Hypertensive nephropathy (or "hypertensive nephrosclerosis", or "Hypertensive renal disease") is a medical condition referring to damage to the kidney due to chronic high blood pressure.It should be distinguished from "renovascular hypertension" (I15.0), which is a form of secondary hypertension.In the kidneys, as a result of benign arterial hypertension, hyaline (pink, amorphous, homogeneous material) accumulates in the wall of small arteries and arterioles, producing the thickening of their walls and the narrowing of the lumina — hyalinearteriolosclerosis. Consequent ischemia will produce tubular atrophy, interstitial fibrosis, glomerular alterations (smallerglomeruli with different degrees of hyalinization - from mild to sclerosis of glomeruli) and periglomerular fibrosis. In advanced stages, renal failure will occur. Functional nephrons have dilated tubules, often with hyaline casts in the lumens. Additional complications often associated with hypertensive nephropathy include glomerular damage resulting in proteinuria and hematuria.
There are some measures available to prevent this disease, or to manage the kidney damages early to improve the quality of life for patients with Hypertensive Nephropathy. It is necessary to visit a nephrologist to get the most current and effective therapeutic schedule. However, apart from the medical treatment, this disease can also be prevented by diet. And the following are several dietary tips for preventing this disease.
1. Low-salt diet
A delicate diet is appropriate for patients with Hypertensive Nephropathy. And high-salt diet should be limited, for too much salt intake will cause vascular sclerosis and the increase of blood pressure. For patients with Hypertension, just limiting the salt intake can make their blood pressure return to normal; and for those who have moderate or severe Hypertension, limiting the salt intake not only can enhance the curative effect of hypotensor, but also can decrease the patients' need of hypotensor, thus decreasing the side effects of the medicines greatly.
In addition, patients should also pay attention to the invisible salts such as
· monosodium glutamate, soy sauce, ketchup and mustard
· pickles
· cooked food such as sausage, pork luncheon meat, spiced beef and roast chicken
· frozen food, canned food and convenient fast food
· desserts, snacks and drinks
2. Patients with Hypertensive Nephropathy should eat LESS sweet food, for sweet food is high in sugars which will transform into fat and cause arteriosclerosis easily.
3. Fat foods should also be limited, for fat foods are rich in cholesterol which will accelerate the arteriosclerosis.
4. Patients with Hypertensive Nephropathy should get rid of smoking and had better drink less wine, for too much smoking and drinking will cause damages to our heart and kidneys.
5. High-potassium foods are recommended for patients whose renal function is normal, for in our human body potassium can buffer the effect of sodium. And the commonly seen high-potassium foods are soybean, tomatoes, celery, fresh mushroom and various green vegetables, and the fruits mainly are oranges, apples, bananas, pears, kiwis, pineapples and watermelons.
6. It is appropriate for patients to eat more foods which are rich in high-quality protein and vitamins, such as fishes, milk, eggs and lean meat.
7. Patients with Hypertensive Nephropathy should also eat more high-calcium foods, for high-calcium foods are conducive to lower the blood pressure. And the commonly foods are dairy products, sesame paste, dried small shrimps, kelp, black fungus, walnuts, sardines and eggs.
The aforementioned tips are only a partial listing of suggestions for patients with Hypertension or Hypertensive Nephropathy. Your needs may vary depending on your kidney function. For help creating a meal plan that meets your needs, consult your doctor.
Saturday 26 November 2011
How should we Prevent and Treat Diabetic Nephropathy
Diabetic nephropathy also known as Kimmelstiel-Wilson syndrome, or nodular diabetic glomerulosclerosis and intercapillary glomerulonephritis, is a progressive kidney disease caused by angiopathy ofcapillaries in the kidney glomeruli. It is characterized by nephrotic syndrome and diffuse glomerulosclerosis. It is due to longstanding diabetes mellitus, and is a prime indication for dialysis in many Western countries.
Therefore, how to prevent and treat Diabetic Nephropathy is of significant importance for patients withDiabetes. In order to prevent or prolong the progression of Diabetic Nephropathy, what should we do?
The key point of preventing Diabetic Nephropathy is receiving effective treatment as early as possible so as to make the blood sugar level under control. Once Diabetic Nephropathy occurs, the therapeutic schedule should be made according to the patients' condition in different stages.
In stage 1 Diabetic Nephropathy
In this stage, the key point of the treatment should target at controlling the blood sugar. If the blood sugar can be controlled well, the kidney lesion mainly shows the increase of the glomerular filtration rate, which can be reduced to normal level.
In stage 2~3 Diabetic Nephropathy
In these two stages, apart from controlling the blood sugar continuously, the patients should also adopt angiotensin-converting enzyme inhibitor(ACEI) or angiotensin receptor blockers(ARB) timely, no matter whether they have Hypertension. If they do have Hypertension, they should also adopt other antihypertensive drugs at the same time so as to lower the blood pressure.
Stage 1~3 is the best time for treating Diabetic Nephropathy, for in the three stages, the kidney damages can be reversed.
In stage 4~5 Diabetic Nephropathy
In these two stages, besides treating Diabetes, the treatment can only target at the symptoms, including lowering the blood pressure, promoting the urination, removing the edema and regulating the blood lipid. Once End-Stage Renal Failure occurs, renal replacement therapy such as dialysis, kidney transplant, or Stem Cell Transplant should be adopted.
Therefore, how to prevent and treat Diabetic Nephropathy is of significant importance for patients withDiabetes. In order to prevent or prolong the progression of Diabetic Nephropathy, what should we do?
The key point of preventing Diabetic Nephropathy is receiving effective treatment as early as possible so as to make the blood sugar level under control. Once Diabetic Nephropathy occurs, the therapeutic schedule should be made according to the patients' condition in different stages.
In stage 1 Diabetic Nephropathy
In this stage, the key point of the treatment should target at controlling the blood sugar. If the blood sugar can be controlled well, the kidney lesion mainly shows the increase of the glomerular filtration rate, which can be reduced to normal level.
In stage 2~3 Diabetic Nephropathy
In these two stages, apart from controlling the blood sugar continuously, the patients should also adopt angiotensin-converting enzyme inhibitor(ACEI) or angiotensin receptor blockers(ARB) timely, no matter whether they have Hypertension. If they do have Hypertension, they should also adopt other antihypertensive drugs at the same time so as to lower the blood pressure.
Stage 1~3 is the best time for treating Diabetic Nephropathy, for in the three stages, the kidney damages can be reversed.
In stage 4~5 Diabetic Nephropathy
In these two stages, besides treating Diabetes, the treatment can only target at the symptoms, including lowering the blood pressure, promoting the urination, removing the edema and regulating the blood lipid. Once End-Stage Renal Failure occurs, renal replacement therapy such as dialysis, kidney transplant, or Stem Cell Transplant should be adopted.
Clinical Types of IgA Nephropathy
Many patients with IgA Nephropathy may doubt how many types of this disease there are and which type they belong to. This article mainly focuses on solving this problem for the patients.
Type I: Gross hematuria
This type usually occurs secondary to mucomembranous diseases like upper respiratory tract infection, cold, overstrain, prophylactic immunization, pneumonia or enteritis. The urine is usually brown or seems like water where flesh is washed and blood clot is rarely seen. The immune latent period is the shortest, and it will remit spontaneously after lasting for several hours to one week. Those with repeated gross hematuria have a good prognosis while those with one isolated gross hematuria have a poor prognosis because they are usually accompanied with Nephrotic Syndrome and Hypertnesion and even acute oliguria or Acute Renal Failure which is probably related to blocking of the renal tubules by erythrocyte cast or necrosis of tubules.
Type II: Abnormal urinalysis
Onset of this type is latent. It can be divided into two types according to whether it is combined with hematuria.
A. Only persistent microscopic hematuria without proteinuria or hypertension. The cases are mainly mesangial proliferative changes, and renal interstitium and vascular lesions are not obvious.
B. Persistent microscopic hematuria with slight proteinuria. This type is more common and protein quantitation is less than 1.0g/d, without hypertension or hypofunction of the intrinsic cells. Pathological changes of this type vary greatly from mesangial proliferative changes to sclerosis of glomerular intrinsic cells, as well as interstitial lesions.
Type III: Massive proteinuria (Nephrotic Syndrome)
Protein quantitation is more than 2.0g/d and it is one of the factors that lead to a poor prognosis of IgA Nephropathy. This type often occurs in cases with severe glomerular changes and it usually shows focal segmental glomerulosclerosis with foot cell damage and fairly wide tubule-interstitial damage or crescents formation. If it is presented as sudden persistent proteinuria without gross hematuria and hypertension history, it can be further divided into two types.
A: Typical “three highs and one low” Nephrotic syndrome, with its pathological changes dominated by slight mesangial proliferation and usually without sclerosis of the intrinsic cells or obvious interstitial change.
B: massive proteinuria and unobvious swelling, usually with increased nocturia, which is clinically called “dry nephrosis”. The pathological changes are: extensive sclerosis of the glomerular intrinsic cells in renal tissues, interstitial fibrosis, protracted course of disease and poor prognosis.
Type IV: Acute Renal Failure
The features are acute onset, rapid progress and poor prognosis. It can be further divided into two types:
A: large amount of crescents formation and vasculitis-like changes ANCA (+).
B: during gross hematuria, large amounts of erythrocyte cast block the renal tubules, making it easy for the patients who are receiving anticoagulant treatment to have large amount of erythrocyte cast.
Type V: Chronic Renal Insufficiency (End-stage)
At the early stage of this type, renal tissues are often at the stage of “inflammatory reaction period” of the fibrosis. Functions of the renal intrinsic cells especially the “filtratin function” is in a high filtration and compensative state and there is no decrease of GFR. Along with development of the renal fibrosis, mesnagial cells gradually appear apoptosis and necrosis and are rapidly replaced by ECM (Extracellular Matrixes). There is also progressive decline and rapid deterioration of the cellular functions, which is followed by a series of Uremia symptoms. SCR (serum creatinine) >442, GFR<15ml/min. B-ultrasonic test shows atropy of both kidneys and thinning of cortex which becomes more sensitive to light. Gradually the disease enters scar formation period.
Certain period after damage of the mesangial cells, Acute Renal Failure will occur in 5% of patients, chronic renal damage in 10% of patients and 50% to 70% of the patients will develop Uremia after 20 years.
Type VI: Hypertension
Pathological features of this type: pathological changes will occur when endothelial cells are involved by mesangial cells lesions, manifested as functional disorder of endothelial cells which will cause more release of vasoconstrictive agents. Besides hematuria, clinical manifestations may also include hypertension especially in the elderly. This is an important sign of deteriorating progression of mesaangial cell diseases, which must be treated with hypotensive drugs to control the symptoms.
Pathological changes show much discarding changes like focal or global sclerosis of the glomeruli and extensive interstitial fibrosis.
Type I: Gross hematuria
This type usually occurs secondary to mucomembranous diseases like upper respiratory tract infection, cold, overstrain, prophylactic immunization, pneumonia or enteritis. The urine is usually brown or seems like water where flesh is washed and blood clot is rarely seen. The immune latent period is the shortest, and it will remit spontaneously after lasting for several hours to one week. Those with repeated gross hematuria have a good prognosis while those with one isolated gross hematuria have a poor prognosis because they are usually accompanied with Nephrotic Syndrome and Hypertnesion and even acute oliguria or Acute Renal Failure which is probably related to blocking of the renal tubules by erythrocyte cast or necrosis of tubules.
Type II: Abnormal urinalysis
Onset of this type is latent. It can be divided into two types according to whether it is combined with hematuria.
A. Only persistent microscopic hematuria without proteinuria or hypertension. The cases are mainly mesangial proliferative changes, and renal interstitium and vascular lesions are not obvious.
B. Persistent microscopic hematuria with slight proteinuria. This type is more common and protein quantitation is less than 1.0g/d, without hypertension or hypofunction of the intrinsic cells. Pathological changes of this type vary greatly from mesangial proliferative changes to sclerosis of glomerular intrinsic cells, as well as interstitial lesions.
Type III: Massive proteinuria (Nephrotic Syndrome)
Protein quantitation is more than 2.0g/d and it is one of the factors that lead to a poor prognosis of IgA Nephropathy. This type often occurs in cases with severe glomerular changes and it usually shows focal segmental glomerulosclerosis with foot cell damage and fairly wide tubule-interstitial damage or crescents formation. If it is presented as sudden persistent proteinuria without gross hematuria and hypertension history, it can be further divided into two types.
A: Typical “three highs and one low” Nephrotic syndrome, with its pathological changes dominated by slight mesangial proliferation and usually without sclerosis of the intrinsic cells or obvious interstitial change.
B: massive proteinuria and unobvious swelling, usually with increased nocturia, which is clinically called “dry nephrosis”. The pathological changes are: extensive sclerosis of the glomerular intrinsic cells in renal tissues, interstitial fibrosis, protracted course of disease and poor prognosis.
Type IV: Acute Renal Failure
The features are acute onset, rapid progress and poor prognosis. It can be further divided into two types:
A: large amount of crescents formation and vasculitis-like changes ANCA (+).
B: during gross hematuria, large amounts of erythrocyte cast block the renal tubules, making it easy for the patients who are receiving anticoagulant treatment to have large amount of erythrocyte cast.
Type V: Chronic Renal Insufficiency (End-stage)
At the early stage of this type, renal tissues are often at the stage of “inflammatory reaction period” of the fibrosis. Functions of the renal intrinsic cells especially the “filtratin function” is in a high filtration and compensative state and there is no decrease of GFR. Along with development of the renal fibrosis, mesnagial cells gradually appear apoptosis and necrosis and are rapidly replaced by ECM (Extracellular Matrixes). There is also progressive decline and rapid deterioration of the cellular functions, which is followed by a series of Uremia symptoms. SCR (serum creatinine) >442, GFR<15ml/min. B-ultrasonic test shows atropy of both kidneys and thinning of cortex which becomes more sensitive to light. Gradually the disease enters scar formation period.
Certain period after damage of the mesangial cells, Acute Renal Failure will occur in 5% of patients, chronic renal damage in 10% of patients and 50% to 70% of the patients will develop Uremia after 20 years.
Type VI: Hypertension
Pathological features of this type: pathological changes will occur when endothelial cells are involved by mesangial cells lesions, manifested as functional disorder of endothelial cells which will cause more release of vasoconstrictive agents. Besides hematuria, clinical manifestations may also include hypertension especially in the elderly. This is an important sign of deteriorating progression of mesaangial cell diseases, which must be treated with hypotensive drugs to control the symptoms.
Pathological changes show much discarding changes like focal or global sclerosis of the glomeruli and extensive interstitial fibrosis.
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