury was fibrinoid necrosis, IgA, and C3, and fibrin deposition to support IgAGN gastrointestinal tract has also been compromised. Low back pain associated with urinary retention or temporary oliguria may be of small blood clots occur in the urinary tract caused by a temporary obstruction.
Second, the nephrotic syndrome
Individually or in some cases associated with hypertension, hematuria. If the histopathological glomerular sclerosis and renal vascular sclerosis poor prognosis.Shanghai Children's Hospital have reported 20 cases IgAGN, which manifested as nephrotic-type, 9 cases (47%), showing that this type of a certain proportion of children IgAGN.
Third, the nephritic syndrome
This type of performance with / without mild edema of asymptomatic microscopic hematuria, often misdiagnosed as the chain sense glomerulonephritis more common in urine screening examination and confirmed by biopsy.
Fourth, the simple proteinuria
Proteinuria as the first symptom in the pediatric majority showed mild or moderate proteinuria without edema and other symptoms of kidney damage.
Fifth, rapidly progressive glomerulonephritis
Rare. Continuous gross hematuria, proteinuria associated with heart, brain involvement, the abrupt deterioration of short-term renal function, renal biopsy widely (50% -100%) glomerular crescent form. Severe hematuria hemoglobin on renal tubular toxicity and tubular obstruction with acute tubular necrosis.
Sunday, April 8, 2012
IgA nephritis should be treated?
IgA nephritis should be treated?
The traditional method of treatment of IgA there is no satisfactory treatment options. Of the disease associated with renal insufficiency adrenal corticosteroids with or without immunosuppressants results are not consistent. Recent data suggest that the proteinuria of more than 1g / d, and subjected to every other day medication adrenal cortex hormone beneficial to the improvement of proteinuria. IgA deposition of minimal change nephropathy may alleviate proteinuria. Used in combination with cyclophosphamide, dipyridamole and warfarin to reduce proteinuria and glomerular filtration rate; combined use of cyclosporin A may also reduce proteinuria, and then also reduced creatinine clearance. Efficacy of phenytoin, anti-platelet drugs, the anthocyanin acid disodium diphenyl Sealand due to such drugs is uncertain. Notwithstanding the reports of urokinase may have a role to protect the glomerular filtration rate, but far from conclusive.Recurrent tonsillitis, tonsillectomy may be useful; antibiotics to prevent and treat infections that may be helpful to some acute nephritic syndrome and acute renal failure for the performers. A small series of observations found that the use of fish oil preparations reducing the role of proteinuria and increased glomerular filtration rate.Severe IgA nephropathy (glomerular filtration rate monthly decline 2 ~ 4ml/min) the use of large doses of immune globulin intravenous infusion period, to stop the glomerular filtration rate, improvement of hematuria and proteinuria, but after stopping often relapse.Cases of hypertension and severe proteinuria, glomerular filtration rate of converting enzyme inhibitors may slow down the rate of descent and reduce proteinuria and severe IgA nephropathy, converting enzyme inhibitors are the preferred antihypertensive drugs.Conversion of normal blood pressure, whether effective inhibitors is unclear.
End-stage IgA nephropathy in a kidney transplant, the transplanted kidney happen soon mesangial IgA deposition; subclinical IgA nephropathy if the donor kidney for renal mesangial IgA deposits after implantation of non-IgA nephropathy uremia often rapidly disappearing. Renal transplantation with recurrence does not necessarily progressive renal failure in IgA nephropathy, however Shi after renal transplantation immunosuppressive therapy including cyclosporine A also did not prevent its development. Cadaveric renal transplantation, 1 year and 3-year graft survival up to 87% and 77%, however, individual IgA antibody IgA anti-HLA antigens of renal transplant recipients, 2-year graft survival of up to 100%. reason to believe that these antibodies against HLA antigens played a useful role in increasing graft survival.
Tuesday, March 20, 2012
Governance experience in the one case of focal proliferative sclerosing IgA nephropathy
Patients with Zhou, male, 42 years old, newly diagnosed on January 22, 2010. The main reason: proteinuria, hematuria 1 month to diagnosis. Patients 1 month before the examination found that urinary protein, occult blood, and many times at the Peking University First Hospital, Xiyuan Hospital of review were seen hematuria, proteinuria, were not system diagnosis and treatment. Wear said: Dongzhimen Hospital, kidney renal biopsies showed 40 glomerular five global sclerosis, 4 ischemic sclerosis, two segmental glomerular sclerosis, the rest of glomerular mesangial cells and matrix light todegree of diffuse hyperplasia, focal segmental severe increase mesangial addicted complex red protein deposition, tubular epithelial vacuoles and granular degeneration, spotty atrophy, multiple foci of the renal mass-like lymph nodes and mononuclear cell infiltration with fibrosis, wall thickening of small arteries, in line with: Home stove proliferative sclerosing IgA nephropathy. Check: 24-hour urine protein excretion 1.76g; protein, occult blood; of creatinine 165.3umol / L, urea nitrogen 8.38mmol / L Blood pressure: 120/80mmHg, oral Aprovel 150mg 1, the pressure's up to 5mg day control of blood pressure. Zheng Jian: fatigue, mouth bitter stick, irritability, foamy urine, lumbar pain, stool viscosity, when the stool, no fever, cough, sputum, lower extremity edema, is satisfied that the poor sleep can red tongue, yellowish greasy, slippery pulse. Diagnosis: focal proliferative sclerosing IgA nephropathy, renal insufficiency, decompensated; hypertension in three high-risk groups. TCM diagnosis: kidney slow wind syndrome is a qi deficiency and liver stagnation and heat block the kidney by blood stasis paralysis.Governing Law: Qi stagnation, heat and dampness, Huoxuetongluo. Recipe: raw Astragalus 50g, the bupleurum 15g, turmeric 15g skullcap 15g, gardenia Health 15g, France Pinellia 10g raw barley 30g, lotus leaf 15g, earthworm 20g, silkworm 20g, raw citrus aurantium 15g, fried betel nut 30g Sophora japonica 15g, Health Burnet 30g, contact Ishido 15g, Atractylodes 20g, Treats 15g, 6 a casual 30g. 7 water, a daily, morning and evening hours service. Antihypertensive drugs to control blood pressure following the service.
29: two clinics in January, fatigue, backache relief, urinary Mo reduced, still upset, irritability, mouth bitter stick, the big can. Red tongue, yellow greasy moss, pulse string.Urine: protein, erythrocyte :10-15 / HP. Stool disappeared, still proteinuria, suggesting that reduce the blood heat; renal wear visible part of the glomerular ball, segmental sclerosis and ischemic sclerosis, renal interstitial multiple spotty fibrosis, Chinese interpreted as network interest into the plot, I strengthen Poxue Xiaozheng products.Recipe: the cases of newly diagnosed party to Huaihua, Health Burnet, plus triangular 15g, Curcuma 15g, Chuan Xiong 18, Smilax glabra 50g in order to strengthen the power of of detoxification Poxue Xiaozheng.
3 attending February 12th: The patient complaint when hypochondriac pain, lumbar pain disappeared, I no obvious discomfort, red tongue, yellow greasy moss, pulse string. 24-hour urinary protein excretion: 0.47g; creatinine: 140umol / L, urea nitrogen 7.9mmol / L,.Prompts the liver qi stagnation, not General pain. Go to the top of a lotus leaf, network Ishido, Yuan Hu 15g, Toosendan 12g Liver Qi to relieve pain.
4 attending March 1: The patient complained of sore throat, irritability, mouth bitter sticky, sticky stool, dark tongue, yellow greasy moss, pulse string. Urine: protein -, 3 - to 5 red blood cells. Show the wind poison off the pharynx into the network, the liver heat.Recipe: the bupleurum 15g, skullcap 15g, Health and gardenia 15g, gentian 10g raw barley 20g, Agastache 15g, Folium 30g, forsythia 15g of Fritillaria 15g, Shegan 15g Mint 15g, Shichangpu 15g earthworm 20g, silkworm 20g, bellflower 15g, the Chuanxiong 18g, black snake 15g, contact Ishido 15g, raw licorice 6g to detoxification LiYan, found the wind Tongluo Soothing heat and dampness.
5 clinic March 15: patients with sore throat disappeared, irritability, mouth bitter sticky stool viscosity. Dark tongue, yellow greasy moss, pulse string. 24-hour urinary protein excretion: 0.41g; the creatinine 115umol / L, urea nitrogen 6.4mmol / L,. . Recipe: top to Agastache, Fritillaria the Shegan, Folium, Fritillaria, Platycodon, the addition pinellia 10g, the Coptis 9g, the Magnolia 9g, lotus leaf 15g, Perrin 15g strengthening heat dampness.
6 attending March 29: patients with stable disease, mouth bitter sticky, no other obvious discomfort, dark tongue yellowish greasy moss, pulse strings. Urine: (-); Biochemical: (-).The cases above the white cardamom 10g continue to take medication.
Thereafter follow-up year, with no discomfort. Urinalysis, blood biochemistry were normal.
IgA nephropathy is one of the world's most common primary glomerular diseases, glomerular mesangial IgA deposition of immunoglobulin, IgA with C3 granular deposition in the mesangial area diseases. IgA nephropathy can be expressed for a variety of different forms of pathology, focal proliferative sclerosing IgAN in the IgAN in a certain proportion, and pathological changes mainly as a glomerular mesangial cell proliferation, extracellular matrix hyperplasia, severe pathological damage can varying degrees of glomerulosclerosis, tubular atrophy, interstitial fibrosis, easy hematuria, proteinuria, edema, hypertension, and renal function decline, if left untreated, can eventually lead to end-stage renal failure ( of ESRD).
Subscribe to:
Posts (Atom)