Mesothelioma Chat Room

Actos and Bladder Cancer : The urinary system (Figure i-i) is very important and has a pretty tough job to do in everyone’s body. It filters your blood and produces waste products in the form of urine. More importantly, it allows you to store urine until it is convenient to urinate. Just think, if we couldn’t store urine, then we would constantly leak waste products. This would make life very difficult and get in the way of things we do during the course of a normal day. The human urinary system is made up of the kidneys, ureters, bladder, and urethra. Men have a prostate gland in addition to the previously mentioned components.

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Your kidneys are two bean-shaped organs that reside in the rear of your abdomen, just under the diaphragm on the left and below the liver on your right side. The kidneys filter blood and produce urine. They are extremely important to life and work extremely hard to filter waste from your bloodstream. Just imagine, the kidneys filter approximately 20 percent of your blood each minute. Although most people have two kidneys, some individuals have one and do just fine. The kidneys function independently, and when one is not working as well, the other compensates and filters more blood. In addition to filtering blood and producing urine, your kidneys help to regulate your blood pressure. They produce special hormones and control the salt and water balance in your body. Normally, the kidneys do not release blood cells into urine. This is why it’s important to be evaluated by a doctor if you have blood in your urine.

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URETERS

After urine is formed by the kidneys, special nerves and muscles in the renal pelvis propel urine downward into the ureters. The ureters are small tubes, very much like the renal pelvis, that allow passage of urine from die kidneys down to the bladder. They function as drainage pipes for the kidney. The ureters have nerves and layers of muscle that propel urine to the bladder. There is so much that your body does that you may not realize. Like the renal pelvis, the ureters are also lined with transitional cells serving as a continuation of die uxothelium.

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BLADDER

The ureters connect to the bladder, which is a muscular, balloon-lilce structure in the pelvis. The bladder functions as the storage unit of the urinary system. It can hold upward of 500-600 mL (2 cups) of urine. Hie bladder is very thick and elastic with multiple layers .

An inner layer made up of transitional cells forming the urothelium; under this lies a thin layer (the lamina propria), with blood vessels supplying the bladder; and finally a thick muscular layer that contracts to empty your bladder. There is a layer of fat surrounding the muscular layer.

The bladder expands in relation to the amount of fluid inside of it Bladder contraction is under complex control by your central nervous system. When your bladder contracts during urination, urine passes though the urethra before leaving your body. The inner cells, closest to the bladder, are transitional cells, whereas the cells closest to the outside of the body are squamous cells resembling skin. Although the urethra has different lengths in men and women, it functions the same. In men, the urethra passes through the prostate gland near the bladder.

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PROSTATE

The prostate, a walnut-sized organ that lies at the base of the bladder in men, plays a role in male fertility. Along with the seminal vesicles, the prostate gland produces fluid that helps sperm after ejaculation. Although the urethra passes through the prostate, the gland itself does not add much, if anything, to the volume of urine that reaches the bladder. As the urethra passes through the prostate, it is lined by transitional cells comprising the urothelium. Therefore, tilings that affect the urothelium can affect the prostate as well. This is very important when it comes to staging bladder cancer.

The urethra is a hollow tube lined with transitional cells at its beginning that connects the bladder to the outside world. The structure of the urethra is different in men and women. The urethra is short in women and is much longer in men due to the presence of the penis. The cells lining the

urethra change along its length. The inner cells, closest to the

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Our use of the term or terms Actos and Bladder Cancer is for descriptive purposes only. There is no relationship between the owners of this website and the maker of the product discussed in this post. Our use of the words Recall, Class Action Lawsuit and other similar words related to an event do not necessarily mean that this event has occurred. Refer to the website of the United States Food and Drug Administration for information on drug or medical device recalls. If a Class Action Lawsuit is formed in relation to the product discussed in this post we will provide that information at the time the Class Action is formed. A Class Action Lawsuit is not required to exist for you to file a lawsuit if you have been injured by the product discussed in this post.

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Multaq Attorneys :

Is Primary Sclerosing Cholangitis Linked to Cancer?

Two possible malignancies are linked to primary sclerosing cholangitis. One is cholangiocarcinoma, or cancer of the bile ducts, and the second is colon cancer. Primary sclerosing cholangitis patients have a 10 to 15 percent lifetime chance of developing cancer in the bile ducts, most often when they have inflammatory bowel disease or cirrhosis. With a higher risk of colon cancer as well (especially patients with both PSC and ulcerative colitis), PSC patients are strongly advised to have annual colonoscopies.

Can Primary Sclerosing Cholangitis Be Cured?

Primary sclerosing cholangitis is an incurable disease, but its symptoms can be treated and its progression slowed. To resolve itching, patients should sample the range of available medications, including prescription medications such as cholestyramine (Questran), which binds bile salts in the intestine and allows them to be eliminated with stool, thereby reducing their accumulation in the liver and skin.

More serious complications of primary sclerosing cholangitis are osteoporosis and osteomalacia (bone-calcium deficiency). Patients are advised to increase their intake of calcium with vitamin D to boost absorption and to consider bone-density medications if these conditions are noted on a bone-density scan.

Gallstones, another complication frequently seen in primary sclerosing cholangitis patients, can be treated as they are in patients who do not have PSC.

If infections occur in the bile ducts, they should be treated with antibiotics. Restricted salt intake as well as use of diuretics can help reduce swelling of the abdomen and feet, once PSC becomes cirrhosis. Patients who are deficient in vitamins A, D, and K can supplement their diets.

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So How Do You Treat Primary Sclerosing Cholangitis?

One of the most successful treatments for primary sclerosing cholangitis is balloon dilation, or stenting, a procedure used to open narrowed bile ducts. During stenting, the physician places a small balloon-tipped tube into the constricted duct; once it is in place, the balloon is inflated to open up the duct and permit bile flow. Success rates of up to 85 percent have been reported with the initial dilation. Stents, or plastic tubes, are often inserted into the ducts to keep them open. In spite of this, renarrowing occurs in up to half of patients, so the procedure usually must be repeated and the stents need to be changed.

Only one drug, ursodeoxycholic acid (marketed as Ursodiol and Actigall), is used to treat PSC patients. However, it has not been definitively shown to improve survival or to delay the need for transplantation.

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chronic liver disease. The survival rate for liver-transplant patients is now well over 90 percent, and transplant patients can expect a high quality of life after their recovery. Patients like Ben, whose symptoms can be managed for years with medications and supplements, can have every expectation of maintaining their normal life expectancies.

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Multaq Warning :Organ transplants strike most people as exotic procedures, but the fact is that liver transplants have been around for about 40 years. The first successful transplant was performed in 1968, and since then this surgery has become almost routine. Even better, the success rate of this transplant has become increasingly predictable, with transplant patients surviving two decades or more after their surgeries. In the vast majority of cases, the patients lead normal lives, with no restriction on vigorous work and play.

About 5,000 liver transplants are performed in the United States each year, at more than 125 transplant centers. When a doctor estimates that the patient cannot live more than two years without a new liver, he or she will enter the patient’s name on the waiting list for a new organ. Indications of liver failure (such as worsening jaundice) or of advanced cirrhosis (such as ascites or encephalophathy) justify a referral, and patients whose chronic liver disease has progressed to liver cancer should also be evaluated for a transplant. Physicians may even order evaluations when the patients symptoms, such as pruritus or fatigue, are dramatically affecting the patient’s quality of life, even if the disease itself may not have progressed to the transplant stage.

Some patients, unfortunately, will not qualify for a transplant because they exhibit certain conditions, known as absolute contraindications, that would prevent the transplants success. Among the absolute contraindications are serious heart or lung disease, active uncontrolled infection, active alcohol or drug abuse, AIDS (but not HIV), metastatic liver cancer (liver cancer that has spread to other parts of the body), and cancer elsewhere that did not originate in the liver.

Borderline candidates for successful transplants are patients who display relative contraindications. These patients are not necessarily denied referrals for a new liver, but they are evaluated very carefully and may or may not be granted a transplant if they exhibit morbid obesity, failed kidneys, advanced age (older than 70 years, with disease of other organs), previous cancer in any organ, malnutrition, HIV, extensive portal vein thrombosis (a blood clot in the portal vein), or a failure thus far to adhere to physicians’ medication or wellness regimens.

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The doctors approval is a patient’s first step toward obtaining a new liver. The patients next step is a meeting with the transplant team-—-liver specialists (hepatologists), a transplant surgeon, an anesthesiologist, a social worker, a psychiatrist, and possibly other doctors, such as heart or lung specialists, depending on the patient’s condition—and an evaluation by the team. Additional MRIs and diagnostic tests such as a colonoscopy, blood tests, and upper endoscopy (to check for esophageal varices) are ordered, and if the medical team concludes that the patient is a suitable candidate for a transplant, he or she is added to a waiting list.

In 2002, the system for distributing new livers was revised. The old system had been widely criticized because of the public’s perception of inequalities based on fame and or financial status. The new system, the Model for End-Stage Liver Disease (MELD), is a mathematical score that does not recognize celebrity or favoritism. Instead, the MELD score calculates the severity of the patient’s liver disease on the basis of the mathematical probability (derived from the results of three blood tests) of the patients dying within three months without a transplant. Patients with liver cancer receive a different MELD score, which measures the status of the cancer. Simply put, the sickest patient gets the new liver.

During the waiting period, patients should be as active as possible because their strength and stamina will be a tremendous help to them in their recovery from the surgery.

Patients who are not hospitalized while waiting for a liver are asked to carry a beeper or a cellular phone so the transplant team can notify them immediately when a liver is located. The transplant center performing the surgery must accept the liver within one hour of it being offered, and if the hospital staff cannot contact the patient, they will call (or beep) the next patient on the list. If the transplant recipient is feeling well when the call comes, with no fever or signs of a developing illness, then he or she should proceed to the transplant center immediately. Considerations such as babysitters, pet care, transportation to the hospital, and a packed suitcase should be arranged in advance so the patient can leave at a moment’s notice.

In the case of complete transplants-—-that is, when the donor’s entire liver is transplanted into the recipient-—-the donor will be a newly deceased or a brain-dead person with a healthy heart and circulatory system. A family member of the donor will have signed a consent form for the donation. However, even if the donor had, in life, indicated a wish to donate his or her liver, several factors can prevent the donation: If the prospective donor has been diagnosed with cancer, AIDS, or active hepatitis B, or tests positive for HIV, then that person’s liver cannot be used. In addition, the donor’s liver function tests should typically be in the normal range, and the liver shouldn’t contain more than 30 percent fat, as fatty livers typically are rejected by the recipients body shortly after the transplant. The donor should be relatively young (under 60, if possible), and the body size and blood type should be similar to the recipient’s. Livers from donors up to age 70 have been successfully transplanted, as have those from donors who have been diagnosed with hepatitis C, if the recipient is also a hepatitis C patient.

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Multaq Warnings : Insulin, the substance that keeps our glucose (blood sugar) levels from becoming too elevated, guides glucose from our bloodstream into the body’s muscle, fat, and liver cells. The cells convert the glucose into energy, but if the glucose isn’t metabolized correctly (i.e., if the cells resist the insulin and won’t allow it to do its job), then we produce less energy and feel fatigued.

People who are insulin-resistant can’t use insulin efficiently, and glucose builds in the blood, prompting the pancreas to produce even more insulin in an attempt to rid the body of the excess glucose. The result is an abundance of fatty acids that are converted to fat, which is stored in the liver, creating nonalcoholic fatty liver disease. Almost all people with NAFLD are insulin-resistant. Although overweight people are more likely to exhibit insulin resistance than people of normal weight, a sedentary lifestyle and a high-fat, high-sugar diet triggers insulin resistance regardless of body weight or body mass index.

The combination of factors and related disorders of metabolism (obesity, insulin resistance, diabetes, hypertriglyceridemia, and hypertension) comprises the group of findings known as the metabolic syndrome. People with the metabolic syndrome generally also have NAFLD, which in some cases will have progressed to NASH.

An easy way to distinguish between nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) is to put them into alphabetical order: NAFLD, or fatty liver disease, comes before NASH, or nonalcoholic steatohepatitis. This mnemonic is helpful because it reflects the order in which the two diseases occur: fatty liver disease arises first and can progress to nonalcoholic steatohepatitis.

Here are some facts at a glance:

•       Simple fatty liver (which is, just as its name describes, an accumulation of fat in the liver) is the beginning stage of nonalcoholic fatty liver disease. It is caused by insulin resistance, meaning that the insulin produced in the body is less effective than it should be. The primary factor in the development of insulin resistance is obesity, especially central obesity, or the accumulation of a disproportionate amount of weight in the abdomen. Simple fatty liver is relatively harmless and often disappears with weight loss.

•       The next stage of nonalcoholic fatty liver disease is nonalcoholic steatohepatitis. When NASH occurs, the liver is still fatty, but it also becomes inflamed (hepatitis) and liver cells can be destroyed. It can progress to scarring of the liver (fibrosis) and development of severe liver diseases, including cirrhosis, which is the last stage of NAFLD.

The Centers for Disease Control estimates that an astonishing 90 percent of people who are obese or have been diagnosed with type 2 diabetes also have simple fatty liver. About 20 percent of them have NASH, and 10 percent have cirrhosis.

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A high-fat diet, obesity, and insulin resistance are the most common causes of nonalcoholic fatty liver disease, but there are other, less common causes. One is drug-induced steatohepatitis, or more precisely drug-induced fatty liver, which is caused by medications such as prednisone (a steroid), tamoxifen (used in treating breast cancer), estrogen (a female hormone), methotrexate (used to treat

cancer and autoimmune conditions), amiodarone (used to treat heart conditions), or Arimidex (used to treat breast cancer).

Early symptoms of fatty liver disease are vague and nonspecific and include fatigue, malaise, and/or an ache in the upper right abdomen (where the liver is located).

Symptoms that appear in the advanced stages of nonalcoholic steatohepatitis mimic those of cirrhosis and include fluid in the abdominal cavity (ascites), severe itching, swelling (edema) of the legs and feet, weakness, nausea, easy bruising, yellowing of the skin and eyes (jaundice), dark (cola-colored) urine, and mental confusion.

To diagnose the problem, a physician may prescribe blood tests to rule out other liver-damaging conditions, including hepatitis B and C. Because excessive alcohol consumption can can cause fatty liver and alcoholic steatohepatitis (ASH), you may be asked about how much alcohol you consume. Excessive quantities are defined as three or more drinks a day for men and two or more drinks for women.

If fatty liver is suspected, the doctor will probably order further tests, including a liver-function blood test to measure whether enzymes are elevated (signaling possible liver damage), an ultrasound or a CT scan, and possibly a liver biopsy.

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It is true that iron is essential to good health. Iron helps to form oxygen-carrying hemoglobin in our red blood cells, boosting brain function, producing energy, and giving us strong muscles and immune systems. For people who suffer from iron deficiency, anemia, or whose iron stores become diminished during pregnancy, iron supplementation is essential.

Normally, our bodies absorb only about 10 percent of the iron that we consume in food. Most iron circulates in the body in the form of hemoglobin, but some is also stored in the liver, bone marrow, and spleen. People with hemochromatosis, though, can absorb up to 20 percent or more of the iron they take in—twice as much as they need to replace iron lost from the body.

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Multaq Lawsuit :

Diagnosis

Diagnosis of hepatitis D virus infection is determined by blood testing. In acute co-infection, IgM and IgG antibodies to hepatitis D virus are detectable during the course of infection. IgM antibodies will be detected earlier after acute infection and IgG later or while the patient is recovering. IgG antibody concentrations in blood generally fall to levels that cannot be detected after the acute infection resolves. There is no reliable marker that persists to indicate past infection with hepatitis D virus. In hepatitis D virus superinfection, high levels of both IgxVI and IgG antibodies against the hepatitis D virus become detectable after infection. Both IgM and IgG antibodies persist in serum as long as the patient remains infected.

Hepatitis D virus co-infection often is not diagnosed. In cases in which acute hepatitis B is not too severe, the doctor will not search for hepatitis D co-infection. If liver disease is unusually severe in a highrisk individual, testing for antibodies against hepatitis D virus may be performed and the diagnosis of acute co-infection made. In chronic hepatitis D, which occurs usually as superinfection, the presence of IgG antibodies in blood against hepatitis D virus, in a patient with detectable blood HBsAg, establishes the diagnosis. Testing will usually be performed in a patient with known chronic hepatitis B whose condition deteriorates.

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While tests for IgG against hepatitis D virus are commercially available in the United States, tests for IgM antibodies are available only in research laboratories. Tests for a hepatitis D virus protein known as hepatitis D antigen and PCR tests for hepatitis D virus RNA are also available in research laboratories. They are not part of routine diagnostic testing, however. Tests for hepatitis D antigen and viral RNA directly detect the presence of virus in the patient’s blood.

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Prevention

Because the hepatitis D virus needs hepatitis B’ virus to replicate, coinfection can be prevented if hepatitis B virus infection is prevented. Patients immune to hepatitis B infection cannot get infected with the hepatitis D virus. Therefore, vaccination against hepatitis B virus will eliminate the chance of contracting hepatitis D. As a result, universal vaccination for hepatitis B should theoretically eliminate hepatitis D as a human disease.

Individuals not immune to hepatitis B infection, who have knowingly been exposed to the hepatitis B and hepatitis D viruses, can receive passive immunization with hepatitis B immune globulin (HBIG). Prevention of hepatitis B virus infection by HBIG will not permit hepatitis D virus infection. No vaccine exists to prevent hepatitis D virus superinfection of persons with chronic hepatitis B virus infection. In these cases, prevention rests entirely upon avoiding high-risk behaviors. High-risk sexual activities should be avoided and latex condoms used. Intravenous drugs should not be used.

Treatment

Treatment of acute hepatitis D virus co-infection is supportive. Either the patient gets better spontaneously or develops fulminant hepatic failure. Emergency liver transplantation is an option for fulminant hepatic failure. In chronic hepatitis D infection, treatment with interferon alpha is a consideration. Although not much data are available at present, some studies suggest that higher doses of interferon alpha, such as 10 million units every day, are necessary in hepatitis D co-infection compared to the 5 million units used every day for chronic hepatitis B.

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Hepatitis E

The hepatitis E virus is a small, spherical virus that has been provisionally classified as a member of the Caliciviridae family. It is possible that this family assignment will change because the hepatitis E viral genome is different than that of most other caliciviruses. Its genome is composed of RNA.

The hepatitis E virus causes only acute liver disease. The disease caused by hepatitis E virus infection is known as hepatitis £, which is very similar to hepatitis A in its symptoms and clinical course. The disease can range from extremely mild to fulminant hepatic failure. Some cases of acute infection with hepatitis E virus may not produce any symptoms at all and go undiagnosed. In most hepatitis E outbreaks, the highest rates of clinically evident hepatitis have occurred in young to middle-age adults. It is possible that infected children, as is the case with hepatitis A, are more likely to have no obvious disease after infection. The time from infection to symptoms varies from fifteen to sixty days, with forty days being the average. It is not yet clear when the greatest danger of infecting others occurs, but virus excretion in feces has been demonstrated up to fourteen days after acute illness.

Patients with relatively mild disease may suffer from nausea, vomiting, fever, fatigue, and loss of appetite. Blood tests may reveal elevations in ALT and AST activities and possibly elevations in bilirubin concentration. Patients with more severe disease may develop jaundice, and blood tests will reveal an elevation in bilirubin concentration, a prolongation of prothrombin time, and sometimes markedly elevated

ALT and AST activities. Most patients with mild or moderate hepatitis E recover without complications. Some patients become so sick that they cannot eat or drink. Some patients with hepatitis E infection develop fulminant hepatic failure.

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Transmission

Hepatitis E virus infection does not occur in the United States. Virtually all cases reported in the United States involve travelers returning from parts of the world where hepatitis E is common. Outbreaks have occurred in many geographic locations around the world, mostly In underdeveloped countries. Hepatitis E virus is primarily spread by the fecal-oral route, that is, from feces of infected individuals to food or water thar is then ingested by others. Drinking contaminated water is probably the most common mode of infection. Person-to-person transmission appears to be rare. Similar to hepatitis A, hepatitis E is more common in parts of the world having poor sanitary conditions. Travelers from developed countries to such regions are at increased risk for infection from hepatitis E.

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Diagnosis

The clinical diagnosis of hepatitis E infection is suggested by the sudden onset of liver disease fifteen to sixty days after suspected exposure to the hepatitis E virus. Sometimes, patients will present with new- onset jaundice immediately suggesting acute liver disease. Such patients should be questioned about a risk factor for hepatitis E, which in North America and most European countries is recent travel to an area where the disease is endemic. Southern and central Asia, northern Africa, and Central America are regions of the world where hepatitis E outbreaks are the most common.

The diagnosis of hepatitis E infection is made through blood testing. Tests for antibodies against the hepatitis E virus are not commercially available in the United States but are available at research laboratories or specialized centers, such as the U.S. Centers for Disease Control and Prevention. Both IgM. and IgC antibodies against the hepatitis E virus are elicited following acute viral infection.

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Prevention

The most important issue regarding hepatitis E is prevention, which depends primarily upon avoiding contaminated water. Travelers to developing countries should avoid drinking from local water supplies and consuming beverages with ice of unknown purity. Uncooked shellfish, uncooked fruits, and vegetables that are not peeled or prepared by the traveler should not be consumed. At the present time, there are no postexposure prophylactic measures nor vaccines for hepatitis E.

Treatment

There is no specific treatment for hepatitis E. In many cases, the disease is mild and self-limiting. If the patient is so sick that he or she cannot eat or drink, hospitalization may be necessary for the administration of intravenous fluids. The patient can be discharged once there is adequate oral intake. In serious cases, generally those causing fulminant hepatic failure, hospitalization and intensive care are required. Preferably, these patients should be hospitalized in a medical center where ¡iver transplantation can be performed if necessary.

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Other Viruses That Cause Hepatitis

Hepatitis A, B, C, D, and E viruses are the major hepatotropic viruses that cause liver disease in humans (there is no hepatitis F). Some other viruses can also cause acute liver disease in otherwise healthy individuals. In most cases, these viruses cause systemic diseases that concurrently affect the liver. These viruses include dengue virus, yellow fever virus, and Epstein-Barr virus (EBV), which causes mononucleosis. Individuals with mononucleosis can suffer from a mild form of acute hepatitis that always resolves. Available data suggest that poxvirus and measles virus cause hepatitis in children.

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Some viruses that are generally harmless in healthy individuals may cause liver disease in patients with compromised immune systems. These viruses may infect patients with AIDS or cancer. They may also infect patients who have received organ transplants and are taking medications that suppress their immune systems. The most important of these viruses is cytomegalovirus, or CMV. CMV can cause hepatitis in recipients of organ transplants, including transplanted livers. CMV can also cause hepatitis and serious bile duct abnormalities in patients with AIDS.

Some doctors will test patients with chronic hepatitis for antibodies against CMV and EBV. These viruses are endemic in the human population, and the detection of IgG antibodies means virtually nothing. Furthermore, these two viruses do not cause any significant chronic liver disease in people with normal immune systems. If someone tells you that you have chronic hepatitis caused by EBV or CMV, you should be suspicious and see another doctor.

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Actos Bladder Cancer :

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If the results of your tests-—-either scans or biopsies-—- show that cancer has spread to other tissue or organs, your doctor will want to confirm that. Clarification of the stage of your cancer comes through looking at the cancer cells from those organs under the microscope. Tissue samples may be taken at the time of your biopsy, or sometimes a needle biopsy is done, bypassing the need for additional surgery.

Pathologists stage bladder-cancer tissue by using a standardized system known as TNM, which stands for tumor- nodes-metastases. A typical TNM might be “T2aNlM0” (T-two-a-N-one-M-zero). Looks like mumbo jumbo, doesn’t it? Try thinking of it as medical shorthand, with each letter and numeral having a defined value that gives doctors and pathologists a specific, consistent way to describe how deeply a cancer has invaded the body’s tissue and organs.

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The TNM system uses the letters T, N, and M followed by numerals to describe the stage of invasiveness of your cancer.

The letter T followed by a numeral from one to four (1 to 4) describes the depth of invasiveness of your tumor. The lower the number, the less invasive the cancer.

The T scale has additional, more detailed levels as well. These levels add the lowercase letters a and b to the T score to delineate more precisely how far into the bladder your cancer has spread and whether it has moved into other areas of your body. It fine-tunes the pathology information to help your doctor make treatment recommendations.

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Reclast Side Effects: Numerous health problems can lead to kidney failure. The four main causes are diabetes, hypertension, glomerular diseases, and polycystic kidney disease (PKD). Genetics plays a role in most causes of kidney failure, and kidney failure may result from a specific defect inherited from one or both parents. PKD is primarily an inherited kidney disease.

Genetics is not the whole story, however. Lifestyle and other environmental factors may also be significant influences. This chapter begins with a primer on the genetic and environmental factors contributing to kidney failure. Knowledge of these factors will help you understand how you might slow the progression of your disease.

For all organs of the body, our genes issue the instructions (or blueprints) to make proteins while we are in the womb. For organs to develop correctly, certain processes must happen in an exact way. It starts when a sperm fertilizes the egg. The cells in the resulting embryo, possessing two copies of each gene, one from each parent, begin to divide. As the embryo grows, copies of genes inherited from each parent must be reproduced identically in each new cell, so that all the cells in the developing fetus (and eventually in the person’s body) will have the same set of genetic blueprints. During a person’s lifetime, many of the cells in the body will die and be replaced with new ones. These new cells generally also contain the same blueprints.

Although rare, mistakes can occur when genes are copied. Called mutations, these mistakes can cause the organs to work improperly. If a house’s blueprints are wrong, a door might be located in the wrong place or the lighting system might fail because of incorrect wiring. In people, gene mistakes are passed along to their children and can cause them to inherit a disease. For example, mutations in genes that make or control kidneys can malfunction, leading to disease.

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Behavioral and environmental factors can also contribute to the expression or progression of a disease. In the case of kidney failure, an improper diet and lack of exercise or other lifestyle factors can contribute greatly to a person’s medical status. We do not deliberately set out to make ourselves ill. However, with the stresses of our culture and everyday life, it can be easy to neglect our own health. Between work, family, and social obligations, we are so busy that we may have little time to cat properly or to get adequate exercise. Over time, our health can begin to fail without our even knowing it.

When people don’t eat right and don’t exercise, they are more likely to be overweight or obese. Obesity has reached epidemic proportions in the United States and in other developed countries. According to a rccent study, 66.3 percent of Americans arc overweight, obese, or morbidly obese.¹ African Americans and Hispanic Americans have a higher prevalence of obesity than non-Hispanic whites. Moreover, women across all races are more obese than men. Obesity increases with age, leveling off by age 60 or declining thereafter.

Obesity may lead to other health complications—including kidney failure—because obesity makes people more likely to develop diabetes and hypertension. Excess weight can also cause coronary heart disease, high cholesterol levels, and stroke, which can lead to death. References to the symptoms of kidney disorders by the ancient Greeks suggest that we have known about kidney failure for thousands of years. We weren’t able to analyze kidneys and other organs until the nineteenth century however. In 1827, the English physician Richard Bright first described the symptoms of kidney failure.

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In the twenty-first century kidney failure is still incurable, but it can be prevented and treated. With dialysis and transplantation, people with kidney failure can continue to have productive lives. Nevertheless, failing kidneys take a very high medical, emotional, and financial toll. There is no cure for kidney failure, but knowing its causes can help prevent, delay, or prepare for it.

Approximately one-half million people in the United States are living with kidney failure. In most cases, diabetes and hypertension are the causes. Both are preventable. Glomerular disorders, which can have both environmental and genetic origins, are another cause of kidney failure. There are also inherited causes of kidney failure, like PKD. If a person inherits mutated genes, the disease will develop, although the progression of the disease varies among families and individuals. This chapter presents a brief overview of each of these four leading causes of kidney failure.

Diabetes (also known as diabetes mellitus) is the leading cause of kidney failure in the United States and accounts for 38 percent of cases. Because of rising obesity rates, diabetes rates are increasing, even among children. As many as 20.6 million people have diabetes. As people age, they become more susceptible to diabetes. About one-half of all people with diabetes are over 60 years old. Across the population, slightly more men than women have diabetes, and it disproportionately affects Native Americans, non-Hispanic African Americans, and Hispanic Americans. Understanding the underlying causes of diabetes is essential for learning how to prevent and treat it.

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