Input: What are the treatments for Hyperthyroidism ?

Output:
Health care providers treat hyperthyroidism with medications, radioiodine therapy, or thyroid surgery. The aim of treatment is to bring thyroid hormone levels to a normal state, thus preventing long-term complications, and to relieve uncomfortable symptoms. No single treatment works for everyone.

Treatment depends on the cause of hyperthyroidism and how severe it is. When choosing a treatment, health care providers consider a patients age, possible allergies to or side effects of the medications, other conditions such as pregnancy or heart disease, and the availability of an experienced thyroid surgeon.

Finding the right specialist for treatment is an important first step. Some professional societies, listed under For More Information, and endocrinology departments in local teaching hospitals can provide the names of local specialists.

Medications

Beta blockers. Health care providers may prescribe a medication called a beta blocker to reduce symptoms until other treatments take effect. Beta blockers act quickly to relieve many of the symptoms of hyperthyroidism, such as tremors, rapid heartbeat, and nervousness, but do not stop thyroid hormone production. Most people feel better within hours of taking these medications.

Antithyroid medications. Antithyroid therapy is the easiest way to treat hyperthyroidism. Antithyroid medications interfere with thyroid hormone production but dont usually have permanent results. Antithyroid medications are not used to treat thyroiditis.

Once treatment with antithyroid medications begins, thyroid hormone levels may not move into the normal range for several weeks or months. The average treatment time is about 1 to 2 years, but treatment can continue for many years.

Antithyroid medications can cause side effects in some people, including

- allergic reactions such as rashes and itching  - a decrease in the number of white blood cells in the body, which can lower resistance to infection  - liver failure, in rare cases

Stop your antithyroid medication and call your health care provider right away if you develop any of the following while taking antithyroid medications:   - fatigue   - weakness   - vague abdominal pain   - loss of appetite   - skin rash or itching   - easy bruising   - yellowing of the skin or whites of the eyes, called jaundice   - persistent sore throat   - fever

In the United States, health care providers prescribe the antithyroid medication methimazole (Tapazole, Northyx) for most types of hyperthyroidism.

Antithyroid medications and pregnancy. Because pregnant and breastfeeding women cannot receive radioiodine therapy, they are usually treated with an antithyroid medication instead. However, experts agree that women in their first trimester of pregnancy should not take methimazole due to the rare occurrence of damage to the fetus. Another antithyroid medication, propylthiouracil (PTU), is available for women in this stage of pregnancy or for women who are allergic to or intolerant of methimazole and have no other treatment options.

Health care providers may prescribe PTU for the first trimester of pregnancy and switch to methimazole for the second and third trimesters. Some women are able to stop taking antithyroid medications in the last 4 to 8 weeks of pregnancy due to the remission of hyperthyroidism that occurs during pregnancy. However these women should continue to be monitored for recurrence of thyroid problems following delivery.

Studies have shown that mothers taking antithyroid medications may safely breastfeed. However, they should take only moderate doses, less than 1020 milligrams daily, of the antithyroid medication methimazole. Doses should be divided and taken after feedings, and the infants should be monitored for side effects.4

Women requiring higher doses of the antithyroid medication to control hyperthyroidism should not breastfeed.

Radioiodine Therapy

Radioactive iodine-131 is a common and effective treatment for hyperthyroidism. In radioiodine therapy, patients take radioactive iodine-131 by mouth. Because the thyroid gland collects iodine to make thyroid hormone, it will collect the radioactive iodine from the bloodstream in the same way. The radioactive iodine gradually destroys the cells that make up the thyroid gland but does not affect other body tissues.

More than one round of radioiodine therapy may be needed to bring thyroid hormone production into the normal range. In the meantime, treatment with beta blockers can control symptoms.

Almost everyone who receives radioactive iodine treatment eventually develops hypothyroidism. But health care providers consider this an acceptable outcome because hypothyroidism is easier to treat and has fewer long-term complications than hyperthyroidism. People who develop hypothyroidism must take synthetic thyroid hormone.

Radioiodine and pregnancy. Although iodine-131 is not known to cause birth defects or infertility, radioiodine therapy is not used in pregnant women or women who are breastfeeding. Radioactive iodine can be harmful to the fetus thyroid and can be passed from mother to child in breast milk. Experts recommend that women wait a year after treatment before becoming pregnant.

Thyroid Surgery

The least-used treatment is surgery to remove part or most of the thyroid gland. Sometimes surgery may be used to treat

- pregnant women who cannot tolerate antithyroid medications  - people with large goiters  - people who have cancerous thyroid nodules, though hyperthyroidism does not cause cancer

Before surgery, the health care provider may prescribe antithyroid medications to temporarily bring a patients thyroid hormone levels into the normal range. This presurgical treatment prevents a condition called thyroid storma sudden, severe worsening of symptomsthat can occur when hyperthyroid patients have general anesthesia.

When part of the thyroid is removedas a treatment for toxic nodules, for examplethyroid hormone levels may return to normal. But some surgical patients may still develop hypothyroidism and need to take synthetic thyroxine, a medication that is identical to the hormone, T4, made by the thyroid. If the entire thyroid is removed, lifelong thyroid hormone medication is necessary. After surgery, health care providers will continue to monitor patients thyroid hormone levels.

Although uncommon, certain problems can occur in thyroid surgery. The parathyroid glands can be damaged because they are located very close to the thyroid. These glands help control calcium and phosphorus levels in the body. Damage to the laryngeal nerve, also located close to the thyroid, can lead to voice changes or breathing problems. But when surgery is performed by an experienced surgeon, less than 1 percent of patients have permanent complications.5 People who need help finding a surgeon can contact one of the organizations listed under For More Information. </s>


Input: What to do for Hyperthyroidism ?

Output:
Experts recommend that people eat a balanced diet to obtain most nutrients. More information about diet and nutrition is provided by the National Agricultural Library at www.nutrition.gov.

Dietary Supplements

Iodine is an essential mineral for the thyroid. However, people with autoimmune thyroid disease may be sensitive to harmful side effects from iodine. Taking iodine drops or eating foods containing large amounts of iodinesuch as seaweed, dulse, or kelpmay cause or worsen hyperthyroidism. More information about iodine is provided by the National Library of Medicine in the fact sheet, Iodine in diet, available at www.nlm.nih.gov/medlineplus.

Women need more iodine when they are pregnantabout 250 micrograms a daybecause the baby gets iodine from the mothers diet. In the United States, about 7 percent of pregnant women may not get enough iodine in their diet or through prenatal vitamins.6 Choosing iodized saltsalt supplemented with iodineover plain salt and prenatal vitamins containing iodine will ensure this need is met.

To help ensure coordinated and safe care, people should discuss their use of dietary supplements, such as iodine, with their health care provider. Tips for talking with health care providers are available through the National Center for Complementary and Integrative Health. </s>


Input: What to do for Hyperthyroidism ?

Output: - Hyperthyroidism is a disorder that occurs when the thyroid gland makes more thyroid hormone than the body needs.  - Hyperthyroidism is most often caused by Graves disease, an autoimmune disorder. Other causes include thyroid nodules, thyroiditis, consuming too much iodine, and overmedicating with synthetic thyroid hormone.  - Some symptoms of hyperthyroidism are nervousness or irritability, fatigue or muscle weakness, heat intolerance, trouble sleeping, hand tremors, rapid and irregular heartbeat, frequent bowel movements or diarrhea, weight loss, mood swings, and goiter.  - Hyperthyroidism is much more common in women than men.  - Hyperthyroidism is also more common in people older than age 60 and is often caused by thyroid nodules. Hyperthyroidism in this age group is sometimes misdiagnosed as depression or dementia. For people older than age 60, subclinical hyperthyroidism increases their chance of developing atrial fibrillation.  - Women with hyperthyroidism should discuss their condition with their health care provider before becoming pregnant.  - Hyperthyroidism is treated with medications, radioiodine therapy, or thyroid surgery. No single treatment works for everyone. </s>


Input: What is (are) Polycystic Kidney Disease ?

Output:
Polycystic kidney disease is a genetic disorder that causes numerous cysts to grow in the kidneys. A kidney cyst is an abnormal sac filled with fluid. PKD cysts can greatly enlarge the kidneys while replacing much of their normal structure, resulting in chronic kidney disease (CKD), which causes reduced kidney function over time. CKD may lead to kidney failure, described as end-stage kidney disease or ESRD when treated with a kidney transplant or blood-filtering treatments called dialysis. The two main types of PKD are autosomal dominant PKD and autosomal recessive PKD.

PKD cysts are different from the usually harmless simple cysts that often form in the kidneys later in life. PKD cysts are more numerous and cause complications, such as high blood pressure, cysts in the liver, and problems with blood vessels in the brain and heart. </s>


Input: What causes Polycystic Kidney Disease ?

Output:
A gene mutation, or defect, causes polycystic kidney disease. Genes provide instructions for making proteins in the body. A gene mutation is a permanent change in the deoxyribonucleic acid (DNA) sequence that makes up a gene. In most cases of PKD, a person inherits the gene mutation, meaning a parent passes it on in his or her genes. In the remaining cases, the gene mutation develops spontaneously. In spontaneous cases, neither parent carries a copy of the mutated gene.

Researchers have found three different gene mutations associated with PKD. Two of the genes are associated with autosomal dominant PKD. The third gene is associated with autosomal recessive PKD. Gene mutations that cause PKD affect proteins that play a role in kidney development.

Genetic Disorders   Each cell contains thousands of genes that provide the instructions for making proteins for growth and repair of the body. If a gene has a mutation, the protein made by that gene may not function properly, which sometimes creates a genetic disorder. Not all gene mutations cause a disorder.   People inherit two copies of most genes; one copy from each parent. A genetic disorder occurs when one or both parents pass a mutated gene to a child at conception. A genetic disorder can also occur through a spontaneous gene mutation, meaning neither parent carries a copy of the mutated gene. Once a spontaneous gene mutation has occurred, a person can pass it to his or her children.   Read more about genes and genetic conditions in the U.S. National Library of Medicines (NLMs) Genetics Home Reference. </s>


Input: How many people are affected by Polycystic Kidney Disease ?

Output:
Estimates of PKDs prevalence range from one in 400 to one in 1,000 people.1 According to the United States Renal Data System, PKD accounts for 2.2 percent of new cases of kidney failure each year in the United States. Annually, eight people per 1 million have kidney failure as a result of PKD.2

Polycystic kidney disease exists around the world and in all races. The disorder occurs equally in women and men, although men are more likely to develop kidney failure from PKD. Women with PKD and high blood pressure who have had more than three pregnancies also have an increased chance of developing kidney failure. </s>


Input: What is (are) Polycystic Kidney Disease ?

Output:
Autosomal dominant PKD is the most common form of PKD and the most common inherited disorder of the kidneys.3 The term autosomal dominant means a child can get the disorder by inheriting the gene mutation from only one parent. Each child of a parent with an autosomal dominant mutation has a 50 percent chance of inheriting the mutated gene. About 10 percent of autosomal dominant PKD cases occur spontaneously.4

The following chart shows the chance of inheriting an autosomal dominant gene mutation:

Health care providers identify most cases of autosomal dominant PKD between the ages of 30 and 50.4 For this reason, health care providers often call autosomal dominant PKD adult PKD. However, the onset of kidney damage and how quickly the disorder progresses varies. In some cases, cysts may form earlier in life and grow quickly, causing symptoms in childhood.

The cysts grow out of nephrons, the tiny filtering units inside the kidneys. The cysts eventually separate from the nephrons and continue to enlarge. The kidneys enlarge along with the cystswhich can number in the thousandswhile roughly retaining their kidney shape. In fully developed autosomal dominant PKD, a cyst-filled kidney can weigh as much as 20 to 30 pounds. </s>


Input: What are the symptoms of Polycystic Kidney Disease ?

Output: In many cases, PKD does not cause signs or symptoms until cysts are half an inch or larger. When present, the most common symptoms are pain in the back and sidesbetween the ribs and hipsand headaches. The pain can be temporary or persistent, mild or severe. Hematuriablood in the urinemay also be a sign of autosomal dominant PKD. </s>


Input: What are the complications of Polycystic Kidney Disease ?

Output:
The complications of autosomal dominant PKD include the following:

- Pain. Cyst infection, other types of urinary tract infections (UTIs), bleeding into cysts, kidney stones, or stretching of the fibrous tissue around the kidney because of cyst growth can cause pain in the area of the kidneys.  - High blood pressure. High blood pressure is present in about half of the people with autosomal dominant PKD and normal kidney function between the ages of 20 and 35.4 Almost 100 percent of people with kidney failure and autosomal dominant PKD have high blood pressure.1 High blood pressuregreater than 140/90 mm Hgincreases the likelihood of heart disease and stroke, as well as adding to the damage already done to the kidneys by the cysts.  - Kidney failure. Kidney failure means the kidneys no longer work well enough to maintain health. A person with kidney failure may have the following symptoms:      - little or no urination    - edemaswelling, usually in the legs, feet, or ankles and less often in the hands or face    - drowsiness    - fatigue, or feeling tired    - generalized itching or numbness    - dry skin    - headaches    - weight loss    - appetite loss    - nausea    - vomiting    - sleep problems    - trouble concentrating    - darkened skin    - muscle cramps    - shortness of breath    - chest pain

Untreated kidney failure can lead to coma and death. More than half of people with autosomal dominant PKD progress to kidney failure by age 70.1

- UTIs. Kidney cysts block the flow of urine through the kidneys. Stagnant urine can set the stage for infection. Bacteria enter the urinary tract through the urethra and spread up to the kidneys. Sometimes, the kidney cysts become infected. UTIs may cause scarring in the kidneys.  - Kidney stones. About 20 percent of people with autosomal dominant PKD have kidney stones.1 Kidney stones can block the flow of urine and cause pain.  - Liver cysts. Liver cysts are the most common nonkidney complication of autosomal dominant PKD.1 Liver cysts generally cause no symptoms.  - Pancreatic cysts. PKD can also cause cysts in the pancreas. Pancreatic cysts rarely cause pancreatitisinflammation, or swelling, of the pancreas.  - Abnormal heart valves. Abnormal heart valves may occur in up to 25 percent of people with autosomal dominant PKD.1 Insufficient blood flow in the aortathe large artery that carries blood from the heartmay result from the abnormal heart valves.  - Diverticula. Diverticula are small pouches, or sacs, that push outward through weak spots in the colon wall. This complication is more common in people with PKD who have kidney failure.1  - Brain aneurysms. An aneurysm is a bulge in the wall of a blood vessel. Aneurysms in the brain might cause headaches that are severe or feel different from other headaches. Brain aneurysms can rupture, or break open, causing bleeding inside the skull. A ruptured aneurysm in the brain is a life-threatening condition and requires immediate medical attention. </s>


Input: What is (are) Polycystic Kidney Disease ?

Output:
Autosomal recessive PKD is a rare genetic disorder that affects the liver as well as the kidneys. The signs of autosomal recessive PKD frequently appear in the earliest months of life, even in the womb, so health care providers often call it infantile PKD. In an autosomal recessive disorder, the child has to inherit the gene mutation from both parents to have an increased likelihood for the disorder. The chance of a child inheriting autosomal recessive mutations from both parents with a gene mutation is 25 percent, or one in four. If only one parent carries the mutated gene, the child will not get the disorder, although the child may inherit the gene mutation. The child is a carrier of the disorder and can pass the gene mutation to the next generation. Genetic testing can show whether a parent or child is a carrier of the mutated gene. Autosomal recessive disorders do not typically appear in every generation of an affected family.

The following chart shows the chance of inheriting an autosomal recessive mutation from parents who both carry the mutated gene:

Read more about how people inherit genetic conditions at the NLMs Genetics Home Reference. </s>


Input: What are the symptoms of Polycystic Kidney Disease ?

Output:
An early sign of autosomal recessive PKD is an enlarged kidney, seen in a fetus or an infant using ultrasound. Kidney function is crucial for early physical development, so children with autosomal recessive PKD and decreased kidney function are usually smaller-than-average size, a condition called growth failure.

Some people with autosomal recessive PKD do not develop signs or symptoms until later in childhood or even adulthood. </s>


Input: What are the complications of Polycystic Kidney Disease ?

Output:
Babies with the most severe cases of autosomal recessive PKD often die hours or days after birth because they cannot breathe well enough to sustain life. Their lungs do not develop as they should during the prenatal period. Pressure from enlarged kidneys also contributes to breathing problems.

Children born with autosomal recessive PKD often develop kidney failure before reaching adulthood.

Liver scarring occurs in all people with autosomal recessive PKD and is usually present at birth. However, liver problems tend to become more of a concern as people with autosomal recessive PKD grow older. Liver scarring can lead to progressive liver dysfunction and other problems.

Additional complications of autosomal recessive PKD include high blood pressure and UTIs. </s>


Input: How to prevent Polycystic Kidney Disease ?

Output: Scientists have not yet found a way to prevent PKD. However, people with PKD may slow the progression of kidney damage caused by high blood pressure through lifestyle changes, diet, and blood pressure medications. People with PKD should be physically active 30 minutes a day most days of the week. See Eating, Diet, and Nutrition for diet advice on lowering blood pressure and slowing the progression of kidney disease in general. If lifestyle and diet changes do not control a persons blood pressure, a health care provider may prescribe one or more blood pressure medications, including ACE inhibitors or ARBs. </s>


Input: What to do for Polycystic Kidney Disease ?

Output:
A dietitian specializes in helping people who have kidney disease choose the right foods and plan healthy meals. People with any kind of kidney disease, including PKD, should talk with a dietitian about foods that should be added to their diet and foods that might be harmful.

PKD may require diet changes for blood pressure control. Kidney disease in general also calls for certain diet changes.

Following a healthy eating plan can help lower blood pressure. A health care provider may recommend the Dietary Approaches to Stop Hypertension (DASH) eating plan, which focuses on fruits, vegetables, whole grains, and other foods that are heart healthy and lower in sodium, which often comes from salt. The DASH eating plan

- is low in fat and cholesterol  - features fat-free or low-fat milk and dairy products, fish, poultry, and nuts  - suggests less red meat, sweets, added sugars, and sugar-containing beverages  - is rich in nutrients, protein, and fiber

More information about the DASH eating planis available from the National Heart, Lung, and Blood Institute.

As your kidneys become more damaged, you may need to eat foods that are lower in phosphorus and potassium. The health care provider will use lab tests to watch your levels.

Foods high in potassium include

- bananas  - oranges  - potatoes  - tomatoes

Lower-potassium foods include

- apples  - peaches  - carrots  - green beans

Foods higher in phosphorus include

- large portions of meat, fish and dairy foods  - bran cereals and oatmeal  - beans and nuts  - colas

Lower-phosphorus alternatives include

- fresh fruits and vegetables  - breads  - pasta  - rice  - corn and rice cereals  - light-colored sodas

People with kidney disease and high blood pressure should also limit how much sodium they get to 2,300 mg or less each day.5

People with CKD may need to watch how much protein they eat. Everyone needs protein. However, protein breaks down into wastes the kidneys must remove. Large amounts of protein make the kidneys work harder. High-quality proteins such as meat, fish, and eggs create fewer wastes than other sources of protein. Beans, whole grains, soy products, nuts and nut butters, and dairy products can also be good sources of protein. Most people eat more protein than they need. Eating high-quality protein and smaller portions of protein can help protect the kidneys.

More information about nutrition for kidney disease is provided in the NIDDK health topics:

- Nutrition for Children with Chronic Kidney Disease  - Nutrition for Adults with Early Chronic Kidney Disease  - Nutrition for Adults with Advanced Chronic Kidney Disease

The National Kidney Disease Education Program offers a series of easy-to-read fact sheets about nutrition for people with CKD. </s>


Input: What to do for Polycystic Kidney Disease ?

Output: - Polycystic kidney disease (PKD) is a genetic disorder that causes numerous cysts to grow in the kidneys.  - A gene mutation, or defect, causes polycystic kidney disease.  - Autosomal dominant PKD is the most common form of PKD and the most common inherited disorder of the kidneys.  - Health care providers identify most cases of autosomal dominant PKD between the ages of 30 and 50.  - The most common symptoms of PKD are pain in the back and sidesbetween the ribs and hipsand headaches. The pain can be temporary or persistent, mild or severe. Hematuriablood in the urinemay also be a sign of autosomal dominant PKD.  - The complications of autosomal dominant PKD include the following:      - pain    - high blood pressure    - kidney failure    - urinary tract infections (UTIs)    - kidney stones    - liver cysts    - pancreatic cysts    - abnormal heart valves    - diverticula    - brain aneurysms    - A health care provider diagnoses autosomal dominant PKD using imaging tests and genetic testing.  - A radiologista doctor who specializes in medical imagingwill interpret the images produced by the following imaging tests:      - ultrasound    - computerized tomography scans    - magnetic resonance imaging    - Genetic testing can show whether a persons cells carry a gene mutation that causes autosomal dominant PKD. A health care provider may also use genetic testing results to determine whether someone with a family history of PKD is likely to develop the disorder in the future. Prenatal testing can diagnose autosomal recessive PKD in unborn children.  - Although a cure for autosomal dominant PKD is not currently available, treatment can ease symptoms and prolong life.  - Autosomal recessive PKD is a rare genetic disorder that affects the liver as well as the kidneys.  - The complications of autosomal recessive PKD include the following:      - death due to breathing problems    - kidney failure    - liver scarring    - high blood pressure    - UTIs    - A health care provider diagnoses autosomal recessive PKD with ultrasound imaging, even in a fetus or newborn.  - Treatments for autosomal recessive PKD focus on the symptoms and complications.  - Scientists have not yet found a way to prevent PKD. However, people with PKD may slow the progression of kidney damage caused by high blood pressure through lifestyle changes, diet, and blood pressure medications.  - People with any kind of kidney disease, including PKD, should talk with a dietitian about foods they should add to their diet and foods that might be harmful. </s>


Input: What is (are) Nutrition for Advanced Chronic Kidney Disease in Adults ?

Output: CKD usually takes a long time to develop and does not go away. In CKD, the kidneys continue to workjust not as well as they should. Wastes may build up so gradually that the body becomes used to having those wastes in the blood. Salts containing phosphorus and potassium may rise to unsafe levels, causing heart and bone problems. Anemialow red blood cell countcan result from CKD because the kidneys stop making enough erythropoietin, a hormone that causes bone marrow to make red blood cells. After months or years, CKD may progress to permanent kidney failure, which requires a person to have a kidney transplant or regular blood filtering treatments called dialysis. </s>


Input: What is (are) Nutrition for Advanced Chronic Kidney Disease in Adults ?

Output:
MNT is the use of nutrition counseling by a registered dietitian to help promote a medical or health goal. A health care provider may refer a patient to a registered dietitian to help with the patient's food plan. Many insurance policies cover MNT when recommended by a health care provider. Anyone who qualifies for Medicare can receive a benefit for MNT from a registered dietitian or nutrition professional when a health care provider provides a referral indicating that the person has diabetes or kidney disease.

One way to locate a qualified dietitian is to contact the Academy of Nutrition and Dietetics at www.eatright.organd click on "Find a Registered Dietitian." Users can enter their address or ZIP code for a list of dietitians in their area. A person looking for dietary advice to prevent kidney damage should click on "Renal (Kidney) Nutrition" in the specialty field. Dietitians who specialize in helping people with CKD are called renal dietitians.

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Input: What is (are) Nutrition for Advanced Chronic Kidney Disease in Adults ?

Output:
As CKD progresses, people often lose their appetites because they find that foods do not taste the same. As a result, they consume fewer caloriesimportant units of energy in foodand may lose too much weight. Renal dietitians can help people with advanced CKD find healthy ways to add calories to their diet if they are losing too much weight.

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Input: What is (are) Nutrition for Advanced Chronic Kidney Disease in Adults ?

Output:
Protein is an essential part of any diet. Proteins help build and maintain muscle, bone, skin, connective tissue, internal organs, and blood. They help fight disease and heal wounds. But proteins also break down into waste products that must be removed from the blood by the kidneys. Eating more protein than the body needs may put an extra burden on the kidneys and cause kidney function to decline faster.

Health care providers recommend that people with CKD eat moderate or reduced amounts of protein. However, restricting protein could lead to malnutrition, so people with CKD need to be careful. The typical American diet contains more than enough protein. Learning about portion sizes can help people limit protein intake without endangering their health. </s>


Input: What is (are) Nutrition for Advanced Chronic Kidney Disease in Adults ?

Output:
Most peoplewith or without CKDcan get the daily protein they need by eating two 3-ounce servings of meat or meat substitute. A 3-ounce serving of meat is about the size of a deck of cards or the palm of a persons hand.

A renal dietitian can help people learn about the amount and sources of protein in their diet. Animal protein in egg whites, cheese, chicken, fish, and red meats contain more of the essential nutrients a body needs. With careful meal planning, a well-balanced vegetarian diet can also provide these nutrients. A renal dietitian can help people with advanced CKD make small adjustments in their eating habits that can result in significant protein reduction. For example, people can lower their protein intake by making sandwiches using thinner slices of meat and adding lettuce, cucumber slices, apple slices, and other garnishes. The following table lists some higher-protein foods and suggestions for lower-protein alternatives that are better choices for people with CKD trying to limit their protein intake.

Higher- and Lower-protein Foods

Based on about a 3 oz. portion        Higher-Protein Foods    Lower-protein Alternatives        Ground beef Halibut Shrimp Salmon Tuna Chicken breast Roasted chicken     Chili con carne Beef stew Egg substitutes Tofu Imitation crab meat

When kidney function declines to the point where dialysis becomes necessary, patients should include more protein in their diet because dialysis removes large amounts of protein from the blood. </s>


Input: What is (are) Nutrition for Advanced Chronic Kidney Disease in Adults ?

Output:
Everyone should know about fat sources because eating the wrong kinds of fat and too much fat increases the risk of clogged blood vessels and heart problems. Fat provides energy, helps produce hormonelike substances that regulate blood pressure and other heart functions, and carries fat-soluble vitamins. Everyone needs dietary fat, but some fats are healthier than others. People with CKD are at higher risk of having a heart attack or stroke. Therefore, people with CKD should be especially careful about how dietary fat affects their heart health.

People with advanced CKD should talk with a dietitian about healthy and unhealthy sources of fat. Saturated fats and trans-fatty acids can raise blood cholesterol levels and clog blood vessels. Saturated fats are found in animal products such as red meat, poultry, whole milk, and butter. These fats are usually solid at room temperature. Trans-fatty acids are often found in commercially baked goods such as cookies and cakes and in fried foods like doughnuts and french fries.

A dietitian can suggest healthy ways to include fat in the diet, especially if more calories are needed. Vegetable oils such as corn or safflower oil are healthier than animal fats such as butter or lard. Hydrogenated vegetable oils should be avoided because they are high in trans-fatty acids. Monounsaturated fatsolive, peanut, and canola oilsare healthy alternatives to animal fats. The table below shows the sources of fats, broken down into three types of fats that should be eaten less often and good fats that can be eaten more often.

Sources of Fats

Eat Less Often    Eat More Often        Saturated fats          - red meat      - poultry      - whole milk      - butter      - lard        Monounsaturated fats          - corn oil      - safflower oil      - olive oil      - peanut oil      - canola oil            Trans-fatty acids          - commercial baked goods      - french fries      - doughnuts            Hydrogenated vegetable oils          - margarine      - shortening </s>


Input: What is (are) Nutrition for Advanced Chronic Kidney Disease in Adults ?

Output:
Too much sodium in a person's diet can be harmful because it causes blood to hold fluid. People with CKD need to be careful not to let too much fluid build up in their bodies. The extra fluid raises blood pressure and puts a strain on the heart and kidneys. A dietitian can help people find ways to reduce the amount of sodium in their diet. Nutrition labels provide information about the sodium content in food. The U.S. Food and Drug Administration advises that healthy people should limit their daily sodium intake to no more than 2,300 milligrams (mg), the amount found in 1 teaspoon of table salt. People who are at risk for a heart attack or stroke because of a condition such as high blood pressure or kidney disease should limit their daily sodium intake to no more than 1,500 mg. Choosing sodium-free or low-sodium food products will help them reach that goal.

Sodium is found in ordinary table salt and many salty seasonings such as soy sauce and teriyaki sauce. Canned foods, some frozen foods, and most processed meats have large amounts of salt. Snack foods such as chips and crackers are also high in salt.

Alternative seasonings such as lemon juice, salt-free seasoning mixes, and hot pepper sauce can help people reduce their salt intake. People with advanced CKD should avoid salt substitutes that use potassium, such as AlsoSalt or Nu-Salt, because CKD limits the body's ability to eliminate potassium from the blood. The table below provides some high-sodium foods and suggestions for low-sodium alternatives that are healthier for people with any level of CKD who have high blood pressure.

High- and Low-sodium Foods

High-sodium Foods    Low-sodium Alternatives        Salt Regular canned vegetables Hot dogs and canned meat Packaged rice with sauce Packaged noodles with sauce Frozen vegetables with sauce Frozen prepared meals Canned soup Regular tomato sauce Snack foods    Salt-free herb seasonings Low-sodium canned foods Frozen vegetables without sauce Fresh, cooked meat Plain rice without sauce Plain noodles without sauce Fresh vegetables without sauce Homemade soup with fresh ingredients Reduced-sodium tomato sauce Unsalted pretzels Unsalted popcorn </s>


Input: What is (are) Nutrition for Advanced Chronic Kidney Disease in Adults ?

Output:
Keeping the proper level of potassium in the blood is essential. Potassium keeps the heart beating regularly and muscles working right. Problems can occur when blood potassium levels are either too low or too high. Damaged kidneys allow potassium to build up in the blood, causing serious heart problems. Potassium is found in many fruits and vegetables, such as bananas, potatoes, avocados, and melons. People with advanced CKD may need to avoid some fruits and vegetables. Blood tests can indicate when potassium levels have climbed above normal range. A renal dietitian can help people with advanced CKD find ways to limit the amount of potassium they eat. The potassium content of potatoes and other vegetables can be reduced by boiling them in water. The following table gives examples of some high-potassium foods and suggestions for low-potassium alternatives for people with advanced CKD.

High- and Low-potassium Foods

High-potassium Foods    Low-potassium Alternatives        Oranges and orange juice Melons Apricots Bananas Potatoes Tomatoes Sweet potatoes Cooked spinach Cooked broccoli Beans (baked, kidney, lima, pinto)    Apples and apple juice Cranberries and cranberry juice Canned pears Strawberries, blueberries, raspberries Plums Pineapple Cabbage Boiled Cauliflower </s>


Input: What is (are) Nutrition for Advanced Chronic Kidney Disease in Adults ?

Output:
Damaged kidneys allow phosphorus, a mineral found in many foods, to build up in the blood. Too much phosphorus in the blood pulls calcium from the bones, making the bones weak and likely to break. Too much phosphorus may also make skin itch. Foods such as milk and cheese, dried beans, peas, colas, canned iced teas and lemonade, nuts, and peanut butter are high in phosphorus. A renal dietitian can help people with advanced CKD learn how to limit phosphorus in their diet.

As CKD progresses, a person may need to take a phosphate binder such as sevelamer hydrochloride (Renagel), lanthanum carbonate (Fosrenol), calcium acetate (PhosLo), or calcium carbonate (Tums) to control the phosphorus in the blood. These medications act like sponges to soak up, or bind, phosphorus while it is in the stomach. Because it is bound, the phosphorus does not get into the blood. Instead, it is removed from the body in the stool.

The table below lists some high-phosphorus foods and suggestions for low-phosphorus alternatives that are healthier for people with advanced CKD.

High- and Low-phosphorus Foods

High-phosphorus Foods    Low-phosphorus Alternatives        Dairy foods (milk, cheese, yogurt) Beans (baked, kidney, lima, pinto) Nuts and peanut butter Processed meats (hot dogs, canned meat) Cola Canned iced teas and lemonade Bran cereals Egg yolks     Liquid non-dairy creamer Sherbet Cooked rice Rice, wheat, and corn cereals Popcorn Peas Lemon-lime soda Root beer Powdered iced tea and lemonade mixes </s>


Input: What to do for Nutrition for Advanced Chronic Kidney Disease in Adults ?

Output: - A person may prevent or delay some health problems from chronic kidney disease (CKD) by eating the right foods and avoiding foods high in sodium, potassium, and phosphorus.  - The kidneys remove wastes and extra water from the blood and make urine.  - Medical nutrition therapy (MNT) is the use of counseling by a registered dietitian to help promote a medical or health goal.  - Dietitians who specialize in helping people with CKD are called renal dietitians.  - People with advanced CKD often lose their appetites and consume fewer caloriesimportant units of energy in foodand may lose too much weight.  - Eating more protein than the body needs may put an extra burden on the kidneys and cause kidney function to decline faster. Most peoplewith or without CKDcan get the daily protein they need by eating two 3-ounce servings of meat or meat substitute.  - People with CKD are at higher risk of having a heart attack or stroke.  - Everyone needs dietary fat, but some fats are healthier than others.  - Too much sodium in a persons diet can be harmful because it causes blood to hold fluid. People with CKD need to be careful not to let too much fluid build up in their bodies.  - People with advanced CKD should avoid salt substitutes that use potassium because CKD limits the bodys ability to eliminate potassium from the blood.  - Damaged kidneys allow potassium to build up in the blood, causing serious heart problems. Potassium is found in many fruits and vegetables, such as bananas, potatoes, avocados, and melons.  - Too much phosphorus in the blood pulls calcium from the bones, making the bones weak and likely to break.  - People with advanced CKD may need to limit how much they drink because damaged kidneys can't remove extra fluid.  - Many patients find that keeping track of their test results helps them see how their treatment is working. Patients can ask their health care provider for copies of their lab reports and ask to have them explained, noting any results out of the normal range. </s>


Input: What is (are) Nutrition for Advanced Chronic Kidney Disease in Adults ?

Output:
The NIDDK Nutrition for Chronic Kidney Disease Series includes three fact sheets:

- Nutrition for Early Chronic Kidney Disease in Adults  - Nutrition for Advanced Chronic Kidney Disease in Adults  - Nutrition for Chronic Kidney Disease in Children </s>


Input: What is (are) Causes of Diabetes ?

Output:
Diabetes is a complex group of diseases with a variety of causes. People with diabetes have high blood glucose, also called high blood sugar or hyperglycemia.

Diabetes is a disorder of metabolismthe way the body uses digested food for energy. The digestive tract breaks down carbohydratessugars and starches found in many foodsinto glucose, a form of sugar that enters the bloodstream. With the help of the hormone insulin, cells throughout the body absorb glucose and use it for energy. Diabetes develops when the body doesnt make enough insulin or is not able to use insulin effectively, or both.

Insulin is made in the pancreas, an organ located behind the stomach. The pancreas contains clusters of cells called islets. Beta cells within the islets make insulin and release it into the blood.

If beta cells dont produce enough insulin, or the body doesnt respond to the insulin that is present, glucose builds up in the blood instead of being absorbed by cells in the body, leading to prediabetes or diabetes. Prediabetes is a condition in which blood glucose levels or A1C levelswhich reflect average blood glucose levelsare higher than normal but not high enough to be diagnosed as diabetes. In diabetes, the bodys cells are starved of energy despite high blood glucose levels.

Over time, high blood glucose damages nerves and blood vessels, leading to complications such as heart disease, stroke, kidney disease, blindness, dental disease, and amputations. Other complications of diabetes may include increased susceptibility to other diseases, loss of mobility with aging, depression, and pregnancy problems. No one is certain what starts the processes that cause diabetes, but scientists believe genes and environmental factors interact to cause diabetes in most cases.

The two main types of diabetes are type 1 diabetes and type 2 diabetes. A third type, gestational diabetes, develops only during pregnancy. Other types of diabetes are caused by defects in specific genes, diseases of the pancreas, certain drugs or chemicals, infections, and other conditions. Some people show signs of both type 1 and type 2 diabetes. </s>


Input: What causes Causes of Diabetes ?

Output:
Type 1 diabetes is caused by a lack of insulin due to the destruction of insulin-producing beta cells in the pancreas. In type 1 diabetesan autoimmune diseasethe bodys immune system attacks and destroys the beta cells. Normally, the immune system protects the body from infection by identifying and destroying bacteria, viruses, and other potentially harmful foreign substances. But in autoimmune diseases, the immune system attacks the bodys own cells. In type 1 diabetes, beta cell destruction may take place over several years, but symptoms of the disease usually develop over a short period of time.

Type 1 diabetes typically occurs in children and young adults, though it can appear at any age. In the past, type 1 diabetes was called juvenile diabetes or insulin-dependent diabetes mellitus.

Latent autoimmune diabetes in adults (LADA) may be a slowly developing kind of type 1 diabetes. Diagnosis usually occurs after age 30. In LADA, as in type 1 diabetes, the bodys immune system destroys the beta cells. At the time of diagnosis, people with LADA may still produce their own insulin, but eventually most will need insulin shots or an insulin pump to control blood glucose levels.

Genetic Susceptibility

Heredity plays an important part in determining who is likely to develop type 1 diabetes. Genes are passed down from biological parent to child. Genes carry instructions for making proteins that are needed for the bodys cells to function. Many genes, as well as interactions among genes, are thought to influence susceptibility to and protection from type 1 diabetes. The key genes may vary in different population groups. Variations in genes that affect more than 1 percent of a population group are called gene variants.

Certain gene variants that carry instructions for making proteins called human leukocyte antigens (HLAs) on white blood cells are linked to the risk of developing type 1 diabetes. The proteins produced by HLA genes help determine whether the immune system recognizes a cell as part of the body or as foreign material. Some combinations of HLA gene variants predict that a person will be at higher risk for type 1 diabetes, while other combinations are protective or have no effect on risk.

While HLA genes are the major risk genes for type 1 diabetes, many additional risk genes or gene regions have been found. Not only can these genes help identify people at risk for type 1 diabetes, but they also provide important clues to help scientists better understand how the disease develops and identify potential targets for therapy and prevention.

Genetic testing can show what types of HLA genes a person carries and can reveal other genes linked to diabetes. However, most genetic testing is done in a research setting and is not yet available to individuals. Scientists are studying how the results of genetic testing can be used to improve type 1 diabetes prevention or treatment.

Autoimmune Destruction of Beta Cells

In type 1 diabetes, white blood cells called T cells attack and destroy beta cells. The process begins well before diabetes symptoms appear and continues after diagnosis. Often, type 1 diabetes is not diagnosed until most beta cells have already been destroyed. At this point, a person needs daily insulin treatment to survive. Finding ways to modify or stop this autoimmune process and preserve beta cell function is a major focus of current scientific research.

Recent research suggests insulin itself may be a key trigger of the immune attack on beta cells. The immune systems of people who are susceptible to developing type 1 diabetes respond to insulin as if it were a foreign substance, or antigen. To combat antigens, the body makes proteins called antibodies. Antibodies to insulin and other proteins produced by beta cells are found in people with type 1 diabetes. Researchers test for these antibodies to help identify people at increased risk of developing the disease. Testing the types and levels of antibodies in the blood can help determine whether a person has type 1 diabetes, LADA, or another type of diabetes.

Environmental Factors

Environmental factors, such as foods, viruses, and toxins, may play a role in the development of type 1 diabetes, but the exact nature of their role has not been determined. Some theories suggest that environmental factors trigger the autoimmune destruction of beta cells in people with a genetic susceptibility to diabetes. Other theories suggest that environmental factors play an ongoing role in diabetes, even after diagnosis.

Viruses and infections. A virus cannot cause diabetes on its own, but people are sometimes diagnosed with type 1 diabetes during or after a viral infection, suggesting a link between the two. Also, the onset of type 1 diabetes occurs more frequently during the winter when viral infections are more common. Viruses possibly associated with type 1 diabetes include coxsackievirus B, cytomegalovirus, adenovirus, rubella, and mumps. Scientists have described several ways these viruses may damage or destroy beta cells or possibly trigger an autoimmune response in susceptible people. For example, anti-islet antibodies have been found in patients with congenital rubella syndrome, and cytomegalovirus has been associated with significant beta cell damage and acute pancreatitisinflammation of the pancreas. Scientists are trying to identify a virus that can cause type 1 diabetes so that a vaccine might be developed to prevent the disease.

Infant feeding practices. Some studies have suggested that dietary factors may raise or lower the risk of developing type 1 diabetes. For example, breastfed infants and infants receiving vitamin D supplements may have a reduced risk of developing type 1 diabetes, while early exposure to cows milk and cereal proteins may increase risk. More research is needed to clarify how infant nutrition affects the risk for type 1 diabetes.

Read more in the Centers for Disease Control and Preventions (CDCs) publication  National Diabetes Statistics Report, 2014 at  www.cdc.gov for information about research studies related to type 1 diabetes. </s>


Input: What causes Causes of Diabetes ?

Output:
Type 2 diabetesthe most common form of diabetesis caused by a combination of factors, including insulin resistance, a condition in which the bodys muscle, fat, and liver cells do not use insulin effectively. Type 2 diabetes develops when the body can no longer produce enough insulin to compensate for the impaired ability to use insulin. Symptoms of type 2 diabetes may develop gradually and can be subtle; some people with type 2 diabetes remain undiagnosed for years.

Type 2 diabetes develops most often in middle-aged and older people who are also overweight or obese. The disease, once rare in youth, is becoming more common in overweight and obese children and adolescents. Scientists think genetic susceptibility and environmental factors are the most likely triggers of type 2 diabetes.

Genetic Susceptibility

Genes play a significant part in susceptibility to type 2 diabetes. Having certain genes or combinations of genes may increase or decrease a persons risk for developing the disease. The role of genes is suggested by the high rate of type 2 diabetes in families and identical twins and wide variations in diabetes prevalence by ethnicity. Type 2 diabetes occurs more frequently in African Americans, Alaska Natives, American Indians, Hispanics/Latinos, and some Asian Americans, Native Hawaiians, and Pacific Islander Americans than it does in non-Hispanic whites.

Recent studies have combined genetic data from large numbers of people, accelerating the pace of gene discovery. Though scientists have now identified many gene variants that increase susceptibility to type 2 diabetes, the majority have yet to be discovered. The known genes appear to affect insulin production rather than insulin resistance. Researchers are working to identify additional gene variants and to learn how they interact with one another and with environmental factors to cause diabetes.

Studies have shown that variants of the TCF7L2 gene increase susceptibility to type 2 diabetes. For people who inherit two copies of the variants, the risk of developing type 2 diabetes is about 80 percent higher than for those who do not carry the gene variant.1 However, even in those with the variant, diet and physical activity leading to weight loss help delay diabetes, according to the Diabetes Prevention Program (DPP), a major clinical trial involving people at high risk.

Genes can also increase the risk of diabetes by increasing a persons tendency to become overweight or obese. One theory, known as the thrifty gene hypothesis, suggests certain genes increase the efficiency of metabolism to extract energy from food and store the energy for later use. This survival trait was advantageous for populations whose food supplies were scarce or unpredictable and could help keep people alive during famine. In modern times, however, when high-calorie foods are plentiful, such a trait can promote obesity and type 2 diabetes.

Obesity and Physical Inactivity

Physical inactivity and obesity are strongly associated with the development of type 2 diabetes. People who are genetically susceptible to type 2 diabetes are more vulnerable when these risk factors are present.

An imbalance between caloric intake and physical activity can lead to obesity, which causes insulin resistance and is common in people with type 2 diabetes. Central obesity, in which a person has excess abdominal fat, is a major risk factor not only for insulin resistance and type 2 diabetes but also for heart and blood vessel disease, also called cardiovascular disease (CVD). This excess belly fat produces hormones and other substances that can cause harmful, chronic effects in the body such as damage to blood vessels.

The DPP and other studies show that millions of people can lower their risk for type 2 diabetes by making lifestyle changes and losing weight. The DPP proved that people with prediabetesat high risk of developing type 2 diabetescould sharply lower their risk by losing weight through regular physical activity and a diet low in fat and calories. In 2009, a follow-up study of DPP participantsthe Diabetes Prevention Program Outcomes Study (DPPOS)showed that the benefits of weight loss lasted for at least 10 years after the original study began.2

Read more about the DPP, funded under National Institutes of Health (NIH) clinical trial number NCT00004992, and the DPPOS, funded under NIH clinical trial number NCT00038727 in  Diabetes Prevention Program.

Insulin Resistance

Insulin resistance is a common condition in people who are overweight or obese, have excess abdominal fat, and are not physically active. Muscle, fat, and liver cells stop responding properly to insulin, forcing the pancreas to compensate by producing extra insulin. As long as beta cells are able to produce enough insulin, blood glucose levels stay in the normal range. But when insulin production falters because of beta cell dysfunction, glucose levels rise, leading to prediabetes or diabetes.

Abnormal Glucose Production by the Liver

In some people with diabetes, an abnormal increase in glucose production by the liver also contributes to high blood glucose levels. Normally, the pancreas releases the hormone glucagon when blood glucose and insulin levels are low. Glucagon stimulates the liver to produce glucose and release it into the bloodstream. But when blood glucose and insulin levels are high after a meal, glucagon levels drop, and the liver stores excess glucose for later, when it is needed. For reasons not completely understood, in many people with diabetes, glucagon levels stay higher than needed. High glucagon levels cause the liver to produce unneeded glucose, which contributes to high blood glucose levels. Metformin, the most commonly used drug to treat type 2 diabetes, reduces glucose production by the liver.

The Roles of Insulin and Glucagon in Normal Blood Glucose Regulation

A healthy persons body keeps blood glucose levels in a normal range through several complex mechanisms. Insulin and glucagon, two hormones made in the pancreas, help regulate blood glucose levels:

- Insulin, made by beta cells, lowers elevated blood glucose levels.  - Glucagon, made by alpha cells, raises low blood glucose levels.

- Insulin helps muscle, fat, and liver cells absorb glucose from the bloodstream, lowering blood glucose levels.  - Insulin stimulates the liver and muscle tissue to store excess glucose. The stored form of glucose is called glycogen.  - Insulin also lowers blood glucose levels by reducing glucose production in the liver.

- Glucagon signals the liver and muscle tissue to break down glycogen into glucose, which enters the bloodstream and raises blood glucose levels.  - If the body needs more glucose, glucagon stimulates the liver to make glucose from amino acids.

Metabolic Syndrome

Metabolic syndrome, also called insulin resistance syndrome, refers to a group of conditions common in people with insulin resistance, including

- higher than normal blood glucose levels  - increased waist size due to excess abdominal fat  - high blood pressure  - abnormal levels of cholesterol and triglycerides in the blood

Cell Signaling and Regulation

Cells communicate through a complex network of molecular signaling pathways. For example, on cell surfaces, insulin receptor molecules capture, or bind, insulin molecules circulating in the bloodstream. This interaction between insulin and its receptor prompts the biochemical signals that enable the cells to absorb glucose from the blood and use it for energy.

Problems in cell signaling systems can set off a chain reaction that leads to diabetes or other diseases. Many studies have focused on how insulin signals cells to communicate and regulate action. Researchers have identified proteins and pathways that transmit the insulin signal and have mapped interactions between insulin and body tissues, including the way insulin helps the liver control blood glucose levels. Researchers have also found that key signals also come from fat cells, which produce substances that cause inflammation and insulin resistance.

This work holds the key to combating insulin resistance and diabetes. As scientists learn more about cell signaling systems involved in glucose regulation, they will have more opportunities to develop effective treatments.

Beta Cell Dysfunction

Scientists think beta cell dysfunction is a key contributor to type 2 diabetes. Beta cell impairment can cause inadequate or abnormal patterns of insulin release. Also, beta cells may be damaged by high blood glucose itself, a condition called glucose toxicity.

Scientists have not determined the causes of beta cell dysfunction in most cases. Single gene defects lead to specific forms of diabetes called maturity-onset diabetes of the young (MODY). The genes involved regulate insulin production in the beta cells. Although these forms of diabetes are rare, they provide clues as to how beta cell function may be affected by key regulatory factors. Other gene variants are involved in determining the number and function of beta cells. But these variants account for only a small percentage of type 2 diabetes cases. Malnutrition early in life is also being investigated as a cause of beta cell dysfunction. The metabolic environment of the developing fetus may also create a predisposition for diabetes later in life.

Risk Factors for Type 2 Diabetes

People who develop type 2 diabetes are more likely to have the following characteristics:

- age 45 or older  - overweight or obese  - physically inactive  - parent or sibling with diabetes  - family background that is African American, Alaska Native, American Indian, Asian American, Hispanic/Latino, or Pacific Islander American  - history of giving birth to a baby weighing more than 9 pounds  - history of gestational diabetes  - high blood pressure140/90 or aboveor being treated for high blood pressure  - high-density lipoprotein (HDL), or good, cholesterol below 35 milligrams per deciliter (mg/dL), or a triglyceride level above 250 mg/dL  - polycystic ovary syndrome, also called PCOS  - prediabetesan A1C level of 5.7 to 6.4 percent; a fasting plasma glucose test result of 100125 mg/dL, called impaired fasting glucose; or a 2-hour oral glucose tolerance test result of 140199, called impaired glucose tolerance  - acanthosis nigricans, a condition associated with insulin resistance, characterized by a dark, velvety rash around the neck or armpits  - history of CVD

The American Diabetes Association (ADA) recommends that testing to detect prediabetes and type 2 diabetes be considered in adults who are overweight or obese and have one or more additional risk factors for diabetes. In adults without these risk factors, testing should begin at age 45. </s>


Input: What causes Causes of Diabetes ?

Output:
Insulin Resistance and Beta Cell Dysfunction

Hormones produced by the placenta and other pregnancy-related factors contribute to insulin resistance, which occurs in all women during late pregnancy. Insulin resistance increases the amount of insulin needed to control blood glucose levels. If the pancreas cant produce enough insulin due to beta cell dysfunction, gestational diabetes occurs.

As with type 2 diabetes, excess weight is linked to gestational diabetes. Overweight or obese women are at particularly high risk for gestational diabetes because they start pregnancy with a higher need for insulin due to insulin resistance. Excessive weight gain during pregnancy may also increase risk.

Family History

Having a family history of diabetes is also a risk factor for gestational diabetes, suggesting that genes play a role in its development. Genetics may also explain why the disorder occurs more frequently in African Americans, American Indians, and Hispanics/Latinos. Many gene variants or combinations of variants may increase a womans risk for developing gestational diabetes. Studies have found several gene variants associated with gestational diabetes, but these variants account for only a small fraction of women with gestational diabetes.

Future Risk of Type 2 Diabetes

Because a womans hormones usually return to normal levels soon after giving birth, gestational diabetes disappears in most women after delivery. However, women who have gestational diabetes are more likely to develop gestational diabetes with future pregnancies and develop type 2 diabetes.3 Women with gestational diabetes should be tested for persistent diabetes 6 to 12 weeks after delivery and at least every 3 years thereafter.

Also, exposure to high glucose levels during gestation increases a childs risk for becoming overweight or obese and for developing type 2 diabetes later on. The result may be a cycle of diabetes affecting multiple generations in a family. For both mother and child, maintaining a healthy body weight and being physically active may help prevent type 2 diabetes. </s>


Input: What causes Causes of Diabetes ?

Output:
Other types of diabetes have a variety of possible causes.

Genetic Mutations Affecting Beta Cells, Insulin, and Insulin Action

Some relatively uncommon forms of diabetes known as monogenic diabetes are caused by mutations, or changes, in a single gene. These mutations are usually inherited, but sometimes the gene mutation occurs spontaneously. Most of these gene mutations cause diabetes by reducing beta cells ability to produce insulin.

The most common types of monogenic diabetes are neonatal diabetes mellitus (NDM) and MODY. NDM occurs in the first 6 months of life. MODY is usually found during adolescence or early adulthood but sometimes is not diagnosed until later in life. More information about NDM and MODY is provided in the NIDDK health topic, Monogenic Forms of Diabetes.

Other rare genetic mutations can cause diabetes by damaging the quality of insulin the body produces or by causing abnormalities in insulin receptors.

Other Genetic Diseases

Diabetes occurs in people with Down syndrome, Klinefelter syndrome, and Turner syndrome at higher rates than the general population. Scientists are investigating whether genes that may predispose people to genetic syndromes also predispose them to diabetes.

The genetic disorders cystic fibrosis and hemochromatosis are linked to diabetes. Cystic fibrosis produces abnormally thick mucus, which blocks the pancreas. The risk of diabetes increases with age in people with cystic fibrosis. Hemochromatosis causes the body to store too much iron. If the disorder is not treated, iron can build up in and damage the pancreas and other organs.

Damage to or Removal of the Pancreas

Pancreatitis, cancer, and trauma can all harm the pancreatic beta cells or impair insulin production, thus causing diabetes. If the damaged pancreas is removed, diabetes will occur due to the loss of the beta cells.

Endocrine Diseases

Endocrine diseases affect organs that produce hormones. Cushings syndrome and acromegaly are examples of hormonal disorders that can cause prediabetes and diabetes by inducing insulin resistance. Cushings syndrome is marked by excessive production of cortisolsometimes called the stress hormone. Acromegaly occurs when the body produces too much growth hormone. Glucagonoma, a rare tumor of the pancreas, can also cause diabetes. The tumor causes the body to produce too much glucagon. Hyperthyroidism, a disorder that occurs when the thyroid gland produces too much thyroid hormone, can also cause elevated blood glucose levels.

Autoimmune Disorders

Rare disorders characterized by antibodies that disrupt insulin action can lead to diabetes. This kind of diabetes is often associated with other autoimmune disorders such as lupus erythematosus. Another rare autoimmune disorder called stiff-man syndrome is associated with antibodies that attack the beta cells, similar to type 1 diabetes.

Medications and Chemical Toxins

Some medications, such as nicotinic acid and certain types of diuretics, anti-seizure drugs, psychiatric drugs, and drugs to treat human immunodeficiency virus (HIV), can impair beta cells or disrupt insulin action. Pentamidine, a drug prescribed to treat a type of pneumonia, can increase the risk of pancreatitis, beta cell damage, and diabetes. Also, glucocorticoidssteroid hormones that are chemically similar to naturally produced cortisolmay impair insulin action. Glucocorticoids are used to treat inflammatory illnesses such as rheumatoid arthritis, asthma, lupus, and ulcerative colitis.

Many chemical toxins can damage or destroy beta cells in animals, but only a few have been linked to diabetes in humans. For example, dioxina contaminant of the herbicide Agent Orange, used during the Vietnam Warmay be linked to the development of type 2 diabetes. In 2000, based on a report from the Institute of Medicine, the U.S. Department of Veterans Affairs (VA) added diabetes to the list of conditions for which Vietnam veterans are eligible for disability compensation. Also, a chemical in a rat poison no longer in use has been shown to cause diabetes if ingested. Some studies suggest a high intake of nitrogen-containing chemicals such as nitrates and nitrites might increase the risk of diabetes. Arsenic has also been studied for possible links to diabetes.

Lipodystrophy

Lipodystrophy is a condition in which fat tissue is lost or redistributed in the body. The condition is associated with insulin resistance and type 2 diabetes. </s>


Input: What causes Causes of Diabetes ?

Output:
Other types of diabetes have a variety of possible causes.

Genetic Mutations Affecting Beta Cells, Insulin, and Insulin Action

Some relatively uncommon forms of diabetes known as monogenic diabetes are caused by mutations, or changes, in a single gene. These mutations are usually inherited, but sometimes the gene mutation occurs spontaneously. Most of these gene mutations cause diabetes by reducing beta cells ability to produce insulin.

The most common types of monogenic diabetes are neonatal diabetes mellitus (NDM) and MODY. NDM occurs in the first 6 months of life. MODY is usually found during adolescence or early adulthood but sometimes is not diagnosed until later in life. More information about NDM and MODY is provided in the NIDDK health topic, Monogenic Forms of Diabetes.

Other rare genetic mutations can cause diabetes by damaging the quality of insulin the body produces or by causing abnormalities in insulin receptors.

Other Genetic Diseases

Diabetes occurs in people with Down syndrome, Klinefelter syndrome, and Turner syndrome at higher rates than the general population. Scientists are investigating whether genes that may predispose people to genetic syndromes also predispose them to diabetes.

The genetic disorders cystic fibrosis and hemochromatosis are linked to diabetes. Cystic fibrosis produces abnormally thick mucus, which blocks the pancreas. The risk of diabetes increases with age in people with cystic fibrosis. Hemochromatosis causes the body to store too much iron. If the disorder is not treated, iron can build up in and damage the pancreas and other organs.

Damage to or Removal of the Pancreas

Pancreatitis, cancer, and trauma can all harm the pancreatic beta cells or impair insulin production, thus causing diabetes. If the damaged pancreas is removed, diabetes will occur due to the loss of the beta cells.

Endocrine Diseases

Endocrine diseases affect organs that produce hormones. Cushings syndrome and acromegaly are examples of hormonal disorders that can cause prediabetes and diabetes by inducing insulin resistance. Cushings syndrome is marked by excessive production of cortisolsometimes called the stress hormone. Acromegaly occurs when the body produces too much growth hormone. Glucagonoma, a rare tumor of the pancreas, can also cause diabetes. The tumor causes the body to produce too much glucagon. Hyperthyroidism, a disorder that occurs when the thyroid gland produces too much thyroid hormone, can also cause elevated blood glucose levels.

Autoimmune Disorders

Rare disorders characterized by antibodies that disrupt insulin action can lead to diabetes. This kind of diabetes is often associated with other autoimmune disorders such as lupus erythematosus. Another rare autoimmune disorder called stiff-man syndrome is associated with antibodies that attack the beta cells, similar to type 1 diabetes.

Medications and Chemical Toxins

Some medications, such as nicotinic acid and certain types of diuretics, anti-seizure drugs, psychiatric drugs, and drugs to treat human immunodeficiency virus (HIV), can impair beta cells or disrupt insulin action. Pentamidine, a drug prescribed to treat a type of pneumonia, can increase the risk of pancreatitis, beta cell damage, and diabetes. Also, glucocorticoidssteroid hormones that are chemically similar to naturally produced cortisolmay impair insulin action. Glucocorticoids are used to treat inflammatory illnesses such as rheumatoid arthritis, asthma, lupus, and ulcerative colitis.

Many chemical toxins can damage or destroy beta cells in animals, but only a few have been linked to diabetes in humans. For example, dioxina contaminant of the herbicide Agent Orange, used during the Vietnam Warmay be linked to the development of type 2 diabetes. In 2000, based on a report from the Institute of Medicine, the U.S. Department of Veterans Affairs (VA) added diabetes to the list of conditions for which Vietnam veterans are eligible for disability compensation. Also, a chemical in a rat poison no longer in use has been shown to cause diabetes if ingested. Some studies suggest a high intake of nitrogen-containing chemicals such as nitrates and nitrites might increase the risk of diabetes. Arsenic has also been studied for possible links to diabetes.

Lipodystrophy

Lipodystrophy is a condition in which fat tissue is lost or redistributed in the body. The condition is associated with insulin resistance and type 2 diabetes. </s>


Input: What to do for Causes of Diabetes ?

Output: - Diabetes is a complex group of diseases with a variety of causes. Scientists believe genes and environmental factors interact to cause diabetes in most cases.  - People with diabetes have high blood glucose, also called high blood sugar or hyperglycemia. Diabetes develops when the body doesnt make enough insulin or is not able to use insulin effectively, or both.  - Insulin is a hormone made by beta cells in the pancreas. Insulin helps cells throughout the body absorb and use glucose for energy. If the body does not produce enough insulin or cannot use insulin effectively, glucose builds up in the blood instead of being absorbed by cells in the body, and the body is starved of energy.  - Prediabetes is a condition in which blood glucose levels or A1C levels are higher than normal but not high enough to be diagnosed as diabetes. People with prediabetes can substantially reduce their risk of developing diabetes by losing weight and increasing physical activity.  - The two main types of diabetes are type 1 diabetes and type 2 diabetes. Gestational diabetes is a third form of diabetes that develops only during pregnancy.  - Type 1 diabetes is caused by a lack of insulin due to the destruction of insulin-producing beta cells. In type 1 diabetesan autoimmune diseasethe bodys immune system attacks and destroys the beta cells.  - Type 2 diabetesthe most common form of diabetesis caused by a combination of factors, including insulin resistance, a condition in which the bodys muscle, fat, and liver cells do not use insulin effectively. Type 2 diabetes develops when the body can no longer produce enough insulin to compensate for the impaired ability to use insulin.  - Scientists believe gestational diabetes is caused by the hormonal changes and metabolic demands of pregnancy together with genetic and environmental factors. Risk factors for gestational diabetes include being overweight and having a family history of diabetes.  - Monogenic forms of diabetes are relatively uncommon and are caused by mutations in single genes that limit insulin production, quality, or action in the body.  - Other types of diabetes are caused by diseases and injuries that damage the pancreas; certain chemical toxins and medications; infections; and other conditions. </s>


Input: What is (are) Childhood Nephrotic Syndrome ?

Output:
Childhood nephrotic syndrome is not a disease in itself; rather, it is a group of symptoms that

- indicate kidney damageparticularly damage to the glomeruli, the tiny units within the kidney where blood is filtered  - result in the release of too much protein from the body into the urine

When the kidneys are damaged, the protein albumin, normally found in the blood, will leak into the urine. Proteins are large, complex molecules that perform a number of important functions in the body.

The two types of childhood nephrotic syndrome are

- primarythe most common type of childhood nephrotic syndrome, which begins in the kidneys and affects only the kidneys  - secondarythe syndrome is caused by other diseases

A health care provider may refer a child with nephrotic syndrome to a nephrologista doctor who specializes in treating kidney disease. A child should see a pediatric nephrologist, who has special training to take care of kidney problems in children, if possible. However, in many parts of the country, pediatric nephrologists are in short supply, so the child may need to travel. If traveling is not possible, some nephrologists who treat adults can also treat children. </s>


Input: What is (are) Childhood Nephrotic Syndrome ?

Output:
The kidneys are two bean-shaped organs, each about the size of a fist. They are located just below the rib cage, one on each side of the spine. Every day, the kidneys filter about 120 to 150 quarts of blood to produce about 1 to 2 quarts of urine, composed of wastes and extra fluid. Children produce less urine than adults and the amount produced depends on their age. The urine flows from the kidneys to the bladder through tubes called ureters. The bladder stores urine. When the bladder empties, urine flows out of the body through a tube called the urethra, located at the bottom of the bladder.

Kidneys work at the microscopic level. The kidney is not one large filter. Each kidney is made up of about a million filtering units called nephrons. Each nephron filters a small amount of blood. The nephron includes a filter, called the glomerulus, and a tubule. The nephrons work through a two-step process. The glomerulus lets fluid and waste products pass through it; however, it prevents blood cells and large molecules, mostly proteins, from passing. The filtered fluid then passes through the tubule, which sends needed minerals back to the bloodstream and removes wastes. </s>


Input: What causes Childhood Nephrotic Syndrome ?

Output:
While idiopathic, or unknown, diseases are the most common cause of primary childhood nephrotic syndrome, researchers have linked certain diseases and some specific genetic changes that damage the kidneys with primary childhood nephrotic syndrome.

The cause of secondary childhood nephrotic syndrome is an underlying disease or infection. Called a primary illness, its this underlying disease or infection that causes changes in the kidney function that can result in secondary childhood nephrotic syndrome.

Congenital diseasesdiseases that are present at birthcan also cause childhood nephrotic syndrome.

Primary Childhood Nephrotic Syndrome

The following diseases are different types of idiopathic childhood nephrotic syndrome:

- Minimal change disease involves damage to the glomeruli that can be seen only with an electron microscope. This type of microscope shows tiny details better than any other microscope. Scientists do not know the exact cause of minimal change disease. Minimal change disease is the most common cause of idiopathic childhood nephrotic syndrome.1  - Focal segmental glomerulosclerosis is scarring in scattered regions of the kidney:     - Focal means that only some of the glomeruli become scarred.    - Segmental means damage affects only part of an individual glomerulus.    - Membranoproliferative glomerulonephritis is a group of disorders involving deposits of antibodies that build up in the glomeruli, causing thickening and damage. Antibodies are proteins made by the immune system to protect the body from foreign substances such as bacteria or viruses.

Secondary Childhood Nephrotic Syndrome

Some common diseases that can cause secondary childhood nephrotic syndrome include

- diabetes, a condition that occurs when the body cannot use glucosea type of sugarnormally  - Henoch-Schnlein purpura, a disease that causes small blood vessels in the body to become inflamed and leak  - hepatitis, inflammation of the liver caused by a virus  - human immunodeficiency virus (HIV), a virus that alters the immune system  - lupus, an autoimmune disease that occurs when the body attacks its own immune system  - malaria, a disease of the blood that is spread by mosquitos  - streptococcal infection, an infection that results when the bacteria that causes strep throat or a skin infection is left untreated

Other causes of secondary childhood nephrotic syndrome can include certain medications, such as aspirin, ibuprofen, or other nonsteroidal anti-inflammatory drugs, and exposure to chemicals, such as mercury and lithium.

Congenital Diseases and Childhood Nephrotic Syndrome

Congenital nephrotic syndrome is rare and affects infants in the first 3 months of life.2 This type of nephrotic syndrome, sometimes called infantile nephrotic syndrome, can be caused by

- inherited genetic defects, which are problems passed from parent to child through genes  - infections at the time of birth

More information about underlying diseases or infections that cause changes in kidney function is provided in the NIDDK health topic, Glomerular Diseases. </s>


Input: What are the symptoms of Childhood Nephrotic Syndrome ?

Output:
The signs and symptoms of childhood nephrotic syndrome may include

- edemaswelling, most often in the legs, feet, or ankles and less often in the hands or face  - albuminuriawhen a childs urine has high levels of albumin  - hypoalbuminemiawhen a childs blood has low levels of albumin  - hyperlipidemiawhen a childs blood cholesterol and fat levels are higher than normal

In addition, some children with nephrotic syndrome may have

- blood in their urine  - symptoms of infection, such as fever, lethargy, irritability, or abdominal pain  - loss of appetite  - diarrhea  - high blood pressure </s>


Input: What are the complications of Childhood Nephrotic Syndrome ?

Output:
The complications of childhood nephrotic syndrome may include

- infection. When the kidneys are damaged, a child is more likely to develop infections because the body loses proteins that normally protect against infection. Health care providers will prescribe medications to treat infections. Children with childhood nephrotic syndrome should receive the pneumococcal vaccine and yearly flu shots to prevent those infections. Children should also receive age-appropriate vaccinations, although a health care provider may delay certain live vaccines while a child is taking certain medications.  - blood clots. Blood clots can block the flow of blood and oxygen through a blood vessel anywhere in the body. A child is more likely to develop clots when he or she loses proteins through the urine. The health care provider will treat blood clots with blood-thinning medications.  - high blood cholesterol. When albumin leaks into the urine, the albumin levels in the blood drop. The liver makes more albumin to make up for the low levels in the blood. At the same time, the liver makes more cholesterol. Sometimes children may need treatment with medications to lower blood cholesterol levels. </s>


Input: How to diagnose Childhood Nephrotic Syndrome ?

Output:
A health care provider diagnoses childhood nephrotic syndrome with

- a medical and family history  - a physical exam  - urine tests  - a blood test  - ultrasound of the kidney  - kidney biopsy

Medical and Family History

Taking a medical and family history is one of the first things a health care provider may do to help diagnose childhood nephrotic syndrome.

Physical Exam

A physical exam may help diagnose childhood nephrotic syndrome. During a physical exam, a health care provider most often

- examines a childs body  - taps on specific areas of the childs body

Urine Tests

A health care provider may order the following urine tests to help determine if a child has kidney damage from childhood nephrotic syndrome.

Dipstick test for albumin. A dipstick test performed on a urine sample can detect the presence of albumin in the urine, which could mean kidney damage. The child or a caretaker collects a urine sample in a special container. For the test, a nurse or technician places a strip of chemically treated paper, called a dipstick, into the childs urine sample. Patches on the dipstick change color when albumin is present in urine.

Urine albumin-to-creatinine ratio. A health care provider uses this measurement to estimate the amount of albumin passed into the urine over a 24-hour period. The child provides a urine sample during an appointment with the health care provider. Creatinine is a waste product filtered in the kidneys and passed in the urine. A high urine albumin-to-creatinine ratio indicates that the kidneys are leaking large amounts of albumin into the urine.

Blood Test

A blood test involves drawing blood at a health care providers office or a commercial facility and sending the sample to a lab for analysis. The lab tests the sample to estimate how much blood the kidneys filter each minute, called the estimated glomerular filtration rate, or eGFR. The test results help the health care provider determine the amount of kidney damage. Health care providers may also order other blood tests to help determine the underlying disease that may be causing childhood nephrotic syndrome.

Ultrasound of the Kidney

Ultrasound uses a device, called a transducer, that bounces safe, painless sound waves off organs to create an image of their structure. A specially trained technician performs the procedure in a health care providers office, an outpatient center, or a hospital. A radiologista doctor who specializes in medical imaginginterprets the images to see if the kidneys look normal; a child does not need anesthesia.

Kidney Biopsy

Biopsy is a procedure that involves taking a small piece of kidney tissue for examination with a microscope. A health care provider performs the biopsy in an outpatient center or a hospital. The health care provider will give the child light sedation and local anesthetic; however, in some cases, the child will require general anesthesia. A pathologista doctor who specializes in diagnosing diseasesexamines the tissue in a lab. The test can help diagnose childhood nephrotic syndrome.

When the health care provider suspects a child has minimal change disease, he or she often starts treatment with medications without performing a biopsy. If the medication is effective, the child does not need a biopsy. In most cases, a health care provider does not perform a biopsy on children younger than age 12 unless he or she thinks that another disease is the cause. </s>


Input: What are the treatments for Childhood Nephrotic Syndrome ?

Output:
Health care providers will decide how to treat childhood nephrotic syndrome based on the type:

- primary childhood nephrotic syndrome: medications  - secondary childhood nephrotic syndrome: treat the underlying illness or disease  - congenital nephrotic syndrome: medications, surgery to remove one or both kidneys, and transplantation

Primary Childhood Nephrotic Syndrome

Health care providers treat idiopathic childhood nephrotic syndrome with several types of medications that control the immune system, remove extra fluid, and lower blood pressure.

- Control the immune system. Corticosteroids are a group of medications that reduce the activity of the immune system, decrease the amount of albumin lost in the urine, and decrease swelling. Health care providers commonly use prednisone or a related corticosteroid to treat idiopathic childhood nephrotic syndrome. About 90 percent of children achieve remission with daily corticosteroids for 6 weeks and then a slightly smaller dose every other day for 6 weeks.2 Remission is a period when the child is symptom-free.  Many children relapse after initial therapy, and health care providers treat them with a shorter course of corticosteroids until the disease goes into remission again. Children may have multiple relapses; however, they most often recover without long-term kidney damage.  When a child has frequent relapses or does not respond to treatment, a health care provider may prescribe other medications that reduce the activity of the immune system. These medications prevent the body from making antibodies that can damage kidney tissues. They include      - cyclophosphamide    - mycophenolate (CellCept, Myfortic)    - cyclosporine    - tacrolimus (Hecoria, Prograf)   A health care provider may use these other immune system medications with corticosteroids or in place of corticosteroids.  - Remove extra fluid. A health care provider may prescribe a diuretic, a medication that helps the kidneys remove extra fluid from the blood. Removing the extra fluid can often help to lower blood pressure.  - Lower blood pressure. Some children with childhood nephrotic syndrome develop high blood pressure and may need to take additional medications to lower their blood pressure. Two types of blood pressure-lowering medications, angiotensin-converting enzyme inhibitors and angiotensin receptor blockers, have the additional benefit of slowing the progression of kidney disease. Many children with nephrotic syndrome require two or more medications to control their blood pressure.

Secondary Childhood Nephrotic Syndrome

Health care providers treat secondary childhood nephrotic syndrome by treating the underlying cause of the primary illness. For example, a health care provider may treat children by

- prescribing antibiotics for an infection  - adjusting medications to treat lupus, HIV, or diabetes  - changing or stopping medications that are known to cause secondary childhood nephrotic syndrome

While treating the underlying cause, the health care provider will also treat the child to improve or restore kidney function with the same medications used to treat primary childhood nephrotic syndrome.

Caretakers should make sure that children take all prescribed medications and follow the treatment plan recommended by their health care provider.

More information about specific treatments for secondary childhood nephrotic syndrome is provided in the NIDDK health topic, Glomerular Diseases.

Congenital Nephrotic Syndrome

Researchers have found that medications are not effective in treating congenital nephrotic syndrome, and that most children will need a kidney transplant by the time they are 2 or 3 years old. A kidney transplant is surgery to place a healthy kidney from someone who has just died or a living donor, most often a family member, into a persons body to take over the job of the failing kidney. To keep the child healthy until the transplant, the health care provider may recommend the following:

- albumin injections to make up for the albumin lost in urine  - diuretics to help remove extra fluid that causes swelling  - antibiotics to treat the first signs of infection  - growth hormones to promote growth and help bones mature  - removal of one or both kidneys to decrease the loss of albumin in the urine  - dialysis to artificially filter wastes from the blood if the kidneys fail

More information is provided in the NIDDK health topic, Treatment Methods for Kidney Failure in Children. </s>


Input: How to prevent Childhood Nephrotic Syndrome ?

Output: Researchers have not found a way to prevent childhood nephrotic syndrome when the cause is idiopathic or congenital. </s>


Input: What to do for Childhood Nephrotic Syndrome ?

Output:
Children who have nephrotic syndrome may need to make changes to their diet, such as

- limiting the amount of sodium, often from salt, they take in each day  - reducing the amount of liquids they drink each day  - eating a diet low in saturated fat and cholesterol to help control elevated cholesterol levels

Parents or caretakers should talk with the childs health care provider before making any changes to the childs diet.

More information is provided in the NIDDK health topic, Nutrition for Chronic Kidney Disease in Children. </s>


Input: What to do for Childhood Nephrotic Syndrome ?

Output: - Childhood nephrotic syndrome is not a disease in itself; rather, it is a group of symptoms that      - indicate kidney damageparticularly damage to the glomeruli, the tiny units within the kidney where blood is filtered    - result in the release of too much protein from the body into the urine    - The two types of childhood nephrotic syndrome are      - primarythe most common type of childhood nephrotic syndrome, which begins in the kidneys and affects only the kidneys    - secondarythe syndrome is caused by other diseases    - The signs and symptoms of childhood nephrotic syndrome may include      - edemaswelling, most often in the legs, feet, or ankles and less often in the hands or face    - albuminuriawhen a childs urine has high levels of albumin    - hypoalbuminemiawhen a childs blood has low levels of albumin    - hyperlipidemiawhen a childs blood cholesterol and fat levels are higher than normal    - A health care provider may order urine tests to help determine if a child has kidney damage from childhood nephrotic syndrome.  - Health care providers will decide how to treat childhood nephrotic syndrome based on the type:      - primary childhood nephrotic syndrome: medications    - secondary childhood nephrotic syndrome: treat the underlying illness or disease    - congenital nephrotic syndrome: medications, surgery to remove one or both kidneys, or transplantation </s>


Input: What is (are) Renal Tubular Acidosis ?

Output:
Renal tubular acidosis (RTA) is a disease that occurs when the kidneys fail to excrete acids into the urine, which causes a person's blood to remain too acidic. Without proper treatment, chronic acidity of the blood leads to growth retardation, kidney stones, bone disease, chronic kidney disease, and possibly total kidney failure.

The body's cells use chemical reactions to carry out tasks such as turning food into energy and repairing tissue. These chemical reactions generate acids. Some acid in the blood is normal, but too much acidacidosiscan disturb many bodily functions. Healthy kidneys help maintain acid-base balance by excreting acids into the urine and returning bicarbonatean alkaline, or base, substanceto the blood. This "reclaimed" bicarbonate neutralizes much of the acid that is created when food is broken down in the body. The movement of substances like bicarbonate between the blood and structures in the kidneys is called transport.

One researcher has theorized that Charles Dickens may have been describing a child with RTA in the character of Tiny Tim from A Christmas Carol. Tiny Tim's small stature, malformed limbs, and periods of weakness are all possible consequences of the chemical imbalance caused by RTA.1 In the story, Tiny Tim recovers when he receives medical treatment, which would likely have included sodium bicarbonate and sodium citrate, alkaline agents to neutralize acidic blood. The good news is that medical treatment can indeed reverse the effects of RTA. </s>


Input: What is (are) Renal Tubular Acidosis ?

Output:
Renal tubular acidosis (RTA) is a disease that occurs when the kidneys fail to excrete acids into the urine, which causes a person's blood to remain too acidic. Without proper treatment, chronic acidity of the blood leads to growth retardation, kidney stones, bone disease, chronic kidney disease, and possibly total kidney failure.

The body's cells use chemical reactions to carry out tasks such as turning food into energy and repairing tissue. These chemical reactions generate acids. Some acid in the blood is normal, but too much acidacidosiscan disturb many bodily functions. Healthy kidneys help maintain acid-base balance by excreting acids into the urine and returning bicarbonatean alkaline, or base, substanceto the blood. This "reclaimed" bicarbonate neutralizes much of the acid that is created when food is broken down in the body. The movement of substances like bicarbonate between the blood and structures in the kidneys is called transport.

One researcher has theorized that Charles Dickens may have been describing a child with RTA in the character of Tiny Tim from A Christmas Carol. Tiny Tim's small stature, malformed limbs, and periods of weakness are all possible consequences of the chemical imbalance caused by RTA.1 In the story, Tiny Tim recovers when he receives medical treatment, which would likely have included sodium bicarbonate and sodium citrate, alkaline agents to neutralize acidic blood. The good news is that medical treatment can indeed reverse the effects of RTA. </s>


Input: How to diagnose Renal Tubular Acidosis ?

Output: To diagnose RTA, doctors check the acid-base balance in blood and urine samples. If the blood is more acidic than it should be and the urine less acidic than it should be, RTA may be the reason, but additional information is needed to rule out other causes. If RTA is the reason, additional information about the sodium, potassium, and chloride levels in the urine and the potassium level in the blood will help identify which type of RTA a person has. In all cases, the first goal of therapy is to neutralize acid in the blood, but different treatments may be needed to address the different underlying causes of acidosis. </s>


Input: How to diagnose Renal Tubular Acidosis ?

Output: To diagnose RTA, doctors check the acid-base balance in blood and urine samples. If the blood is more acidic than it should be and the urine less acidic than it should be, RTA may be the reason, but additional information is needed to rule out other causes. If RTA is the reason, additional information about the sodium, potassium, and chloride levels in the urine and the potassium level in the blood will help identify which type of RTA a person has. In all cases, the first goal of therapy is to neutralize acid in the blood, but different treatments may be needed to address the different underlying causes of acidosis. </s>