显示标签为“Diabetic nephropathy”的博文。显示所有博文
显示标签为“Diabetic nephropathy”的博文。显示所有博文

2014年11月14日星期五

Shijiazhuang Kidney Disease Hospital in the treatment of diabetes

Shijiazhuang Kidney Disease Hospital
Shijiazhuang Kidney Disease Hospital
Diabetic nephropathy is the renal function due to diabetes and manifested clinically by proteinuria usually several years after the onset of hyperglycemia. The earliest clinical sign of diabetic nephropathy is the appearance of a small posotitaslefkomatinis  in the urine. In particular, as microalbuminuria bounded albumin excretion 30-300mg / 24 hours or 20-200 micrograms / min or 30-300 mg albumin / g creatinine in random deigmaouron. When albumin excretion exceeds these limits, refer to macroalbuminuria or more precisely for albuminuria . The categories given in Table albuminuria.

Diabetes can also go to the nerve. Diabetic neuropathy is a nerve damage as a result permanently elevated blood sugar levels. It is one of the most consequential of diabetes - probably at about every third patient with diabetes is neuropathy before. This can be affected to a peripheral nerve, thus the sensitive sensory nerves and the motor movement. But often also suffers from the vegetative (also: autonomic) nervous system, which can not be consciously influence and controls a variety of functions in the body, such as the activity of internal organs or perspiration.

Shijiazhuang Kidney Disease Hospital in the treatment of diabetes: high blood sugar is a major factor leading to diabetic nephropathy.High incidence of obesity, often associated with hypertension, dyslipidemia, atherosclerosis and other diseases. Insidious onset, early without any symptoms, or only mild fatigue, thirst, blood sugar tolerance test is not obvious who need to do in order to be confirmed. Serum insulin levels were normal or increased early and late low. Suggestion: patient blood glucose levels can be adjusted at any time according to hypoglycemic drugs

Shijiazhuang Kidney Disease Hospital Diet therapy: clinical and experimental studies have observed that high-protein diets can increase blood flow and glomerular pressure, increased renal blood flow caused by high blood sugar dynamics change. Oral antidiabetic drug therapy (2) antihypertensive treatment: Hypertension is an important factor to accelerate the progression of diabetic nephropathy. General treatment of hypertension: should include limiting sodium intake, quit alcohol limit, weight loss and adequate exercise, especially for obese people with type 2 diabetes, even mild weight loss but also conducive to blood pressure control.

2014年8月29日星期五

How Does Diabetes Cause Kidney Disease?

Diabetic nephropathy
Kidneys are remarkable organs. Inside them are millions of tiny blood vessels that act as filters. Their job is to remove waste products from the blood.

Nephropathy means kidney disease or damage. Diabetic nephropathy is damage to your kidneys caused by diabetes. In severe cases it can lead to kidney failure. But not everyone with diabetes has kidney damage.

Sometimes this filtering system breaks down. Diabetes can damage the kidneys and cause them to fail. Failing kidneys lose their ability to filter out waste products, resulting in kidney disease.

How Does Diabetes Cause Kidney Disease?

When our bodies digest the protein we eat, the process creates waste products. In the kidneys, millions of tiny blood vessels (capillaries) with even tinier holes in them act as filters. As blood flows through the blood vessels, small molecules such as waste products squeeze through the holes. These waste products become part of the urine. Useful substances, such as protein and red blood cells, are too big to pass through the holes in the filter and stay in the blood.

Diabetes can damage this system. High levels of blood sugar make the kidneys filter too much blood. All this extra work is hard on the filters. After many years, they start to leak and useful protein is lost in the urine. Having small amounts of protein in the urine is called microalbuminuria.

When kidney disease is diagnosed early, during microalbuminuria, several treatments may keep kidney disease from getting worse. Having larger amounts of protein in the urine is called macroalbuminuria. When kidney disease is caught later during macroalbuminuria, end-stage renal disease, or ESRD, usually follows.

Diagnosing Diabetic Nephropathy

Screening for diabetic nephropathy should start within five years of a diagnosis of type 1 diabetes, or at the onset of puberty, whichever comes first. Screening for diabetic nephropathy in people with type 2 diabetes should take place within one year of diagnosis. All people with diabetes should then be screened annually, particularly after microalbuminuria has been detected.

Diabetic nephropathy and microalbuminuria are best diagnosed with a urine sample. It is important to avoid urine testing during an ongoing urinary tract infection or another acute illness, after strenuous exercise, or with uncontrolled high blood pressure or heart failure. Any of these conditions can cause blood and albumin to show up in the urine, resulting in an inaccurate measurement.

Treatment of Diabetic Nephropathy

The first line of defense against diabetic nephropathy is a healthy lifestyle, including a low-fat diet, light-to-moderate exercise regimen, smoking cessation, and avoiding excessive alcohol consumption in an effort to keep blood sugar levels in check and reduce blood pressure.

Albuminuria can be reversed by taking certain blood pressure medications, such as angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers, which are particularly beneficial for both lowering blood pressure and protecting the kidneys in people with diabetes. A blood pressure under 130/80 mmHg should be targeted by people with diabetes. Reaching this goal often requires taking more than one blood pressure medication.

Another important factor in managing diabetic nephropathy is to keep blood sugars in check using insulin and possibly other medications as well. The target A1C level (a measure of average blood sugar levels during the last few months) for a patient with diabetic nephropathy is less than 7%.

Along with managing blood pressure and blood sugars, patients with diabetic nephropathy also benefit from lowering cholesterol and preventing obesity. There is some evidence that reducing protein in the diet will help prevent the progression of kidney disease. There is, however, some controversy regarding this theory.

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Treatment and prevention of diabetic nephropathy

Diabetic nephropathy
Diabetic nephropathy is treated with medicines that lower blood pressure and protect the kidneys. These medicines may slow down kidney damage and are started as soon as any amount of protein is found in the urine (microalbuminuria). The use of these medicines before nephropathy occurs may also help prevent nephropathy in people who have normal blood pressure.

Diabetic nephropathy is the leading cause of chronic kidney disease in patients starting renal replacement therapy (1) and is associated with increased cardiovascular mortality (2). Diabetic nephropathy has been classically defined by the presence of proteinuria >0.5 g/24 h. This stage has been referred to as overt nephropathy, clinical nephropathy, proteinuria, or macroalbuminuria. In the early 1980s, seminal studies from Europe revealed that small amounts of albumin in the urine, not usually detected by conventional methods, were predictive of the later development of proteinuria in type 1 (3–5) and type 2 (6) diabetic patients. This stage of renal involvement was termed microalbuminuria or incipient nephropathy.

If you have high blood pressure, two or more medicines may be needed to lower your blood pressure enough to protect the kidneys. Medicines are added one at a time as needed.

If you take other medicines, avoid ones that damage or stress the kidneys, especially nonsteroidal anti-inflammatory drugs (NSAIDs). NSAIDs include ibuprofen and naproxen.

Diabetic nephropathy has been didactically categorized into stages based on the values of urinary albumin excretion (UAE): microalbuminuria and macroalbuminuria. The cutoff values adopted by the American Diabetes Association (14) (timed, 24-h, and spot urine collection) for the diagnosis of micro- and macroalbuminuria, as well as the main clinical features of each stage, are depicted in Table 1. There is accumulating evidence suggesting that the risk for developing diabetic nephropathy (15–18) and cardiovascular disease (19,20) starts when UAE values are still within the normoalbuminuric range. Progression to micro- or macroalbuminuria was more frequent in patients with type 2 diabetes with baseline UAE above the median (2.5 mg/24 h) (15). After 10 years of follow-up, the risk of diabetic nephropathy was 29 times greater in patients with type 2 diabetes with UAE values >10 μg/min (16). The same was true for patients with type 1 diabetes (17). This favors the concept that the risk associated with UAE is a continuum, as is the case with blood pressure levels (21). Possibly, values of UAE lower than those currently used for microalbuminuria diagnosis should be established.

It is also important to keep your blood sugar within your target range. Maintaining blood sugar levels within your target range prevents damage to the small blood vessels in the kidneys.

Limiting the amount of salt in your diet can help keep your high blood pressure from getting worse. You may also want to restrict the amount of protein in your diet. If diabetes has affected your kidneys, limiting how much protein you eat may help you preserve kidney function. Talk to your doctor or dietitian about how much protein is best for you.

Initial treatment
Medicines that are used to treat diabetic nephropathy are also used to control blood pressure. If you have a very small amount of protein in your urine, these medicines may reverse the kidney damage. Medicines used for initial treatment of diabetic nephropathy include:

Angiotensin-converting enzyme (ACE) inhibitors, such as captopril, enalapril, lisinopril, and ramipril. ACE inhibitors can lower the amount of protein being lost in the urine. Also, they may reduce your risk of heart and blood vessel (cardiovascular) disease.
Angiotensin II receptor blockers (ARBs), such as candesartan cilexetil, irbesartan, losartan potassium, and telmisartan. You may be given both an ACE inhibitor and an ARB. The combination of these medicines may provide greater protection for your kidneys than either medicine alone.
If you also have high blood pressure, two or more medicines may be needed to lower your blood pressure enough to protect your kidneys. Medicines are added one at a time as needed.

If you take other medicines, avoid ones that damage or stress the kidneys, especially nonsteroidal anti-inflammatory drugs (NSAIDs).

It is also important to keep your blood sugar within your target range to prevent damage to the small blood vessels in the kidneys.

Ongoing treatment
As diabetic nephropathy progresses, blood pressure usually rises, making it necessary to add more medicine to control blood pressure.

Your doctor may advise you to take the following medicines that lower blood pressure. You may need to take different combinations of these medicines to best control your blood pressure. By lowering your blood pressure, you may reduce your risk of kidney damage. Medicines include:

A combination of angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs). A combination of these medicines may be more effective in controlling blood pressure than either used alone.

Calcium channel blockers, which lower blood pressure by making it easier for blood to flow through the vessels. Examples include amlodipine, diltiazem, or verapamil.
Diuretics. Medicines such as chlorthalidone, hydrochlorothiazide, or spironolactone help lower blood pressure by removing sodium and water from the body.

Beta-blockers lower blood pressure by slowing down your heartbeat and reducing the amount of blood pumped with each heartbeat. Examples include atenolol, carvedilol, or metoprolol.

Continue to avoid other medicines that may damage or stress the kidneys, especially nonsteroidal anti-inflammatory drugs (NSAIDs). And it is still important to keep your blood sugar within your target range, eat healthy foods, get regular exercise, and not smoke.

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2014年8月19日星期二

Early symptoms of diabetic nephropathy

Diabetic nephropathy
There are no symptoms in the early stages of diabetic nephropathy. If you have kidney damage, you may have small amounts of protein leaking into your urine (microalbuminuria). Normally, protein is not found in urine except during periods of high fever, strenuous exercise, pregnancy, or infection.

Not everyone with diabetes will develop diabetic nephropathy. In people with type 1 diabetes, diabetic nephropathy is more likely to develop 5 to 10 years or more after the onset of diabetes. People with type 2 diabetes may find out that they already have a small amount of protein in the urine (microalbuminuria) at the time diabetes is diagnosed, because they may have had diabetes for several years.

Diabetes affects the arteries of the body and as the kidneys filter blood from many arteries, kidney problems are a particular risk for people with diabetes.

What is Diabetic Nephropathy?
Nephropathy is the deterioration of the kidneys. Diabetic Nephropathy is damage to your kidneys caused by Diabetes. The end-stage of Diabetic Nephropathy is called kidney failure, end-stage kidney disease, or ESRD.

Diabetic Nephropathy develops through five clinical stages, of which the fifth is end-stage kidney failure. Early prevention, detection and treatment are essential for Diabetics to delay or control progression of Diabetic Nephropathy into the next stage.

Micro-Chinese Medicine Osmotherapy treats Diabetic Kidney Disease starting from removing initiating factors of renal fibrosis by Diabetes and creates a favorable environment for repairing injured renal intrinsic cells.

Healthy kidneys are responsible for filtrating bloodstream, carrying away wasteful products and stopping leakage of nutrients out of the body. In Diabetic Nephropathy, glomerular filtering cells are impaired thus causing loss of proteins and retention of wastes (such as urea and blood urea nitrogen). Micro-Chinese Medicine Osmotherapy removes blood stasis, stabilizes blood pressure and removes inflammations, which will stop renal fibrosis and transport sufficient nutrients and blood for fixing damaged glomerular cells. By the treatment kidney function is improved and symptoms can be got rid of effectively.

Diet for Diabetic Nephropathy
Restrict intake of sodium. Heavy sodium consumption will aggravate fluid accumulation in the body. In this way blood volume is increased and blood pressure is even higher. This is very harmful for the kidneys. Limiting sodium helps protect the kidneys and slow down kidney damage.

Balance intake of water. Fluid restriction should be performed carefully if one has severe swelling, obviously reduced urine output, or high blood pressure. In others, if there is no obvious kidney function reduction or fluid retention, there is no need to restrict your intake of water. Talk with your doctor to get individualized instructions.

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Notes diabetic nephropathy

Diabetic nephropathy
Diabetic nephropathy in diabetic nephropathy patients must pay attention to nursing. Diabetic nephropathy is a common complication of diabetes. Diabetic nephropathy patients tend to focus only on medication to control the disease, an important role but ignore the daily nursing care in the treatment of diabetic nephropathy. Nursing of diabetic nephropathy pay attention to what matters.

For the diabetes nephrosis patient's diet, should be divided into two aspects, first, what cannot eat in diabetic nephropathy patients; second, diabetic nephropathy patients eat what is good. Below we have a detailed introduction.

For the diabetes nephrosis patient's diet, should be divided into two aspects, first, what cannot eat in diabetic nephropathy patients; second, diabetic nephropathy patients eat what is good. Below we have a detailed introduction.

Diabetic nephropathy patients eat what is good

Bean Products.Because soy contains large amounts of protein, inorganic salts, vitamins, and unsaturated fatty acids, can reduce blood cholesterol, can reduce blood glycerin three fat effect, contains sitosterol also have lipid-lowering effect.

Crude sugar,Generally contain a variety of trace elements, vitamin B and dietary fiber, such as oat noodles, buckwheat noodles.

Good control of emotions, maintain a good attitude.In patients with diabetic nephropathy in diabetic patients can't control HERSHEY'S, easy to elevated serum cholesterol, resulting in diabetic vascular complications, coronary heart disease.

What cannot eat diabetes nephropathy patients

Can not eat the blood glucose increased food,For example, white sugar, brown sugar, rock sugar, glucose, maltose, etc..

Caution: no hypertension for patients with mild symptoms, not obvious, edema, no impairment of renal function, protein is not much, this kind of patient can do more physical exercise. For edema is obvious, patients or renal insufficiency patients with higher blood pressure, need to rest in bed.

Daily monitoring can not be ignored: restriction of fluid intake, water intake should be controlled in the urine volume before a day plus 500ml is appropriate. Pay more attention to observe the urine volume, color, character change. If there is abnormal when the need for timely report to the physician at least once a week, urine routine and urine specific gravity 1 times.

Pay more attention to the daily symptom changing: To observe the changes of blood pressure, edema, urine volume, urine test results and the patient's renal function; close observation and biochemical indexes: Observation of patients without anemia, electrolyte, acid-base imbalance, urea nitrogen rise higher situation. Such as abnormal timely report to the physician treatment.

Diet control: control of plant protein intake on renal function insufficiency patients, to reduce the burden on the kidneys. In the usual diet to ensure the intake of carbohydrates in the diet, intake, blood glucose control and control carbohydrate, to reduce the decomposition of autologous protein by providing sufficient heat. Limit sodium intake, dietary sodium should be lower than 3G, oliguria, should control the intake of potassium, and ensure comprehensive nutrition.

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Prevention of diabetic nephropathy

Early Diabetes
Diabetic nephropathy is becoming increasingly common with the aging of our population and the obesity epidemic. The major ways to prevent or slow its progression are by reducing blood pressure, controlling blood sugar, and inhibiting the renin-angiotensin-aldosterone axis. New therapeutic agents are also being tried.

The progression from no proteinuria to microalbuminuria to clinical proteinuria parallels glomerular changes of thickening of the basement membrane, mesangial expansion, and the development of Kimmelstiel-Wilson nodules and sclerosis.

Blood pressure control to 130/80 mm Hg slows microvascular and macrovascular disease, but the goal should not be lower in older patients with diabetes.

Glycemic control slows microvascular disease: the goal for most patients for hemoglobin A1c is 7.0%. Tighter control may increase cardiovascular risk.

Either an angiotensin-converting enzyme inhibitor or an angiotensin receptor blocker is the first-line treatment for diabetic nephropathy; combining the two is no longer recommended.

If more aggressive treatment is needed, a diuretic or spironolactone (with potassium monitoring) can be added.

The role of sodium bicarbonate and new agents such as blockers of transcription factors is still emerging.

Keeping your blood sugar tightly controlled every day is a big commitment. It requires constant monitoring and, if you take insulin, frequent doses of medication. But keeping your blood sugar as close to normal as possible is the best way to help prevent neuropathy and other complications of diabetes. Consistency is important because shifts in blood sugar levels can accelerate nerve damage.

For the best control, aim for a blood glucose level from 70 to 130 mg/dL (3.9 to 7.2 mmol/L) before meals and an A1C reading that is less than 7 percent. An A1C test measures your average blood sugar level over a period of two to three months. The American Diabetes Association recommends that people with diabetes have an A1C test at least twice a year if blood sugar levels are consistently in a healthy range. If your blood sugar isn't well controlled or you change medications, get tested more often.

Early in the course of diabetic nephropathy, blood pressure is normal and microalbuminuria is not evident, but many patients have a high glomerular filtration rate (GFR), indicating temporarily “enhanced” renal function or hyperfiltration. The next stage is characterized by microalbuminuria, correlating with glomerular mesangial expansion: the GFR falls back into the normal range and blood pressure starts to increase. Finally, macroalbuminuria occurs, accompanied by rising blood pressure and a declining GFR, correlating with the histologic appearance of glomerulosclerosis and Kimmelstiel-Wilson nodules.4

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2014年8月13日星期三

Late treatment of diabetic nephropathy

Late treatment of diabetic nephropathy
Recently, attention has been called to atypical presentations of diabetic nephropathy with dissociation of proteinuria from reduced kidney function. Also noted is that microalbuminuria is not always predictive of diabetic nephropathy.[1] Nevertheless, a majority of the cases of diabetic nephropathy presents with proteinuria, which progressively gets worse as the disease progresses, and is almost uniformly associated with hypertension.

diabetes is an ever-growing problem worldwide. Approximately 40% of the patients with type 2 diabetes will develop diabetic kidney disease. In the United States, diabetes has become the most common single cause of endstage renal disease defined by the need for dialysis or transplantation. Patients with type 2 diabetes and diabetic nephropathy have a dramatically increased cardiovascular risk. The Irbesartan Diabetic Nephropathy Trial was designed to determine whether the use of irbesartan or a calcium channel blocker would provide protection against the progression of nephropathy due to type 2 diabetes beyond that attributable to the lowering of blood pressure. In that study, 1715 hypertensive patients with nephropathy due to type 2 diabetes were randomly assigned to irbesartan 300 mg/day or amlodipine 10 mg/day, or placebo.

All patients randomized in this trial had more than 900 mg of protein in their urine and serum creatinines between 1.0 mg/dl and 3.0 mg/dl. The target blood pressure was 135/85 mmHg or less in all groups. The primary outcome was time to a combined endpoint of doubling of their baseline serum creatinine concentration, the development of endstage renal disease, or death from any cause. The mean duration of follow-up was 2.6 years. Treatment with irbesartan was associated with a risk of the primary composite endpoint that was 20% lower than that in the placebo group ( P = 0.02) and 23% lower than that in the amlodipine group ( P = 0.006). The risk of doubling of the serum creatinine concentration was 33% lower in the irbesartan group than in the placebo group ( P = 0.003) and 37% lower in the irbesartan group than in the amlodipine group ( P < 0.001). Treatment with irbesartan was associated with a relative risk of endstage renal disease that was 23% lower than that in both other groups.

 These differences were not accounted for by differences in the blood pressures that were achieved. Proteinuria was reduced on average by 33% in the irbesartan group as compared with 6% in the amlodipine group and 10% in the placebo group. The angiotensin II receptor blocker irbesartan was shown to be effective in protecting against the progression of nephropathy due to type 2 diabetes. In a study done in patients with type 2 diabetes and early nephropathy as manifested by microalbuminuria, 590 hypertensive patients with type 2 diabetes and microalbuminuria were randomized to receive either irbesartan 150 mg/day or irbesartan 300 mg/day and followed for 2 years. The primary outcome in that trial was the time to the onset of diabetic nephropathy, defined by persistent albuminuria in overnight specimens, with a urinary albumin excretion rate that was more than 200 mg/min or at least 30% higher than the baseline level. The irbesartan 150 mg/day group demonstrated a 39% relative risk reduction versus the control group in the development of overt proteinuria. The irbesartan 300 mg/day group demonstrated a highly significant 70% risk reduction versus the control group ( P < 0.001). The albumin excretion rate was reduced in the two irbesartan groups throughout the study (-11% and -38% at 24 months compared with baseline in the irbesartan 150-mg and 300-mg groups, respectively).

The albumin excretion rate remained unchanged in the control group. Irbesartan was demonstrated in the above study to be renoprotective, independent of its blood pressure-lowering effect, in patients with type 2 diabetes and microalbuminuria. Thus, irbesartan, an angiotensin receptor blocker, was demonstrated to be significantly renoprotective in patients with type 2 diabetes with either early nephropathy (microalbuminuria) or late nephropathy (proteinuria). The renoprotective effects of irbesartan were above and beyond the effects irbesartan had on systemic blood pressure. Patients with type 2 diabetes and either early or late diabetic nephropathy should be treated with the angiotensin II receptor blocker irbesartan.


Currently, diabetic nephropathy is the leading cause of chronic kidney disease in the United States and other Western societies. It is also one of the most significant long-term complications in terms of morbidity and mortality for individual patients with diabetes. Diabetes is responsible for 30-40% of all end-stage renal disease (ESRD) cases in the United States. (See Prognosis.)

Good evidence suggests that early treatment delays or prevents the onset of diabetic nephropathy or diabetic kidney disease. (See Treatment and Management.)

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Diabetic Nephropathy: Preventing Progression

Diabetic Nephropathy: Preventing Progression
Microalbuminuria can also be caused by hypertension, which often complicates type 2 diabetes and makes the diagnosis more difficult.
Diabetic nephropathy increases the risk of end-stage renal disease (ESRD) and mortality, and is associated with increased cardiovascular risk.
In persons with type 1 diabetes, angiotensin-converting enzyme inhibitors reduce progression of early nephropathy, whereas in persons with late nephropathy, they reduce the risk of end-stage renal failure and death.

Intensive glycemic control reduces progression of nephropathy compared with conventional control in persons with early renal disease, but we do not know whether glycemic control is effective in persons with late nephropathy.
We do not know whether angiotensin-II receptor blockers, dietary protein restriction, or tight control of blood pressure reduce the risks of renal or cardiovascular disease, or improve survival, in persons with early or late nephropathy.

In persons with type 2 diabetes, angiotensin-converting enzyme inhibitors reduce progression from early to late nephropathy and may reduce cardiovascular events, but we do not know whether they are beneficial in late nephropathy.

Angiotensin-II receptor blockers may reduce progression of nephropathy in persons with early or late nephropathy.
Lowering of diastolic blood pressure, even if not raised initially, reduces the risk of progression of early nephropathy, but we do not know whether it is effective in late nephropathy.
We do not know whether protein restriction or tight glycemic control are beneficial in early or late nephropathy.
Clinical Questions
Definition
Diabetic nephropathy is a clinical syndrome in persons with diabetes, characterized by albuminuria on at least two occasions separated by three to six months. Diabetic nephropathy is usually accompanied by hypertension, progressive rise in proteinuria, and decline in renal function. In type 1 diabetes, five stages have been proposed. Of these, stages 1 and 2 are equivalent to preclinical nephropathy and are detected only by imaging or biopsy. Stage 3 is synonymous with early nephropathy—the clinical term used in this review. Stage 4 nephropathy is also known clinically as late nephropathy, and this term will be used for the remainder of this review. Stage 5 represents the progression to ESRD.

Population: For the purpose of this review, we have included persons with diabetes and early or late nephropathy. Early nephropathy presents as microalbuminuria, usually defined by an albuminuria level of 30 to 300 mg per day (or urine albumin-to-creatinine ratio of 30 to 300 mg per g [3.4 to 34.0 mg per mmol]). Late nephropathy presents as macroalbuminuria, characterized by an albuminuria level greater than 300 mg per day (or urine albumin-to-creatinine ratio greater than 300 mg per g). The treatment of persons with diabetes and ESRD is not covered in this review.

Incidence and Prevalence
After 20 years of having type 1 or 2 diabetes, the cumulative risk of proteinuria is 27 to 28 percent, and the overall prevalence of microalbuminuria and macroalbuminuria is 30 to 35 percent. In addition, the incidence of diabetic nephropathy is increasing, partly due to the growing epidemic of type 2 diabetes, and because of increased life expectancies. For example, the incidence in the United States has increased by 150 percent in the past decade.

Etiology and Risk Factors
Duration of diabetes, older age, male sex, smoking, and poor glycemic control have all been found to be risk factors in the development of nephropathy. In addition, certain ethnic groups seem at greater risk (see Prognosis). Microalbuminuria is less pathognomonic of nephropathy among persons with type 2 diabetes because hypertension, which is a common complication of type 2 diabetes, can also cause microalbuminuria. Hypertension can also cause renal insufficiency; therefore, the time to development of renal insufficiency can be shorter in type 2 diabetes than in type 1. Renal biopsy may be advisable in persons who have an atypical course. In addition, there are some differences in the progression of type 1 and type 2 diabetic nephropathy. In persons with type 2 diabetes, albuminuria is more often present at diagnosis. Hypertension is also more common in type 2 diabetic nephropathy. Finally, microalbuminuria is less predictive of late nephropathy in persons with type 2 diabetes compared with type 1.

Prognosis
Persons with microalbuminuria are at increased risk for progression to macroalbuminuria and end-stage renal disease. The course of renal function is similar between types 1 and 2 diabetes. The natural history of diabetic nephropathy is better defined in type 1 than in type 2 diabetes. In type 2 diabetes, the course can be more difficult to predict, primarily because the date of onset of diabetes is less commonly known and because comorbid conditions can contribute to renal disease. Without specific interventions, about 80 percent of persons with type 1 diabetes and 20 to 40 percent of persons with type 2 diabetes who have microalbuminuria will develop macroalbuminuria.9 Diabetic nephropathy is associated with poor outcomes. Diabetic nephropathy is the most common cause of end-stage renal disease in the United Kingdom, accounting for 20 percent of all cases,10 whereas in the United States, diabetes accounts for 48 percent of all new cases of end-stage renal disease.11 Persons with type 1 diabetes and proteinuria have been found to have a 40-fold greater risk of all-cause mortality than persons without proteinuria.12 The prognostic significance of proteinuria is less extreme in type 2 diabetes, although persons with proteinuria have a fourfold risk of death compared with persons without proteinuria.13 In addition, increased cardiovascular risk has been associated with albuminuria in persons with diabetes.14 Blacks, Native Americans, and Hispanics have a much higher risk of developing end-stage renal disease in the setting of diabetes compared with whites.9,15 In the United States, blacks with diabetes develop end-stage renal disease at a considerably more rapid rate than whites with diabetes.16 In the United Kingdom, the rates for initiating treatment for end-stage renal disease are 4.2 times higher for Afro-Caribbeans and 3.7 times higher for Indo-Asians compared with whites.17 The Pima tribe of Native Americans, located in the southwestern United States, have much higher rates of diabetic nephropathy compared with whites, and they also develop end-stage renal disease at a faster rate.18
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Diabetic Nephropathy: Diagnosis

Diabetic Nephropathy: Diagnosis
Diabetic nephropathy is the leading cause of kidney disease in patients starting renal replacement therapy and affects ∼40% of type 1 and type 2 diabetic patients. It increases the risk of death, mainly from cardiovascular causes, and is defined by increased urinary albumin excretion (UAE) in the absence of other renal diseases. Diabetic nephropathy is categorized into stages: microalbuminuria (UAE >20 μg/min and ≤199 μg/min) and macroalbuminuria (UAE ≥200 μg/min). Hyperglycemia, increased blood pressure levels, and genetic predisposition are the main risk factors for the development of diabetic nephropathy. Elevated serum lipids, smoking habits, and the amount and origin of dietary protein also seem to play a role as risk factors. Screening for microalbuminuria should be performed yearly, starting 5 years after diagnosis in type 1 diabetes or earlier in the presence of puberty or poor metabolic control. In patients with type 2 diabetes, screening should be performed at diagnosis and yearly thereafter. Patients with micro- and macroalbuminuria should undergo an evaluation regarding the presence of comorbid associations, especially retinopathy and macrovascular disease. Achieving the best metabolic control (A1c <7%), treating hypertension (<130/80 mmHg or <125/75 mmHg if proteinuria >1.0 g/24 h and increased serum creatinine), using drugs with blockade effect on the renin-angiotensin-aldosterone system, and treating dyslipidemia (LDL cholesterol <100 mg/dl) are effective strategies for preventing the development of microalbuminuria, in delaying the progression to more advanced stages of nephropathy and in reducing cardiovascular mortality in patients with type 1 and type 2 diabetes.
Diabetic nephropathy is the leading cause of chronic kidney disease in patients starting renal replacement therapy (1) and is associated with increased cardiovascular mortality (2). Diabetic nephropathy has been classically defined by the presence of proteinuria >0.5 g/24 h. This stage has been referred to as overt nephropathy, clinical nephropathy, proteinuria, or macroalbuminuria. In the early 1980s, seminal studies from Europe revealed that small amounts of albumin in the urine, not usually detected by conventional methods, were predictive of the later development of proteinuria in type 1 (3–5) and type 2 (6) diabetic patients. This stage of renal involvement was termed microalbuminuria or incipient nephropathy.

The cumulative incidence of microalbuminuria in patients with type 1 diabetes was 12.6% over 7.3 years according to the European Diabetes (EURODIAB) Prospective Complications Study Group (7) and ∼33% in an 18-year follow-up study in Denmark (8). In patients with type 2 diabetes, the incidence of microalbuminuria was 2.0% per year and the prevalence 10 years after diagnosis 25% in the U.K. Prospective Diabetes Study (UKPDS) (9). Proteinuria occurs in 15–40% of patients with type 1 diabetes, with a peak incidence around 15–20 years of diabetes (8,10,11). In patients with type 2 diabetes, the prevalence is highly variable, ranging from 5 to 20% (2,9).

People with diabetes have a lot to juggle when it comes to their healthcare. Having diabetes puts you at risk of other health problems, including heart attacks, strokes, vision loss, nerve damage, and kidney disease. While all of that may sound overwhelming, there is some good news; many of the steps you need to take to prevent one of those complications may actually help to prevent them all.

The kidneys play an important role in the body: they filter the blood, removing waste products and excess salt and water. If the kidneys become diseased, they falter in their task, leaving the blood polluted.

Finding out that you have early diabetic nephropathy can alert you that your kidneys are in danger. It is important to take steps to protect your kidneys before the problem advances. Information about advanced kidney disease is also available (see "Patient information: Chronic kidney disease (Beyond the Basics)").

In some cases, diabetic nephropathy can eventually cause the kidneys to stop working altogether. If that happens to you, you will need to have a kidney transplant or dialysis, a procedure that filters the blood artificially several times a week. (See "Patient information: Dialysis or kidney transplantation — which is right for me? (Beyond the Basics)".)

DIABETIC NEPHROPATHY SYMPTOMS

Diabetic nephropathy usually causes no symptoms, and people who have the condition often produce normal amounts of urine. To detect diabetic nephropathy, healthcare providers rely on tests that measure protein levels in the urine and blood tests to evaluate the level of kidney function.

When the kidneys are working normally, they prevent protein from leaking into the urine, so finding protein in the urine is a sign that the kidneys are in trouble. Often people who have diabetic nephropathy also have high blood pressure.

DIABETIC NEPHROPATHY RISK FACTORS

There are several factors that can increase your risk of developing diabetic nephropathy. These include:

●Having chronically elevated blood sugar levels
●Being overweight or obese
●Smoking
●Having a diabetes-related vision problem (diabetic retinopathy) or nerve damage (diabetic neuropathy) (see "Patient information: Diabetic neuropathy (Beyond the Basics)")
Having a family history of kidney disease or belonging to certain ethnic groups (eg, African American, Mexican, Pima Indian) can also increase your risk of diabetic nephropathy.

To learn more, please contact me:sjzhospitalrenal@hotmail.com

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