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Children and ADPKD: It's Not Just an Adult Disease. PKD Progress. 23(2): 18. Summer 2007.

This brief article presents an excerpt from the recently updated Polycystic Kidney Disease (PKD) Patient's Manual: Understanding and Living with Autosomal Dominant Polycystic Kidney Disease (ADPKD), a publication available free of charge from the PKD Foundation at www.pkdcure.org. This article reminds readers that children can have autosomal dominant PKD, and that these children tend to fall into two groups: those who are diagnosed before birth or in the first year of life with large kidneys or cysts, and those who are diagnosed after the age of 1 year. The number of cysts a child has affects his or her signs and symptoms. Almost all children who are diagnosed after the first year of life have perfectly normal kidney function that seems to stay normal throughout childhood. Most of these children will maintain normal kidney function until they are into their mid-20s. The article also considers whether or not children should be told they are at risk of ADPKD, whether children of parents with ADPKD should be tested for the disease, and recommendations for routine screening. Sidebars review the characteristics of ADPKD in children.

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Dialysis and PKD Patients: An Analysis. Nephrology News & Issues. 21(9): 36, 37. August 2007.

This article focuses on the treatment of patients with polycystic kidney disease (PKD) before the need for renal replacement therapy and during chronic dialysis. The authors discuss the complications of PKD, including renal pain, hematuria, and renal infection; the extrarenal manifestations of PKD, including gastrointestinal involvement, hepatic synthetic dysfunction, cardiac valve abnormalities, hypertension, and brain aneurysms in patients with a strong family or personal history of same; the use of heparin in these patients; the use of dietary sodium restriction, diuretics, and antihypertensive medications used to control volume and blood pressure; the role of remaining kidney function, even in patients who require dialysis to maintain health; patient candidacy for dialysis; the decision between home dialysis versus in-center care; the choice between hemodialysis and peritoneal dialysis; and the importance of adequate nutrition to decrease hospitalizations, improve survival, increase independence, and improve sense of well-being. The authors note that PKD patients are generally good candidates for survival and have a survival advantage compared with patients with end-stage renal disease (ESRD) from other causes.

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Eating Healthy From the Start: Kid and Kidney-Friendly Nutrition Tips. PKD Progress. 23(2): 10-11. Summer 2007.

It is likely that eating well in childhood may offer some protection to the kidneys and influence the early progression of polycystic kidney disease (PKD) in children at risk for the condition. This article offers kid-friendly and kidney-friendly nutrition tips for parents of children who have healthy kidney function whether or not they have been diagnosed with PKD. Specific food and nutrition items discussed include flaxseeds, sodium, fruits and vegetables, protein intake, and soy-based foods. Suggestions for increasing a child's sense of adventure and willingness to try new foods are also provided and focus on families eating meals together, the need to offer new foods on at least 10 different occasions, letting children serve themselves, and including children in shopping and cooking activities. One sidebar reviews how much protein is recommended for children in different age groups—the recommended Dietary Reference Intake for children.

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Exercise and PKD. PKD Progress. 23(3): 12-13. Fall 2007.

This article reviews the importance of exercise for people who have polycystic kidney disease (PKD). The author interviews Dr. Richard M. Fine, a fitness trainer, who emphasizes that for most people, the ability to exercise is more about overcoming a mental barrier than a physical one. Dr. Fine reviews the steps that can help a patient implement and maintain an exercise plan, including exercising with other people, learning about the emotional benefits of exercise, and incorporating movement and exercise into all one’s daily activities. Two charts summarize a group of exercises for everyone and a group of exercises for people with specific disorders, including diabetes, hypertension, coronary heart disease, and osteoporosis. The charts list the modes of exercise; goals; recommended intensity, frequency, and duration; and expected time to see results.

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Getting Back on the Wagon and Rid of the Saddle. PKD Progress. 23(1): 16-17. Spring 2007.

This brief article offers a list of 25 ideas for health improvement for people who are in the early stages of polycystic kidney disease (PKD). Designed to capture the attention of people who are making New Year's resolutions, the article suggests that readers enlist the help of friends, trim fat from their diet, eat smaller portions, include more fiber in their diet, learn new recipes or take a cooking class, plan ahead, bring healthy food when traveling or visiting, limit liquid calories, add more movement to the day, try soy foods, include treats that are not food-based, learn about herbs and spices, eat fish, focus on reducing sodium, exercise to fight stress or fatigue, limit artificial sweeteners, use a smaller size plate, do not eat while distracted by television or reading, do not have high fat snack foods in the house, chew food thoroughly, keep a diet diary, wait 20 minutes before taking a second helping of food, avoid fried foods, eat soup, and try to prevent getting over hungry. For each item, the authors offer one or two sentences of explanation and encouragement.

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Polycystic Kidney Disease. Bethesda, MD: National Kidney and Urologic Diseases Information Clearinghouse. 2007. 7 p.

Polycystic kidney disease (PKD) is a genetic disorder characterized by the growth of numerous cysts in the kidneys. The cysts are filled with fluid. PKD cysts can slowly replace much of the mass of the kidneys, reducing kidney function and leading to kidney failure. This fact sheet reviews PKD, focusing on two major inherited forms of PKD and a noninherited form: autosomal dominant PKD, autosomal recessive PKD, and acquired cystic kidney disease (ACKD). Written in a question-and-answer format, the fact sheet covers the definition of each type, symptoms, diagnostic tests used to confirm the condition, and treatment options. The symptoms and signs of PKD include pain in the back and lower sides, headaches, urinary tract infections (UTIs), blood in the urine, and cysts in the kidneys and other organs. Diagnosis of PKD is accomplished by ultrasound imaging of kidney cysts, the ultrasound imaging of cysts in other organs, and family medical testing, including genetic testing. Although there is no cure for PKD, treatments include medicine and surgery to reduce pain, antibiotics to resolve infections, dialysis to replace functions of failed kidneys, and transplantation. The fact sheet concludes with a summary of research programs in this area, a list of resource organizations for readers wanting additional information, and a brief description of the activities of the National Kidney and Urologic Diseases Information Clearinghouse (NKUDIC). 2 figures.

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Renal Transplantation for ADPKD Patients: A 2007 Update. Nephrology News & Issues. 21(4): 24-27. March 2007.

This article updates readers on the recommendations and advances in the field of kidney transplantation for people with autosomal dominant polycystic kidney disease (ADPKD). The author first considers the benefits of transplantation over other treatments for ADPKD, noting that even when adjusted for diabetes and concomitant heart disease, the transplant patient has a greater life expectancy despite the risks of surgery and the perioperative period. Patients with ADPKD have as good or better outcomes than patients with other kinds of kidney failure. The author also considers the issue of whether to remove the native kidneys as part of a kidney transplant in this patient population. The absolute indications for removal of native polycystic kidneys prior to transplantation are active kidney infections, kidney malignancy, or kidneys that are so large that they mechanically preclude transplantation into the recipient's pelvis. The article also covers family donors in families with ADPKD, costs, living versus cadaveric donation, the kidney allocation process, and immunosuppressive medications.

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Talking to Your Kids About PKD: A Mommy's Perspective. PKD Progress. 23(2): 13. Summer 2007.

In this brief article, the author shares her experience helping her young son understand why her kidney disease requires her to have special medical care. Diagnosed with polycystic kidney disease (PKD) when the boy was 4 years old, the author reports that the child became troubled and anxious when he suddenly had to go to a babysitter while his mother had weekly doctor appointments. The author describes how she explained the disease and kidney function to the child, and how the approach of providing a lot of information about what is going on has helped to calm him and help him feel more secure. The author concludes by considering the kinds of information she will need to share with her son when she gets ready to have a kidney transplant. 1 figure.

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Vasopressin Receptor Antagonists. Dialysis and Transplantation. 36(5): 266-74. May 2007.

This article brings readers up-to-date on advances in vasopressin receptor antagonists, drugs that are used to reduce urine osmolality and increase free water excretion while preserving sodium and raising serum sodium concentration. These drugs offer an improvement over traditional diuretics, which increase sodium excretion along with water excretion. The authors first review vasopressin physiology and vasopressin receptors, then discuss specific vasopressin receptor antagonists, including conivaptan, lixivaptan, tolvaptan, and satavaptan. Conivaptan is approved for the treatment of euvolemic hyponatremia, and more trials are needed to investigate its role in the management of acutely decompensated and chronic congestive heart failure (CHF). Tolvaptan may benefit patients with polycystic kidney disease. The authors conclude that vasopressin receptor antagonists are likely to become a key treatment in hospitalized patients who need diuretics. 5 tables. 23 references.

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Ways You Can Help Promote PKD During National Kidney Month. PKD Progress. 23(1): 4-5. Spring 2007.

This brief article offers a list of 25 ideas to help promote polycystic kidney disease (PKD) awareness during National Kidney Month, which takes place in March of each year. The ideas include hanging up promotional posters; passing along informational packets to health care providers; speaking to community groups and friends about PKD; adding references to PKD to email signatures, websites, and voice mail; contacting local newspapers, television, and radio stations about airing public service announcements; sending bookmarks to local schools; planning chapter events; wearing PKD merchandise; forming a Walk for PKD team; and attending the PKD National Convention. The article describes some promotional materials that are available through the Polycystic Kidney Disease Foundation at pkdcure@pkdcure.org or 800-PKD-CURE.

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Childhood Kidney Disease Gene Identified. Nephrology News & Issues. 20(3): 16. March 2006.

This brief article reports on the recent identification of a new gene linked to the inherited kidney disorder called Meckel-Gruber syndrome (MKS). Children with MKS have central nervous system deformities as well as abnormal cysts in their kidneys, and usually die shortly after birth. The news of the gene identification is important to MKS families who might have their blood screened for the defect and seek genetic counseling. The finding also is important for better understanding of common birth defects, such as neural tube abnormalities, and for related disorders, such as more common forms of polycystic kidney disease (PKD). The author notes that the current work is an extension of Mayo Clinic researchers' work for more than a decade that has helped to reveal the genetic basis of PKD and to develop therapies. The author briefly reports on the research study methodology and the investigators from different institutions who were part of the research team.

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Cystic Diseases of the Kidney. IN: Kellogg Parsons, J.; James Wright, E., eds. Brady Urology Manual. New York, NY: Informa Healthcare USA. 2006. pp 107-114.

This chapter about cystic diseases of the kidney is from a reference handbook that offers a comprehensive overview of urology, presented in outline and bulleted formats for ease of access in the busy health care world of hospital emergency rooms and outpatient clinics. The author notes that simple renal cyst is a common, benign condition that is usually detected incidentally. The chapter covers general information, presentation, diagnosis, and treatment of simple renal cyst, acquired renal cystic disease, autosomal dominant polycystic kidney disease (ADPKD), and autosomal recessive polycystic kidney disease (ARPKD). The Bosniak classification system is recommended to distinguish simple cysts from complex renal cysts and cystic renal cell carcinoma (RCC). Acquired renal cystic disease occurs in patients with kidney failure and is characterized by bilateral cortical and/or medullary cysts. ADPKD is an inherited disease of the collecting duct characterized by multiple large renal cysts, progressive renal insufficiency, and extrarenal manifestations, including hepatic cysts and cerebral artery aneurysm. Treatment for ADPKD and ARPKD is supportive care. The chapter concludes with a list of references for additional reading. 19 references.

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Diagnosing PKD, Determining Options. Nephrology News & Issues. 20(3): 62-65. March 2006.

This article provides information about the diagnosis of polycystic kidney disease (PKD). Symptoms lead to the diagnosis of PKD in approximately 34 percent of queried patients. The second most common theme that led to the diagnosis of PKD was a known family history. Almost 32 percent of PKD patients were diagnosed during evaluation of hypertension or asymptomatic microscopic hematuria (blood in the urine). The author outlines the typical types of pain experienced by patients with PKD, describes the diagnostic tests that are used to confirm PKD, and offers suggestions for dealing with patients (particularly regarding health insurance issues and treatment options that may delay or halt the progression of the disease). For example, aggressive and early treatment of hypertension conveys the promise of slowing the progression of the disease. In addition, addressing abnormalities of mineral metabolism, anemia, and dyslipidemia can forestall serious problems. 13 references.

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Eating for Optimal Health. PKD Progress. 21(2): 12-13, 24. Summer 2006.

This article reviews the use of dietary modifications to help slow the progression of polycystic kidney disease (PKD). Written primarily for newly-diagnosed patients with PKD who are not yet on dialysis, the article discusses lifestyle and dietary tips that are recommended to help patients stay as healthy as possible. These tips are: reduce stress, avoid inflammation in the kidney, use plant-based proteins that are high in antioxidants, incorporate soybeans in the diet, choose low-sodium foods and condiments, limit caffeine and alcohol, increase potassium consumption, include omega-3 fatty acids in the diet, consume high-fiber carbohydrates, maintain an optimal weight, and limit dietary fat intake. The author reminds readers that all of these recommendations are useful to improve anyone’s health, not just the family member with PKD. Readers are also encouraged to start slowly and to incorporate changes into their overall program of nutrition and health.

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Family and ADPKD: A Guide for Children and Parents. Kansas City, MO: Polycystic Kidney Disease Foundation. 2006. 18 p.

This document provides basic information for the parents of a child that has just been diagnosed with autosomal dominant polycystic kidney disease (ADPKD), a genetic disease that affects the kidneys and other parts of the body. In ADPKD, cysts can form in the kidney, anywhere along the nephron. This fact sheet answers common questions in the areas of general information, inheritance, diagnosis, health promotion, prognosis, extra-renal manifestations, psychosocial factors, and current research on PKD. Specific topics include the anatomy and function of the kidneys, how PKD can damage the good parts of the kidney, diagnosis in people who have no symptoms, dietary approaches to preventing disease progression, limiting protein intake, avoiding dehydration, sodium, sports and recreation, medications, high blood pressure, mortality due to ADPKD, dialysis and kidney transplantation, organ donation, disclosing health information to a child, screening in siblings, complications in ADPKD, cerebral aneurysms, coping with pain, and finding information resources. The information is presented in a kid-friendly fashion, so an adolescent would be comfortable reading the fact sheet by him or herself.

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Just Diagnosed with Polycystic Kidney Disease (PKD). PKD Progress. 21(2): 6-9. Summer 2006.

This newsletter article helps readers newly diagnosed with polycystic kidney disease (PKD) understand the condition and how they can take an active part in their own health care. The author uses the story of one woman’s experiences with diagnosis, educating herself, and treatment, to help readers understand the process of coping with the disease. PKD is a common, life-threatening, genetic kidney disease that causes cysts to grow, usually on both kidneys. Eventually, the cysts multiply, usually leading to kidney failure, for which transplantation or dialysis are the only treatments. The author reviews symptoms and diagnosis, the tests used to confirm PKD, and possible problems getting health insurance coverage. The author emphasizes the importance of patients getting appropriate medical care for PKD and the complications it may cause (notably hypertension, abnormalities of mineral metabolism, anemia, and dyslipidemia). Readers are encouraged to contact their local chapter of the PKD Foundation. The article concludes with a list of 10 web sites for additional information.

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Making an Earlier Diagnosis of ADPKD: Implications for the Treatment of Hypertension. Nephrology News & Issues. 20(7): 32-36. June 2006.

This article discusses the problem of hypertension in patients with autosomal dominant polycystic kidney disease (ADPKD). The authors review the incidence and prevalence of hypertension in ADPKD, which usually develops in the second or third decade of life, even before the loss of significant kidney function. Hypertension is associated with increased kidney size, a faster decline in kidney function, left ventricular hypertrophy, premature cardiovascular disease, and mortality. The authors make a case for the earlier diagnosis of ADPKD, in part to start anti-hypertensive therapy earlier and to ensure the correct anti-hypertensive agent is chosen. The authors conclude by recommending screening for at-risk and already-diagnosed adolescents and young adults for hypertension at least annually. Early detection and aggressive treatment can reduce the future likelihood of cardiac and renal injury. 2 figures. 19 references.

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PKD Patient's Manual: Understanding and Living with Autosomal Dominant Polycystic Kidney Disease. Kansas City, MO: Polycystic Kidney Disease Foundation. 2006. 33 p.

This booklet provides information about autosomal dominant polycystic kidney disease (ADPKD) to those who have the disease, those who are at risk due to an affected family member, and people who care about someone who has been diagnosed with ADPKD. The primary manifestation of ADPKD is cysts in the kidney, cysts as well as other abnormalities can occur in other areas of the body. Written in a question-and-answer format, this booklet covers the epidemiology of ADPKD, symptoms, genetics and inheritance, the ADPKD genes, screening tests for ADPKD, kidney anatomy and function, cysts and their impact on the kidney, high blood pressure (hypertension), weight loss, exercise, sodium, potassium, tobacco use, acute and chronic pain in ADPKD, blood in the urine, urinary tract infection (UTI), kidney stones, liver cysts, dialysis and transplantation, mitral valve prolapse, intracranial aneurysms, hernias, diverticula, pregnancy, diet therapy, fluids, caffeine, children with ADPKD, symptoms of kidney failure, and common tests that are done to diagnose and monitor cystic disease. The booklet concludes with a list of resource organizations through which readers can get more information. 12 figures. 1 table. 2 references.

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Q & A on PKD [Polycystic Kidney Disease]. Kansas City, MO: Polycystic Kidney Disease Foundation. 2006. 47 p.

This patient education packet covers a wide variety of information about polycystic kidney disease (PKD). The first article brings readers up-to-date on autosomal dominant PKD (ADPKD) genes and proteins; the second section reviews strategies that can be used to treat hypertension and end-organ damage in patients with ADPKD. The remainder of the fact sheet answers questions that patients may have in the areas of diagnosis and genetics, extra-renal manifestations, renal manifestations, pregnancy and birth control, menopause, kidney failure, dialysis and transplantation, diet and drug therapy, surgery, the role of exercise, and pain management. Specific topics covered include multicystic kidneys, multicystic versus polycystic kidney, natural course of the disease in families, spontaneous onset of ADPKD, diagnostic criteria, fetal testing for PKD, medullary sponge kidney, symptom-free PKD, race and ethnic background as risk factors, screening family members for PKD, pancreatic cysts, diverticulosis and diverticulitis in people with PKD, malabsorption problems, polycystic liver disease, hernia and polycystic kidney, neurologic involvement, cerebral aneurysms in people with PKD, cardiovascular problems associated with PKD, pregnancy, drug therapy, blood pressure considerations, kidney infections, the use of antibiotics, urinary tract infections, kidney stones, estrogen replacement therapy, renal function tests, dialysis therapy, peritoneal dialysis, vascular access, recurrence of PKD in a newly-transplanted kidney, the impact of immunosuppressive drugs on PKD, nutrition, protein intake, soy protein versus animal protein, flax seed, phosphorus, sodium restriction, vitamins, chemotherapy, exercise, medical nutrition therapy (MNT), the relationship between primary care physicians and nephrologists, medications that can be damaging to the kidneys, diagnostic tests used to monitor PKD, and pain management. The fact sheet includes many brief case-report type questions to help readers with specific issues.

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Volume Progression in Polycystic Kidney Disease. New England Journal of Medicine. 354(20): 2122-2130. May 18, 2006.

This article considers the problem of volume progression in autosomal dominant polycystic kidney disease (ADPKD). ADPKD is characterized by progressive enlargement of cyst-filled kidneys. The authors report on a 3-year study in which they measured the rates of change in total kidney volume, total cyst volume, and iothalamate clearance in patients with ADPKD (n = 232, aged 15 to 46 years). Results showed that total kidney volume and total cyst volume increased exponentially, a result consistent with an expansion process dependent on growth. Total cyst volume increased by a mean of 203 milliliters-plus or minus 246 milliliters-over a 3-year period among 214 patients. The baseline total kidney volume predicted the subsequent rate of increase in volume, independent of age. A baseline total kidney volume above 1500 milliliters in 51 patients was associated with a declining glomerular filtration rate (GFR). Total kidney volume increased more in 135 patients with PKD1 mutations than in 28 patients with PKD2 mutations. The authors conclude that kidney enlargement resulting from the expansion of cysts in patients with AKPKD is continuous and quantifiable and is associated with the decline of renal function. 4 figures. 1 table. 29 references.

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Eating Well for Two. PKD Progress. 21(1): 12-13, 24. Spring 2005.

This newsletter article discusses nutrition in pregnant women with polycystic kidney disease (PKD). The author contends that most women with PKD can have healthy, uncomplicated pregnancies, especially if they start out with a creatinine level less than 2 milligrams per deciliter and do not have hypertension (high blood pressure). Two potential, nutritionally-modifiable risk factors for pregnant women with PKD are hypertension and urinary tract infections. The article focuses on the role of nutrition in a healthy pregnancy in this patient population. Topics include increased protein needs during pregnancy, how to maintain a healthy sodium balance, calcium, cranberry juice, high fruit and vegetable intake, the use of iron supplements, omega-3 fatty acids, and the importance of not gaining weight during pregnancy. One sidebar refers readers to the Nutrient Analysis Database on the U.S. Department of Agriculture website (www.nal.usda.gov/fnic/foodcomp/search).

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Evaluation and Preparation of Renal Transplant Candidates. IN: Danovitch, G.M. Handbook of Kidney Transplantation. Philadelphia, PA: Lippincott Williams and Wilkins. 2005. pp. 169-192.

The preparation of patients with end-stage renal disease for kidney transplantation should start from the time of recognition of progressive chronic kidney disease (CKD). This chapter on the evaluation and preparation of renal transplant candidates is from a handbook that offers a practical guide for health care providers who manage kidney transplant patients. The authors note that the management of these patients consists of an initial evaluation followed, if they are appropriate transplant candidates, by their supervision while awaiting transplantation. Initial evaluation is designed not only to assess the chances of recovery from surgery, but also to increase short- and long-term patient survival. The limited number of organs available has changed the focus of the transplant evaluation toward better long-term outcome over short-term benefits. The authors first focus on the initial recipient evaluation and then consider the management of the waiting list for deceased donor transplantation. Specific topics covered include the benefits of early referral, patient education, the routine evaluation, the evaluation of specific transplant risk factors related to organ system disease (cardiovascular disease, cerebrovascular and peripheral vascular disease, malignancy, infections, gastrointestinal disease, pulmonary disease, urologic evaluation, renal osteodystrophy and metabolic bone disease, and hypercoagulable states), and risk factors related to specific patient characteristics (aged, obesity, highly sensitized patients, previously transplanted patients, and candidates for double-organ transplants). An additional section considers the relevance of the etiology of renal disease to the transplant evaluation, including diabetes mellitus, focal and segmental glomerulosclerosis, recurrent glomerulonephritis, thrombotic thrombocytopenic purpura, systemic lupus erythematosus and vasculitis, oxalosis and oxaluria, Fabry disease, Alport syndrome, sickle cell disease, amyloidosis and plasma cell dyscrasias, and polycystic kidney disease. 1 figure. 5 tables. 16 references.

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Facts About Kidney Disease. Rockville, MD: American Kidney Fund. 2005. 8 p.

This brochure provides basic information about kidney disease. Topics include the anatomy and physiology of kidneys, common kidney diseases, risks for kidney disease, the symptoms of kidney disease, diagnostic tests used to confirm kidney disease, treatments for kidney failure, and prevention of kidney disease. Kidney diseases discussed include chronic kidney disease (CKD), which can occur from many different causes, kidney stones, polycystic kidney disease (PKD), kidney infections (pyelonephritis), simple kidney cysts, kidney cancer, and the nephritic syndrome. Diagnostic tests described include glomerular filtration rate (GFR), urine tests, blood pressure monitoring, blood glucose testing, kidney biopsy, and imaging tests (CT, MRI). Treatment options include hemodialysis, peritoneal dialysis, and kidney transplantation. Readers are encouraged to contact the American Kidney Fund (AKF) HelpLine (800–638–8299 or HelpLine@kidneyfund.org). The brochure is illustrated with black-and-white photographs. 5 figures.

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Getting Back on the Wagon and Getting Rid of the Saddle. PKD Progress. 18(1): 8-9. Spring 2005.

This article, from a journal for people with polycystic kidney disease (PKD), emphasizes the importance of weight management as part of a complete program of disease management. The author cautions that excess body weight can increase blood pressure and may lead to hormonal changes (hyperinsulinemia) that could accelerate the progression of PKD. The author then outlines recommendations for healthy weight loss, including working out with friends, reducing the amount of fat in one's diet, eating smaller portions, avoiding high-calorie snack foods, increasing fiber in one's diet, meal planning, packing healthy food, avoiding liquid calories (sodas, alcohol), and exercising. The author concludes by reminding readers that these healthy approaches are useful not only for weight loss but also for general health and well-being.

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How to Pick a Good Nephrologist. PKD Progress. 20(1): 11-13. Spring 2005.

This article, from a journal for people with polycystic kidney disease (PKD), outlines suggestions to help readers choose a good nephrologist (kidney specialist). The author stresses that selecting a physician who meets one's needs is a multi-step process that includes networking, talking to one's primary care physician, consulting academic resources, and considering issues of insurance. The author also notes that reasonable access to the physician is also important; no matter how good the physician, if the practice is not well-managed, that physician may not be the best choice. A final section discusses advocacy and learning to be one's own health care advocate. One sidebar lists some online resources for finding and learning about doctors and hospitals.

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Mechanistic Approach to Inherited Polycystic Kidney Disease. Pediatric Nephrology. 20(5): 558-566. May 2005.

This article discusses the use of a mechanistic approach to the pathogenesis of inherited polycystic kidney disease. The authors note that although some of these inherited cystic diseases are rarely encountered, the number of affected people (approximately 6.5 million worldwide) justifies the investigations into their pathogenesis. The authors discuss the disease burden worldwide, the genetics of the autosomal dominant diseases, medullary cystic kidney disease, autosomal dominant polycystic kidney disease (ADPKD), tuberous sclerosis complex, autosomal recessive polycystic kidney disease (ARPKD), nephronophthisis, Bardet-Biedl syndrome, the dysregulation of renal tubular epithelial cell biology, the pathogenesis of cysts, tubules, and cilium. 5 figures. 1 table. 55 references.

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Medical and Surgical Aspects of Kidney Donation. IN: Danovitch, G.M. Handbook of Kidney Transplantation. Philadelphia, PA: Lippincott Williams and Wilkins. 2005. pp. 135-168.

The appropriate identification and preparation of kidney donors (both living and deceased) contribute critically to the success of the transplant endeavor on both the individual and the national levels. This chapter on the medical and surgical aspects of kidney donation is from a handbook that offers a practical guide for health care providers who manage kidney transplant patients. The authors divide the chapter into two sections: Part I addresses the selection and evaluation of living donors and the surgical techniques of living donor nephrectomy; Part II discusses these same issues for deceased kidney donors. Specific topics include the role of informed consent, the evaluation process, the psychosocial evaluation, risks of donation, donor age, assessment of surgical risks, the risk of disease transmission to the recipient, evaluation of future risk to the donor, assessment of renal function (glomerular filtration rate, proteinuria, hematuria, hypertension, diabetes, obesity, nephrolithiasis, inherited renal disease, autosomal dominant polycystic kidney disease, Alport syndrome, familial primary glomerulonephritis, and systemic lupus erythematosus), surgical evaluation of the living kidney donor, surgical techniques for living donor nephrectomy, long-term postnephrectomy issues (renal function, pregnancy, employment and insurance, and long-term medical care), and controversies and innovations in living kidney donor practice, including biologically unrelated donors, incompatible donor and recipient, paid donation, and the living donor registry. The second section discusses contraindications to deceased donor donation, the role of donor age, expanded criteria donors, donor biopsy, nephron dose, donation after cardiac death, diagnosis of brain death, techniques of deceased donor organ retrieval, and deceased donor kidney preservation. 2 figures. 10 tables. 32 references.

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PKD: A Progress Report, New Directions in Research. Nephrology News & Issues. 19(12): 39-40. November 2005.

Polycystic kidney disease (PKD) causes end-stage renal disease (ESRD) in 50 percent of affected individuals. This article brings readers up-to-date about research activities into understanding the molecular basis of PKD. The author discusses advances in gene identification, including mapping, cloning, and sequencing; analysis of the genes and encoded proteins; the mechanisms of disease progression; renal functional deterioration; and advances that can contribute to clinical therapies. The author notes that PKD is typically such a slowly progressive disease that it is hard to evaluate potential therapies. The development of surrogate markers for disease progression may address this concern. The author briefly reports on the CRISP study that evaluated renal anatomic changes, measured by periodic magnetic resonance imaging (MRI), in patients with PKD.

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Polycystic Kidney Disease (PKD). American Family Physician. 71(1): 135-136. January 1, 2005.

This patient education fact sheet reviews the problem of polycystic kidney disease (PKD), a condition in which sacs of fluid grow in the kidneys. If too many cysts grow or if they become too big, the kidneys are damaged. The cysts may also be painful or get infected. The fact sheet reviews the symptoms of PKD, the impact of PKD on lifestyle and lifespan, diagnostic tests that may be used to confirm the presence of PKD, who should be tested for PKD, and the diagnosis of PKD in unborn babies. PKD tends to run in families and children of people with PKD have a 50 percent chance of getting the disease. Blank space for notes is also included.

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Pregnancy and PKD. PKD Progress. 21(1): 6-7. Spring 2005.

This newsletter article discusses pregnancy in women with polycystic kidney disease (PKD). The author discusses medications, supplements, the problems of pre-eclampsia and hypertension, decreased kidney function, and other women's health issues. The brochure Health Tips for Living with Polycystic Kidney Disease by Dr. Arlene Chapman is used as a basis for much of the discussion. Many women with PKD can experience a positive and successful pregnancy, but a woman with PKD must be careful to protect her own health and that of her baby. For women with pre-existing hypertension, careful, frequent evaluation of blood pressure during the second and third trimesters is crucial. The author cautions that women with established renal insufficiency have less than a 50 percent chance of having a baby that survives pregnancy. One sidebar offers a brief PKD pregnancy checklist of health issues for women to discuss with their health care providers.

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Understanding Conditions That Lead to Chronic Kidney Disease. Kidney Beginnings. 4(4): 6-7, 22. Special Edition 2005.

This article familiarizes readers with some of the conditions and diseases that can eventually lead to chronic kidney disease (CKD). The author focuses primarily on diabetes mellitus and hypertension (high blood pressure). Of all the patients who experience kidney failure, 43.5 percent have diabetes and 26.5 percent have high blood pressure. High blood glucose levels associated with diabetes can disrupt the structure and function of blood vessels, including those that are involved in the filtration system of the kidneys. Damaged kidneys do not do a good job of cleaning out the body’s waste and extra fluids. Readers are advised to keep their blood glucose and blood pressure levels as close to normal as possible. Other conditions briefly discussed are glomerulonephritis, nephrotic syndrome, and polycystic kidney disease (PKD). Readers are referred to a booklet available from the American Association of Kidney Patients (AAKP) for more information (800-749-2257).

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About Chronic Kidney Disease. El Segundo, CA: DaVita Inc. 2004. 4 p.

Healthy kidneys function to remove extra water and wastes from the body, to help control blood pressure, to keep body chemicals in balance, to keep bones strong, to tell the body to make red blood cells, and to help children grow normally. This patient education fact sheet offers a basic description of chronic kidney disease (CKD), a condition that occurs when the kidneys are no longer able to clean toxins and waste products from the blood or perform their functions to full capacity. Written in a question-and-answer format, the fact sheet discusses acute renal failure and how it differs from CKD, the main causes of kidney disease, diabetes-related kidney disease, kidney stones, parathyroid hormone (PTH) and calcium, polycystic kidney disease (PKD), the symptoms of CKD, and diagnostic tests used to confirm CKD. The fact sheet concludes with information about a patient education program sponsored by DaVita (the producer of the fact sheet and a provider of in-center hemodialysis nationally).

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Polycystic Kidney Disease. New England Journal of Medicine. 350(2): 151-164. January 2004.

This article reviews the mechanisms of polycystic kidney disease (PKD), a leading cause of end-stage renal failure and a common indication for dialysis or renal transplantation. The age at onset, the severity of symptoms, and the rates of progression to end-stage renal disease (ESRD) or death vary widely in this group of diseases. Topics covered include autosomal dominant PKD, autosomal recessive PKD, familial nephronophthisis, medullary cystic kidney disease, cell biology, molecular biology, developmental regulation and programming, and prospects for prognosis and therapy. 5 figures. 2 tables. 98 references.

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Solving the Protein Puzzle for Those Who Are Early-Stage PKD and Not on Dialysis. PKD Progress. 19(1): 10-11. Spring 2004.

Protein is an essential nutrient that is a chief component of cells in the body. Protein is essential for building and repairing body tissues, supporting the immune system, and providing the proper balance of neurotransmitters. For people with polycystic kidney disease (PKD), protein needs vary according to their kidney function. This article considers the protein needs of people with early stage PKD who are not yet on dialysis. Topics include the foods that contain protein, guidelines for amounts of protein to be eaten, the different types of protein (animal versus vegetable), and the use of soy proteins. One chart lists common protein sources (animal and vegetable), and the grams of protein in one serving size (also described). 1 table.

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Autosomal Dominant Polycystic Kidney Disease. In: Johnson, R.J. and Feehally, J. Comprehensive Clinical Nephrology. 2nd ed. Orlando, FL: Mosby, Inc. 2003. p. 597-611.

Autosomal dominant polycystic kidney disease (ADPKD) is a multisystem disorder characterized by multiple, bilateral renal cysts associated with cysts in other organs such as liver, pancreas, and arachnoid membranes. Noncystic, extrarenal (outside the kidney) manifestations of ADPKD include mitral valve prolapse, intracranial aneurysms, and hernias. This chapter on ADPKD is from a comprehensive textbook that covers every clinical condition encountered in nephrology (the study of kidney disease). The authors of this chapter cover an introduction and definitions, epidemiology and pathogenesis, clinical manifestations, pathology, diagnosis and differential diagnosis, natural history, transplantation, and treatment strategies, including those for flank pain, cyst hemorrhage, urinary tract and cyst infection, nephrolithiasis (kidney stones), hypertension (high blood pressure), renal failure, and polycystic liver disease. The chapter is clinically focused and extensively illustrated in full color. 11 figures. 1 table. 39 references.

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Eye and Kidney: From Clinical Findings to Genetic Explanations. Journal of the American Society of Nephrology. 14(2): 516-529. February 2003.

Although the study of embryonic eye and kidney development was first studied in the middle of the 19th century, three decades passed until scientists identified the molecular controls of both renal (kidney) and eye organogenesis. Most of these advances have come from mouse and rodent gene manipulation. Translation of the mouse data to human congenital oculorenal disease has just begun. In this article, the authors propose a clinical diagnostic approach of oculorenal syndromes with their genetic links. Genetic disorders covered include coloboma, aniridia, Alagille syndrome, Zellweger syndrome, autosomal dominant polycystic kidney disease (ADPKD), von Hippel Lindau disease, Sturge-Weber syndrome, Krabble syndrome (phacomatosis pigmentovascularis), tuberous sclerosis complex, Bardet-Biedl syndrome, Alport syndrome, nail patella syndrome, and LCAT deficiency. 1 table. 122 references.

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Living Successfully With the Challenges for ADPKD Patients. PKD Progress. 18(4): 11. Winter 2003.

This brief newsletter article helps people with autosomal dominant polycystic kidney disease (ADPKD) learn some healthy strategies for coping with their illness. The author stresses that living with ADPKD involves a series of events that may trigger grief, from first diagnosis to dealing with symptoms and complications. However, the process of grief helps people normalize the loss and move forward. The author reviews ways to determine whether one is having significant problems with the grief process and also describes strategies that may help patients speed up the grief process and deal more successfully with ADPKD in general. Suggestions are noted in the areas of staying in contact with others, exercise, a positive attitude, and the role of humor.

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Living Successfully With the Challenges of ARPKD for Parents. PKD Progress. 18(4): 12. Winter 2003.

This brief newsletter article helps parents of children with autosomal recessive polycystic kidney disease (ARPKD) learn some healthy strategies for coping with their caregiving and parenting role. The author stresses that feelings of grief after learning of the child's diagnosis are common and notes that it is also natural to feel anger, fear, and shock. The author encourages readers to take an attitude that emphasizes the positive, healthy aspects of the situation. The author introduces the acronym ELAN, as a strategy for achieving a positive attitude. ELAN is from Empowerment, Learn about the disease, Allow time for self-growth (of the caregiver), and Notice the needs of other members of the family.

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Living Successfully With the Challenges of PKD for Caregivers. PKD Progress. 18(4): 13. Winter 2003.

This brief newsletter article helps family caregivers of people with polycystic kidney disease (PKD) learn some healthy strategies for coping with their caregiving role. The author stresses that feelings of helplessness are common for both patients and caregivers and notes that it is also natural to feel angry, guilty, and fearful. The author encourages readers to take an attitude that emphasizes the positive, healthy aspects of the situation and the burdens of care will seem lighter. Readers are also encouraged to seek others in similar positions, to work with support groups and voluntary organizations (such as the PKD Foundation and chapters), and to make sure that their own needs are addressed on a regular basis. The article concludes with the web site address of the National Family Caregivers Association (www.nfcacares.org).

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Phosphorus Levels. PKD Progress. 18(3): 10. Fall 2003.

In patients with renal (kidney) insufficiency, the kidneys may not be able to remove enough phosphorus from the blood, causing the levels of phosphorus to become too high. A high blood phosphorus level may cause itchy skin and a loss of calcium from the bones. This fact sheet from a newsletter for polycystic kidney disease patients briefly reminds readers of the role of phosphorus and the importance of eating fewer foods that are high in phosphorus. The fact sheet also discusses the role of medications such as calcium carbonate (Tums), calcium acetate (PhosLo) or sevelamer hydrochloride (Renagel) that help bind phosphorus in the bowel. Readers are also encouraged to work closely with a dietitian to maximize their kidney function. 1 figure.

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Polycystic Kidney Disease. New York, NY: National Kidney Foundation. 2003. [10 p.].

This brochure, from the National Kidney Foundation, describes polycystic kidney disease (PKD), a condition in which cysts (fluid filled pouches) are found in the kidney. The brochure is written in a question and answer format and considers topics including a definition of PKD, who is at risk for developing the disease, the symptoms of PKD, diagnostic tests used to confirm the condition, the risks of progressing from PKD to kidney failure, treatment options for PKD (particularly those supportive treatments that may prevent or slow down loss of kidney function), dietary modifications that might be indicated in patients with PKD, exercise, pregnancy, and the role of genetics and genetic counseling. The brochure includes current research activities on PKD. Readers are referred to two resource organizations for more information (the National Kidney Foundation at www.kidney.org and the Polycystic Kidney Disease Foundation at www.pkdcure.org). The brochure concludes with a brief description of the goals and activities of the National Kidney Foundation. 1 figure.

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Soy Protein. PKD Progress. 18(4): 17. Winter 2003.

The typical American diet includes few or no soy products. This brief newsletter article describes recent information about soy-based protein sources, particularly in the diets of patients with autosomal dominant polycystic kidney disease (ADPKD). The author notes that, at this point, it is not clear what is causing the beneficial effects of soy-based diets. In human studies, soy-based protein intake has been linked to a reduction in coronary heart disease and has been shown to decrease total cholesterol levels. ADPKD patients with higher HDL cholesterol levels appear to lose renal (kidney) function at a slow rate. This may be the mechanism by which soy protein protects the kidney in ADPKD from progressive damage. Importantly, when soy extracts are used rather than soy-based diets, the same cholesterol-lowering effect is not found, suggesting that other components associated with soy may be important or that digestive processes involving soy in foods are more important than soy itself.

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Understanding Conditions That Lead to Chronic Kidney Disease. Kidney Beginnings. 2(3): 6-8. September-October 2003.

This patient education article helps readers understand the conditions that can lead to chronic kidney disease (CKD). Two of the most common conditions are diabetes and hypertension. Of all the patients who have kidney failure, 43.5 percent have diabetes and 26.5 percent have high blood pressure. The remaining 29.8 percent lost kidney function due to another condition. The author describes the various diseases that can lead to CKD (diabetes and hypertension) in more detail, with brief mention of glomerulonephritis, nephrotic syndrome, and polycystic kidney disease (PKD). Readers are referred to the American Association of Kidney Patients (800-749-2257 or www.aakp.org) for more information.

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ABC's of Vitamins. PKD Progress. 17(4): 14. Winter 2002.

This brief newsletter article helps readers with polycystic kidney disease (PKD) understand the role of vitamins and vitamin supplements. The article stresses that vitamins are an important source of energy, and 13 have been established as essential compounds in the diet (because the human body cannot manufacture them). The article focuses on vitamin C and the problems with excess intake, and vitamin A, also problematic in too-high doses. The article concludes by discussing water soluble vitamins (including folic acid and the B vitamins) that are lost during the process of both hemodialysis and peritoneal dialysis and should be replaced.

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Cilia in PKD: Letting It All Hang Out. JASN. Journal of the American Society of Nephrology. 13 (10): 2614-2616. October 2002.

This editorial serves as an introduction to a research article that considers the role of the primary cilia in tubular epithelial cells in polycystic kidney disease (PKD). The author stresses that the data reported in the accompanying article is a testament to the power of genetics and the importance of animal models. The observations in the animal models undoubtedly steered the polycystin work toward cilia. The cilia may otherwise have been overlooked or simply thought of as unlikely. The author concludes by noting the present challenge is to propose a mechanism to explain how cilia-related functions of polycystin, polaris, and cystin may cause PKD. Of course, cilia may only be part of the story when it comes to understanding what is able to generate cysts from tubules. 41 references.

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From Early CKD to Dialysis: Patient Information-seeking Facilitates Adjustment. Renal Rehabilitation Report. 10(3): S10. Fall 2002.

From the moment of diagnosis, people with kidney disease confront a wide range of questions about their condition, its treatment, and the effects each will have on their lives. This article shares the experiences of one patient who is new to dialysis (6 months) but who has dealt with chronic kidney disease because her father had the same type of polycystic kidney disease (PKD) with which she was diagnosed. The author shares her transition to incorporating dialysis into her life and explains her decision to use home hemodialysis. Readers are encouraged to arm themselves with knowledge, accept reality, and change what they can and need to change.

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In the Know: PKD Glossary. PKD Progress. 17(2): 7. Summer 2002.

This brief article offers a glossary of terms commonly used when discussing polycystic kidney disease (PKD). Terms defined are: anemia, blood urea nitrogen (BUN), creatinine, creatinine clearance, electrolytes, erythropoietin, hematuria, hypertension, nephrotic syndrome, proteinuria, and uremia. Each word is defined in a sentence or two. The article includes a web site recommended for patients who would like additional information (www.pkdcure.org).

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Pain Management in Polycystic Kidney Disease. PKD Progress. 17(2): 12-13. Summer 2002.

This article, from a newsletter for patients with polycystic kidney disease (PKD), outlines pain management strategies. The author stresses that a detailed patient history, physical examination, and examination of the urine can frequently pinpoint the cause of pain. The reasons for acute pain in the patient with PKD can differ from those that cause chronic pain. Physicians must acknowledge that the patient has pain and attempt to understand the cause of it; management of pain can then be done in a stepwise sequence. Noninvasive techniques for pain management can include ice massage, heating pads, whirlpool baths, use of the Alexander Technique, and psychobehavioral modification. The author notes that it is often difficult to cure chronic pain, but the goal is to reduce the frequency and severity of pain so as not to interfere with one's lifestyle. The next step involves analgesics (pain killers), beginning with over the counter drugs, then prescription drugs, including narcotics. If the drugs do not produce relief of pain, then more invasive techniques can be tried, such as transcutaneous electrical nerve stimulation (TENS), acupuncture, spinal cord stimulation (neuromodulation), and injection of narcotic agents directly into the spinal column. The last step is a surgical approach. The author concludes by encouraging readers not to give up hope, but to pursue a detailed evaluation and then a stepwise approach to the management of pain. The goal is to empower patients to be active participants in their own care.

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PKD Pharmacology. PKD Progress. 17(4): 11-13. Winter 2002.

Throughout the course of polycystic kidney disease (PKD), patients face a host of physical and biological challenges. This article describes three common problems associated with PKD and the medications used to treat them. The problems are hypertension (high blood pressure), anemia, and calcium and phosphorus issues. Drugs discussed include ACE inhibitors, beta blockers, calcium channel blockers, darbepoetin (a new form of erythropoietin), calcium carbonate, calcium acetate, sevelamer hydrochloride, and vitamin D.

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Q and A on PKD. Kansas City, MO: PKD (Polycystic Kidney Disease). 2002. 91 p.

In this monograph, scientific advisors from the Polycystic Kidney Foundation (PKF) answer patients' questions about dealing with polycystic kidney disease (PKD). The editors note that advances in basic and clinical science in the PKD field are occurring with encouraging speed and importance. Questions are considered in sixteen chapters: autosomal dominant PKD (ADPKD) genes and proteins; identification of the autosomal recessive polycystic kidney disease (ARPKD) gene; strategies to treat hypertension (high blood pressure) and end organ damage in ADPKD patients; diagnosis and genetics; extra-renal (outside the kidney) manifestations; liver and gastrointestinal involvement; brain (intracranial) aneurysms and cysts; hypertension; renal manifestations; infections and stones; proteinuria (protein in the urine) and hematuria (blood in the urine); pregnancy, birth control and menopause; kidney failure, dialysis, and transplantation; diet, drugs, surgery, and exercise; pain management; and general information. A final section considers PKD in children. A brief subject index concludes the monograph.

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Renal Contraction Therapy for Enlarged Polycystic Kidneys by Transcatheter Arterial Embolization in Hemodialysis Patients. American Journal of Kidney Diseases. 39(3): 571-579. March 2002.

Kidneys of patients with autosomal dominant polycystic kidney disease (ADPKD) usually continue to increase in size, even after patients begin dialysis therapy, and the mass effects may lead to severe complications. Such external conventional therapies as surgical and laparoscopic procedures have not yielded satisfactory results. This article reports on a technique in which the authors attempted renal contraction therapy in patients with ADPKD by renal transcatheter arterial embolization (TAE) using intravascular coils. After obtaining informed consent, the authors selected anuric (without urine formation) patients on dialysis therapy with markedly distended abdomens or macroscopic hematuria (blood in the urine) (n = 64). After therapy, renal sizes decreased to 73.8 percent, 61.7 percent, and 53.4 percent of preinterventional values at 3, 6, and 12 months after therapy, respectively. Abdominal circumference and dry weight were significantly decreased at 3, 6, and 12 months, compared with baseline values before therapy. This therapy was effective for all patients. Serious complications were not seen after this treatment, although such minor complications as fever and flank pain were observed within the first week after the procedure. The authors conclude that treatment with TAE is a safe and effective procedure that has resulted in improvement in the quality of life and nutritional status of patients with ADPKD. 8 figures. 16 references.

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Tips for Caffeine. PKD Progress. 17(2): 10. Summer 2002.

This newsletter article gives readers with polycystic kidney disease (PKD) some tips for drinking caffeinated beverages while still following their special dietary restrictions. The author notes that caffeinated beverages have been reported to be potentially detrimental to people with autosomal dominant PKD (ADPKD), possibly by triggering or promoting cyst expansion. However, caffeine has not been tested in animals or humans with ADPKD to determine its effects on cyst-fluid secretion. Excessive caffeine intake has detrimental health effects whether or not one has ADPKD. Caffeine intake is usually considered excessive when a person drinks more than three or four cups of a caffeinated beverage in a day. The author recommends that readers limit caffeine intake and consider stopping the consumption of caffeine altogether to promote healthy living. One chart lists the caffeine content of nine common sodas, and ten different types of coffee and tea.

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Tips for Eating Out. PKD Progress. 17(2): 11. Summer 2002.

This newsletter article gives readers with polycystic kidney disease (PKD) some tips for eating at restaurants while still following their special dietary restrictions. The author notes that a healthy diet is essential in controlling high blood pressure (hypertension) and prolonging kidney function. The author lists specific strategies for ordering, requesting specially prepared food, and choosing desserts. One sidebar offers strategies for beginning and maintaining an exercise program as an adjunct to dietary approaches.

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ARPKD: A Quick Review. PKD Progress. 16(3): 7. Summer 2001.

ARPKD (autosomal recessive polycystic kidney disease) primarily affects, the kidneys (always both) with progressive cysts and the liver with congenital hepatic fibrosis (CHF), which is malformation and progressive scarring of the bile duct system. This brief article reviews ARPKD, its diagnosis and treatment. The author notes that because of continually improved mechanical ventilation, neonate support, control of systemic and portal hypertension, management of ESRD, and transplantation, the ARPKD population is living longer into adulthood. Unfortunately, 30 to 50 percent of infants with ARPKD die at birthor shortly thereafter, usually as a result of underdeveloped lungs and pulmonary complications. Almost everyone with ARPKD is diagnosed during infancy or childhood; however, the first signs of the disease vary greatly. Approximately 30 percent of the infants experience failure-to-thrive, although the exact cause is unknown. Hypertension (high blood pressure) is thought to be a factor in progression of renal deterioration, and without aggressive treatment, severe hypertension can be life threatening. The same inherited defect that affects the kidneys occurs in the liver, but the two organs react differently with great variability of onset and severity of clinical symptoms. Even for symptomatic individuals, synthetic liver function generally is preserved, as it usually continues to excrete, produce, and regulate hormones and chemicals normally.

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Can Progression of Autosomal Dominant or Autosomal Recessive Polycystic Kidney Disease be Prevented?. Seminars in Nephrology. 21(5): 430-440. September 2001.

Data from animal and human studies suggest that the rate of progression of renal insufficiency can be slowed with careful control of blood pressure, use of a low-protein diet, and the use of lipid-lowering agents. This article reports on research investigating whether progression of autosomal dominant or autosomal recessive polycystic kidney disease (PKD) can be prevented. Several dietary and pharmacologic (drug) intervention strategies, including blood pressure control, dietary modification, and the use of antioxidants as well as lipid (blood fats) lowering agents have been studied in humans and animals with PKD in an effort to slow the rate of renal progression. The authors review the current understanding of the effectiveness of these conventional therapies, as well as new therapies that specifically target the mediators of cyst formation in PKD. These new therapies use tyrosine kinase inhibitors and gene therapy in efforts to identify potential strategies for slowing cyst formation and parenchymal injury (to the body of the kidney organ) in PKD. Current drug and diet strategies fail to show any consistent benefits in preserving renal (kidney) function and reducing renal injury in human PKD. The authors call for randomized, controlled trials in children and adults with early PKD in order to evaluate the effectiveness of these newer therapeutic interventions. 1 table. 113 references.

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Cysts of the Liver. In: Okuda, K., ed.,et al. Hepatobiliary Diseases: Pathophysiology and Imaging. Malden, MA: Blackwell Science, Inc. 2001. p. 505-516.

Nonparasitic liver cyst is defined as a closed cavity that contains liquid and is lined with epithelium (lining cells). Most cysts are derived from the biliary system. Congenital liver cysts may arise from genetic abnormalities and are frequently associated with renal malformations. Some pathologists group and consider these disorders together as cystic disorder complexes syndrome (CDCS) or as hepatic fibropolycystic disease. This chapter on cysts of the liver is from a textbook that familiarizes the reader with various imaging modalities, the information they provide, and the merits of each, in order to facilitate the combined use of different imaging techniques in the diagnosis and management of hepatobiliary (liver and bile tract) diseases. Topics include CDCS, solitary cysts, polycystic disease of the liver, autosomal-recessive polycystic disease, autosomal-dominant polycystic kidney disease, ciliated hepatic foregut cyst, hepatic peribiliary cysts, uncommon cystic lesions of the liver, and issues in imaging. The authors note that typical hepatic cysts are detected easily with any imaging modality. 17 figures. 1 table. 26 references.

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Genetics and Physiology of Polycystic Kidney Disease. Seminars in Nephrology. 21(2): 107-123. March 2001.

Autosomal dominant polycystic kidney disease (ADPKD) is a major, inherited disorder that is characterized by the growth of large, fluid filled cysts from the tubules and collecting ducts of affected kidneys, and by a number of extrarenal manifestations including liver and pancreatic cysts, hypertension, heart valve defects, and cerebral (brain) and aortic aneurysms. This article explores the genetics and physiology of polycystic kidney disease. Mutations in either of 2 different genes (PKD1 or PKD2) give rise to ADPKD. The authors note that most mutations identified in affected families appear to inactivate the PKD genes, and they discuss accumulating evidence that suggests that a 2 hit mechanism, in which the normal PKD1 or PKD2 allele is also mutated, may be required for cyst growth. The pathogenesis of cyst formation is currently thought to involve increased cell proliferation, fluid accumulation, and basement membrane remodeling. In contrast to normal kidney cells whose cell proliferation is inhibited by cyclic AMP (adenosine monophosphate), ADPKD cells are stimulated to proliferate. Cyclic AMP and growth factors, including epidermal growth factor, have complementary effects to accelerate the enlargement of ADPKD cysts, and thereby to contribute to the progression of the disease. The authors hope that this knowledge will facilitate the discovery of inhibitors of signal transduction cascades that can be used in the treatment of ADPKD. 3 figures. 234 references.

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Health Tips for Living with Polycystic Kidney Disease. Kansas City, MO: PKD (Polycystic Kidney Disease) Foundation. 2001. 72 p.

Dietary strategies are now proving to play an important role in alleviating the symptoms of renal (kidney) failure and may, in fact, slow the progression toward renal failure as well. This book helps people with polycystic kidney disease (PKD) adopt a healthy lifestyle. The book covers a rational and practical approach to optimizing the diet, health care information for women with PKD, alternative approaches to maintaining a more comfortable and pain-free existence, and how to find support in the renal community. The book is divided into four sections: a comprehensive section regarding diet and autosomal dominant PKD (ADPKD); a section reviewing issues of pregnancy and estrogen use for women with PKD; a section dealing with chronic pain and exercise; and a section on where to go in the renal community for support and information. Three appendices conclude the book: sodium content of common foods, high-quality protein vegetarian combinations, and protein-wise menus. The addresses and website locations of related resource organizations are also provided. 4 figures.

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Health Tips for Living with Polycystic Kidney Disease. Kansas City, MO: PKD (Polycystic Kidney Disease) Foundation. 2001. 72 p.

Polycystic kidney disease (PKD) has two hereditary forms: autosomal dominant (ADPKD), the most common of all life-threatening genetic diseases, or autosomal recessive (ARPKD), a relatively rare disease that often causes significant mortality in the first month of life. Cysts are sacs of fluid that cause the kidney to enlarge and that can hinder the kidney's filtering ability. Recent research has found certain dietary modifications, hypertension (high blood pressure) treatments, and lifestyle changes to have a favorable, progression-slowing impact on PKD. This book offers strategies for healthy living for people with ADPKD. The book is divided into four sections: a comprehensive section regarding diet and ADPKD; a section reviewing issues of pregnancy and estrogen use for women with PKD; a section dealing with chronic pain and exercise; and a section on where to go in the renal community for support and information. The book concludes with a list of websites for additional information, a listing of National ESRD (End Stage Renal Disease) Network Organizations, and appendices that list sodium content of common foods, high quality protein vegetarian combinations, and special menus. 4 figures.

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Molecular Genetics and Pathogenesis of Autosomal Dominant Polycystic Kidney Disease. In: Coggins, C.H.; Hancock, E.W., Eds. Annual Review of Medicine: Selected Topics in the Clinical Sciences, Volume 52. Palo Alto, CA: Annual Reviews Inc. 2001. p. 93-123.

Autosomal dominant polycystic kidney disease (ADPKD) is a common and systemic disease characterized by formation of focal cysts in the kidneys. Rapid progress has been made over the past few years in identifying the genes responsible for the vast majority of cases of ADPKD, in unraveling the underlying mutations, in localizing the gene products at the cellular and subcellular levels, and in developing animal models that reproduce many of the disease features. This article considers the molecular genetics and pathogenesis of ADPKD. Of the three potential causes of cysts, downstream obstruction, compositional changes in extracellular matrix, and proliferation of partially dedifferentiated cells, evidence strongly supports the latter as the primary abnormality. In the vast majority of cases, the disease is caused by mutations in PKD1 or PKD2, and appears to be recessive at the cellular level. Somatic second hits in the normal allele of cells containing the germ line mutation initiate or accelerate formation of cysts. PKD1 and PKD2 encode a putative adhesive ion channel regulatory protein and an ion channel respectively. The two proteins interact directly in vitro. Their cellular and subcellular localization suggest that they may also function independently in a common signaling pathway that may involve the membrane skeleton and that links cell to cell and cell to matrix adhesion to the development of cell polarity. 2 figures. 225 references.

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Multicystic Dysplastic Kidney Disease. In: Gearhart, J.P.; Rink, R.C.; Mouriquand, P.D. Pediatric Urology. Philadelphia, PA: W.B. Saunders Company. 2001. p. 279-287.

This chapter on multicystic dysplastic kidney disease is from a comprehensive textbook on pediatric urology that emphasizes the pathophysiology of various disorders. The authors note that dysplasia is identified on microscopic examination by the presence of primitive ducts and metaplastic cartilage. It can occur in varied amounts from isolated areas to encompassing the entire kidney. Dysplasia accompanied by cysts is referred to as multicystic dysplasia, whereas dysplasia with a preponderance of cysts encompassing the kidney is known as multicystic dysplastic kidney disease (MCDK). Three morphological types of MCDK exist. Once antenatal screening ultrasonography became routine, a greater number of MCDKs were suspected, and the management as well as the potential complications needed to be elucidated. The authors review histology, etiology, clinical features, diagnosis, natural history, and treatment. 6 figures. 116 references.

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Anemia-Related Fatigue: Feeling Tired Isn't Always Normal. PKR Progress. 15(3): 10. Fall-Winter 2000.

This article from a newsletter for patients with polycystic kidney disease (PKD) explores the problem of anemia related fatigue in patients with kidney diseases. The author notes that since basic treatments are available for PKD, health care providers and researchers are now turning their attention to quality of life medical issues such as anemia. Anemia develops in virtually all patients with renal failure during the course of their disease. Health care providers now know that by intervening earlier in the disease process (in patients with chronic kidney disease who are not yet on dialysis), patients can realize a number of benefits and enhance their overall well being. The kidneys produce about 90 percent of the body's supply of the hormone erythropoietin (EPO); EPO is a major catalyst in the production of red blood cells in the bone marrow, so a reduction in EPO due to kidney disease usually results in fewer red blood cells and insufficient oxygen reaching the body tissues. The author explains the two primary diagnostic tests used to check for anemia, hematocrit (HCT) and hemoglobin. Anemia related fatigue is often described as a total lack of energy or debilitating exhaustion that can last days, weeks, or months. Fatigue can also have mental and emotional effects. The author cautions that because of its gradual onset and insidious nature, fatigue is often overlooked, underrecognized, and undertreated. Readers are encouraged to work with their physicians to address any problems or symptoms of fatigue.

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Evaluation of the Transplant Recipient. In: Danovitch, G.M., ed. Handbook of Kidney Transplantation. 3rd ed. Philadelphia, PA: Lippincott Williams and Wilkins. 2000. p. 130-145.

This chapter on evaluation of the transplant recipient is from a handbook of kidney transplantation that provides practical information on therapy, patient monitoring, and patient care management. In this chapter, the authors stress that the potential kidney transplant recipient must be evaluated by the transplantation team to determine whether he or she is a suitable candidate. The patient must also make a personal evaluation of the transplantation option, and the transplant team must see to it that the patient's evaluation is an educated one. The excellent statistics achieved by most transplantation centers for graft survival and morbidity have changed the attitude of both physicians and patients regarding the appropriateness of transplantation. Now, nearly all patients with end stage renal disease (ESRD) can be regarded as potentially acceptable candidates for transplantation. Instead of denying the option to broad groups of patients, such as the elderly or those with diabetes mellitus and coronary artery disease, each person's candidacy should be evaluated individually. The author of this article outlines and briefly explains contraindications to kidney transplantation, including malignancy, chronic infection, severe extrarenal disease, noncompliance, and psychiatric illness. Other topics include the general medical evaluation of the recipient, urologic evaluation, patient education concerns, special features related to the primary kidney disease (including diabetes mellitus, systemic lupus erythematosus, focal glomerulosclerosis, Goodpasture's syndrome, Alport's syndrome, amyloidosis, paraproteinemia, polycystic kidney disease, Fabry's disease, scleroderma, hyperoxaluria, thrombotic thrombocytopenic purpura, systemic vasculitis and Wegener's granulomatosis, and sickle cell disease), risk factors related to organ system diseases, and risk factors related to individual patient characteristics (age, obesity, malnutrition, peritoneal dialysis, previous transplantations, double organ candidates). 4 tables. 17 references.

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Kidney Disease and Gastrointestinal Involvement. Dialysis and Transplantation. 29(4): 202-204, 206-207. April 2000.

Some kidney diseases may present with gastrointestinal (GI) manifestations. Conversely, in some gastrointestinal diseases, renal involvement is present. In addition, some systemic diseases are associated with both kidney and GI involvement. In this review article, the interrelationship between kidney diseases and GI manifestations is addressed. The interrelationship between the kidney and liver diseases is also covered. Patients with chronic renal failure (CFR) often consult the gastroenterologist first because of anorexia, nausea, vomiting, heartburn, and indigestion of a few months duration. Patients with acute renal failure (ARF) may also present with anorexia (lack of appetite), nausea, vomiting, and GI bleeding. Kidney diseases that may cause GI manifestations include acute glomerulonephritis, nephrotic syndrome, reflux nephropathy and pyelonephritis, analgesic (pain medication) nephropathy, acute tubulointerstitial nephritis following NSAID administration, obstructive uropathy, polycystic kidney disease (PKD), and GI manifestations in patients on dialysis. Gastrointestinal related causes may contribute to the following kidney diseases: prerenal failure resulting from fluid losses related to vomiting, diarrhea, hemorrhage, bowel fistula, or bowel obstruction; acute tubular necrosis resulting from extreme renal ischemia; obstructive uropathy usually due to active inflammatory GI disease; urinary tract infections, which often result in women from E. coli ascending from the GI tract; postinfectious glomerulonephritis; IgA nephropathy, which is often secondary to chronic liver diseases, celiac disease (gluten intolerance), Crohn's disease, adenocarcinomas of the GI tract, and other diseases such as shistosomiasis. 23 references.

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Kidney Disease and Gastrointestinal Involvement. Dialysis and Transplantation. 29(4): 202-204, 206-207. April 2000.

Some kidney diseases may present with gastrointestinal (GI) manifestations. Conversely, in some GI diseases, renal involvement is present. In addition, some systemic diseases are associated with both kidney and GI involvement. In this review article, the interrelationship between kidney diseases and GI manifestations is addressed. The interrelationship between the kidney and liver diseases is also covered. Patients with chronic renal failure often consult a gastroenterologist first because of anorexia, nausea, vomiting, heartburn, and indigestion of a few month's duration. Patients with acute renal failure may also present with anorexia (lack of appetite), nausea, vomiting, and GI bleeding. Kidney diseases that may cause GI manifestations include acute glomerulonephritis, nephrotic syndrome, reflux nephropathy and pyelonephritis, analgesic (pain medication) nephropathy, acute tubulointerstitial nephritis following administration of NSAIDs, obstructive uropathy, polycystic kidney disease, and GI manifestations in patients on dialysis. GI related causes may contribute to the following kidney diseases: prerenal failure, resulting from fluid losses related to vomiting, diarrhea, hemorrhage, bowel fistula, or bowel obstruction; acute tubular necrosis, resulting from extreme renal ischemia; obstructive uropathy, usually due to active inflammatory GI disease; urinary tract infections, which often result in women from E. coli ascending from the GI tract; postinfectious glomerulonephritis; IgA nephropathy, which is often secondary to chronic liver diseases, celiac disease (gluten intolerance), Crohn's disease, adenocarcinomas of the GI tract; and liver disease. 23 references.

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Nephrolithiasis Associated with Autosomal Dominant Polycystic Kidney Disease: Contemporary Urological Management. Journal of Urology. 163(3): 726-729. March 2000.

This article reports on a study undertaken to evaluate the role of contemporary urological intervention in patients with nephrolithiasis (kidney stones) associated with autosomal dominant polycystic kidney disease (ADPKD). Intervention for upper tract stones associated with autosomal dominant polycystic kidney disease was performed in 5 women and 2 men, aged 29 to 65 years old (mean age 47 years). Indications for intervention consisted of flank pain in 6 patients or hematuria (blood in the urine) in 2 patients. A total of 12 procedures (mean 1.7 per patient) were performed, including shock wave lithotripsy (ESWL) in 6 patients, percutaneous nephrolithotomy (surgery 'through the skin' to remove the stones) in 2 patients, retrograde endoscopy or manipulation in 3 patients, and extended pyelonephrolithotomy in 1 patient. All patients were rendered stone free or had only residual 'dust.' Hospital stay for 5 patients was 1 night or less, and there were no complications. Renal (kidney) function for each patient was stable or improved as measured by serum creatinine. The authors conclude that most patients with ADPKD who require intervention for kidney stones can be safely and effectively treated with essentially any or all contemporary, minimally invasive techniques. The choice of intervention can be based primarily on size and location of the upper tract stones rather than the associated presence of polycystic kidneys. 3 figures. 1 table. 7 references.

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Pathogenesis of Autosomal Dominant Polycystic Kidney Disease: An Update. Current Opinion in Nephrology and Hypertension. 9(4): 385-394. July 2000.

The identification of PKD1 and PKD2, the two major genes responsible for autosomal dominant polycystic kidney disease (ADPKD), are the important discoveries upon which much of the current investigation into the pathogenesis of this common heritable disease is based. This article updates readers on the pathogenesis of ADPKD. A major mechanistic insight was achieved with the discovery that ADPKD occurs by a two hit mechanism requiring somatic inactivation of the normal allele in individual polarized epithelial cells. Most recent advances are focused on the function of the respective protein products (polycystin 1 and polycystin 2). Indirect evidence supports and interaction between polycystin 1 and 2, but the authors note that it is unlikely that they work in concert in all tissues and at all times. The authors review the similarities and differences of these protein products and their role in understanding ADPKD. The authors describe ongoing research projects and note that the understanding of this disease is reaching a critical stage at which rational treatment approaches may become reality. Identification of targets for conditional lethality in cyst lining cells will be a major step in modifying the course of this disease. 2 figures. 69 references.

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Surgery for Adult Polycystic Liver Disease. Journal of Gastroenterology and Hepatology. 15(11): 1239-1242. November 2000.

Adult polycystic liver disease, commonly associated with polycystic kidney disease, can result in massive hepatomegaly (enlarged liver) and debilitating symptoms. This article reviews the use of surgery for adult polycystic liver disease (APLD). Surgical intervention for symptomatic APLD, such as cyst fenestration (the creation of an opening in the cyst) or liver resection has been associated with significant morbidity (illness and complications) and inconsistent long term palliation. However, selected patients with severe symptoms benefit from liver resection and extensive fenestration with acceptable morbidity and mortality (death). These procedures can allow the excision of most prominent cysts with minimal resection of liver tissue; liver volume is preserved despite the polycystic disease. Total hepatectomy (removal of the liver) and orthotopic liver transplantation may need to be considered for patients with severe APLD. The author of the review describes the surgical results of various types of operations to help surgeons conceptualize which operation to offer patients with APLD. 1 table. 50 references.

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Your Kidneys: Master Chemists of the Body. New York, NY: National Kidney Foundation. 2000. 14 p.

The schematic drawings of the urinary system in this booklet describe the location of the kidneys in the body and the kidney filtering system. Types and causes of kidney disease are also discussed including diabetes, high blood pressure, glomerulonephritis, polycystic kidney disease, kidney stones, urinary tract infections, and congenital diseases. The warning signs of kidney disease and the treatments available for advanced kidney failure are considered briefly.

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