“Adults would stare, and kids would come up and ask if she had a baby in her tummy,” says Justine Harbin of Weirton, WV, about her daughter, Mia, 4. Mia has polycystic kidney disease (PKD). So does Ms. Harbin, and Mia’s two sisters, Lilly and Kennedy. That’s why the appearance of Mia’s kidneys on the ultrasound didn’t come as much of a surprise to her (“They took up her whole stomach,” she says). Neither did the official diagnosis of PKD that was made shortly after Mia’s birth.
“A year before her transplant, Mia’s kidneys were over three times the normal length, let alone volume. When you picked her up to put her on the examination table, you could feel the cysts between your fingers. I’ve never seen anything remotely like the degree of PKD that Mia had.”
PKD is a genetic disorder in which kidneys develop cysts filled with fluid that can grow and cause damage, leading to kidney failure. Other complications include liver damage and high blood pressure. Mia’s liver wasn’t involved, but her blood pressure became increasingly hard to control, despite being on four different medications at once. Soon, signs of congestive heart failure appeared, and Mia would easily become tired and short of breath. The tiniest kid in her class, she was also falling off the growth curve for her age.
Time to Act
Failing kidneys aren’t always removed, but if they’re infected, or if there isn’t room for them, they will be, in a procedure called a nephrectomy. Nephrectomies and transplants aren’t typically performed together. Patients with PKD most often undergo the nephrectomy first, then stay on dialysis for months or years until his or her doctors determine that the time is right for a transplant.
But not this time. “We thought that Mia was not the best candidate for dialysis, for a couple of reasons,” says Dr. Nguyen. “The family lives an hour-and-a-half away, so the burden of coming to Pittsburgh three, four, five times each week was a huge undertaking.”
As it happens, there was an even better reason: Abhinav Humar, MD, division chief of UPMC Transplant Surgery, was willing to perform the nephrectomy and transplant as part of the same surgery. “Our nephrology team is experienced, and we have the surgical expertise to back it up,” he says “We transplant children that maybe other centers are reluctant to transplant, or they make them wait.”
In June 2016, Mia had both kidneys removed and received a transplant from a live donor. The procedure took under six hours, and during it, Mia went from 35 to 25 pounds—shedding 10 pounds of kidney. “There was almost more kidney than Mia in there,” says Ms. Harbin.
After Transplant
To say that Mia rebounded from the surgery would be an understatement. The blood pressure that Dr. Nguyen characterized as “ridiculously high” went back to normal during her hospital stay, and Dr. Nguyen believes that her symptoms of congestive heart failure will resolve with time. She’s shown great catch-up growth, and is making up with lost time when it comes to running, and, says her mom, bossing everyone around.
“To see her blossom and thrive and chase her sister down the hallway – she’s doing things she could never do before,” says Dr. Nguyen. “It’s like this huge burden was just taken from her, and she’s just the picture of what you want a kid to be at that age. That’s why we transplant.”
PKD & Kidney Research From The Hindu, by TAMIL NADU
CHENNAI: By the end of the decade it may not be necessary to wait for a cadaveric kidney or a donor for a renal transplant. Then, it might b possible to have an artificial device that would take over the function of the kidney.
Research in this regard has been on for the past 15 years and indications are that by end-2017, the device would be tested for its safety on patients. A clinical trial would involve not more than a dozen patients, said Shuvo Roy, researcher from the University of California, San Francisco.
Dr. Roy, who delivered the Mrs. Malathi VenkatesanTANKER Foundation memorial lecture on Wednesday, spoke about the device and how it evolved.
The device is designed in such a way that it would not only carry out the job of a dialysis machine but cell membrane from a cadaveric kidney injected along with the device would ensure a continuous supply of nutrition is available. The device not only dispenses with dialysis but also helps maintain the health of the patient. It also does not require anti-coagulant drugs.
A bioengineer, Dr. Roy said though kidney failure affects only 0.1% of the population in the United States but consumes around 7% of the national budget, that is US$ 33 billion. Given this scenario, and the fact that the safety test and the efficacy test are yet to be done he said it is difficult to speculate over the price of the device. Yet, it would, be a boon as the cost of the device could be either as much as or lower than a renal transplant. And dialysis is three times more expensive than transplant.
While the safety test would be done on not less than a dozen patients the efficacy test would require at least 100 patients. “We envision safety test next year and the efficacy test probably in three years and that would be the proof of the product,” he said.
The shelf life of the device would depend on the data that would be generated during the efficacy test. Even if the device lasts one or two years, easy access to a replacement would have to be ensured, he added.
Sowmya Swaminathan, secretary, Department of Medical Research said in India at least 1% of the population suffers from end stage renal disease. She said Indian start-up companies could collaborate to manufacture the device for the country’s requirement.
The latest Pharmaceutical and Healthcare disease pipeline guide Polycystic Kidney Disease - Pipeline Review, H2 2016, provides an overview of the Polycystic Kidney Disease (Genetic Disorders) pipeline landscape.
Report Highlights
Pharmaceutical and Healthcare latest pipeline guide Polycystic Kidney Disease - Pipeline Review, H2 2016, provides comprehensive information on the therapeutics under development for Polycystic Kidney Disease (Genetic Disorders), complete with analysis by stage of development, drug target, mechanism of action (MoA), route of administration (RoA) and molecule type.
The guide covers the descriptive pharmacological action of the therapeutics, its complete research and development history and latest news and press releases.
The Polycystic Kidney Disease (Genetic Disorders) pipeline guide also reviews of key players involved in therapeutic development for Polycystic Kidney Disease and features dormant and discontinued projects. The guide covers therapeutics under Development by Companies /Universities /Institutes, the molecules developed by Companies in Pre-Registration, Phase III, Phase II, Phase I, Preclinical and Discovery stages are 1, 1, 2, 1, 11 and 2 respectively for Similarly, the Universities portfolio in Preclinical and Discovery stages comprises 2 and 2 molecules, respectively for Polycystic Kidney Disease.
Polycystic Kidney Disease (Genetic Disorders) pipeline guide helps in identifying and tracking emerging players in the market and their portfolios, enhances decision making capabilities and helps to create effective counter strategies to gain competitive advantage. The guide is built using data and information sourced from proprietary databases, company/university websites, clinical trial registries, conferences, SEC filings, investor presentations and featured press releases from company/university sites and industry-specific third party sources.
Additionally, various dynamic tracking processes ensure that the most recent developments are captured on a real time basis.
Polycystic kidney disease (PKD) is a genetic disorder that causes many fluid-filled cysts to grow in your kidneys. Unlike the usually harmless simple kidney cysts that can form in the kidneys later in life, PKD cysts can change the shape of your kidneys, including making them much larger.
PKD is a form of chronic kidney disease (CKD) that reduces kidney function and may lead to kidney failure. PKD also can cause other complications, or problems, such as high blood pressure, cysts in the liver, and problems with blood vessels in your brain and heart.Polycystic kidney disease is a genetic disorder that causes many fluid-filled cysts to grow in your kidneys. What are the types of PKD?
PKD is one of the most common genetic disorders. PKD affects about 500,000 people in the United States.1
ADPKD affects 1 in every 400 to 1,000 people in the world, and ARPKD affects 1 in 20,000 children.2,3 Who is more likely to have PKD?
PKD affects people of all ages, races, and ethnicities worldwide. The disorder occurs equally in women and men.
What causes PKD?
A gene mutation, or defect, causes PKD. In most PKD cases, a child got the gene mutation from a parent. In a small number of PKD cases, the gene mutation developed on its own, without either parent carrying a copy of the mutated gene. This type of mutation is called “spontaneous.” Read more about genes and genetic conditions . What are the signs and symptoms of PKD?
The signs and symptoms of ADPKD, such as pain, high blood pressure, and kidney failure, are also PKD complications. In many cases, ADPKD does not cause signs or symptoms until your kidney cysts are a half inch or larger in size.
Early signs of ARPKD in the womb are larger-than-normal kidneys and a smaller-than-average size baby, a condition called growth failure. The early signs of ARPKD are also complications. However, some people with ARPKD do not develop signs or symptoms until later in childhood or even adulthood.
Can I prevent PKD?
Researchers have not yet found a way to prevent PKD. However, you may be able to slow PKD problems caused by high blood pressure, such as kidney damage. Aim for a blood pressure goal of less than 120/80. Work with a health care team to help manage your or your child’s PKD. The health care team will probably include a general practitioner and a nephrologist, a health care provider specializing in kidney health.
PKD Foundation co-Founder Jared J. Grantham, MD, passed away Sunday, Jan. 22 at 80 years old, the charity announced Jan. 24. He had been undergoing treatment for cancer.
Grantham and Joseph Bruening founded the PKD Foundation in 1982, with a vision to find treatments and a cure for polycystic kidney disease.
Grantham graduated from the University of Kansas School of Medicine and did his residency in internal medicine at the Kansas University Medical Center (KUMC). He also did a research fellowship at the National Heart Institute’s laboratory of kidney and electrolyte metabolism. Grantham became an assistant professor of medicine at KUMC in 1969. He served as Director of the Division of Nephrology from 1970 to 1995.
In 1989, Grantham founded and served as the first Editor-in-Chief of the Journal of the American Society of Nephrology. He also served as Program Chairman of ASN in 1985 and was a member of the Council for 10 years. From 1988–1989, he served as Secretary-Treasurer of ASN.
Memorial services will be held at Indian Heights United Methodist Church at 10211 Nall Ave, Overland Park KS 66207. Visitation services will be on Friday, Jan. 27 from 6:30 to 8:30 p.m., and a Celebration of Life will be held on Saturday, Jan. 28 at 2 p.m.
In lieu of flowers, Grantham’s family is accepting donations to the PKD Foundation to continue to advance his vision.
To see more information on Grantham, and share a memory, visit the PKD Foundation website.
Autosomal dominant polycystic kidney disease (ADPKD) is one of the most common inheritable human diseases and leads to renal failure; however, no effective treatment exists. In a new study, Xueying Lin and colleagues used TALEN-mediated gene editing to establish a zebrafish model of ADPKD and showed that activating autophagy reduces cystogenesis and restores renal function.
“As PKD1 is the most common causative gene for PKD, we generated zebrafish pkd1a mutants,” explains Lin. These pkd1a-null fish had pronephric cysts, mTOR hyperactivation and reduced autophagic flux — a feature also present in kidney epithelial cells from PKD1-null mice and patients with ADPKD.
To pinpoint the contribution of defective autophagy to cystogenesis, the researchers reduced the levels of ATG5 — a core autophagy protein — in pkd1a-deficient fish. This inhibition of autophagy increased the incidence of cyst formation caused by pkd1a depletion at an early time point (48% versus 10%). Conversely, activation of autophagy with a short peptide of beclin-1, with carbamazepine or minoxidil, or through mTOR inhibition with rapamycin reduced cyst formation and restored renal function in pkd1a-deficient fish. “Although abnormal autophagy had previously been shown in PKD models, our study demonstrates that autophagy activation exerts therapeutic benefits in PKD,” says Lin.
Inhibition of the mTOR pathway using rapamycin is a candidate therapy for PKD but high doses of this agent are toxic and have systemic adverse effects. Here, the researchers showed that the combination of a 10-fold reduced dose of rapamycin with carbamazepine had a synergistic effect and suppressed cystogenesis as efficiently as a high dose of rapamycin.
Going forward, the researchers plan to take advantage of the zebrafish embryo, an efficient in vivo model for small molecule screening. “We plan to screen known autophagy modulators, especially those already in clinical use, to identify effective new drugs for PKD.”
The present invention provides compounds of Formula (I) or (II), which are thought to be able to inhibit mTOR (mammalian target of rapamycin) signaling pathway, induce UPR (unfolded protein response), and/or perturb mitochondrial function of a cyst cell (e.g., a cyst cell causing polycystic kidney disease (PKD, e.g., autosomal dominant PKD (ADPKD) or autosomal recessive PKD (ARPKD)) or polycystic liver disease (PLD, e.g., autosomal dominant PLD (ADPLD) or autosomal recessive PLD (ARPLD)). The invention also provides pharmaceutical compositions, kits, and methods involving the compounds described herein for use in treating PKD or PLD, inhibiting the growth of a cyst cell, and/or killing a cyst cell.
DESCRIPCIÓN (El texto procesado por OCR puede contener errores)
METHODS FOR TREATING POLYCYSTIC KIDNEY DISEASE AND
POLYCYSTIC LIVER DISEASE
RELATED APPLICATIONS
[0001] The present application claims priority under 35 U.S.C. § 119(e) to U.S. provisional patent application, U.S. S.N. 61/891,377, filed October 15, 2013, which is incorporated herein by reference.
GOVERNMENT SUPPORT
[0002] This invention was made with U.S. Government support under grant numbers DK079310, CA077743, and DK007276 awarded by the National Institutes of Health and under Contract number W81XWH-06-1-0183 awarded by the Army Medical Research and Material Command. The U.S. Government has certain rights in the invention.
BACKGROUND OF THE INVENTION
[0003] Polycystic kidney disease (PKD) is a genetic disorder characterized by the growth of numerous cysts in the kidneys of a subject. PKD is among the most common life-threatening genetic diseases in the world and is a leading cause of end-stage renal failure and a common indication for dialysis or renal transplantation (Wilson, N. Engl. J. Med. 2004, 350, 151-164). The kidneys filter wastes and extra fluid from the blood to form urine and also regulate amounts of certain vital substances in the subject. When cysts form in the kidneys, they are filled with fluid. PKD cysts can profoundly enlarge the kidneys while replacing much of the normal structure, resulting in reduced kidney function and leading to kidney failure. PKS includes autosomal dominant PKD (ADPKD) and autosomal recessive PKD (ARPKD). ADPKD is the more common inherited form of PKD, whereas ARPKD is a rare inherited form. It has been reported that mutations in two genes, PKD1 and PKD2, which encode polycystin-1 (PCI) and polycystin-2 (PC2), respectively, may be responsible for ADPKD (Gallagher et ah, Adv. Chronic Kidney Dis. 2010, 17(2): 118-130; The European Polycystic Kidney Disease Consortium, Cell 1994, 78:725; The International Polycystic Kidney Disease Consortium, Cell 1995, 81:289-298; Mochizuki et al, Science 1996, 272: 1339-1342; The European Polycystic Kidney Disease Consortium, Cell 1994, 77, 881-894). A causative gene ARPKD has been thought to be PKHD1, which encodes fibrocystin/polyductin (FPC).
[0004] PKD can also cause cysts in the liver and problems in other organs, such as blood vessels in the brain and heart. For example, polycystic liver disease (PLD) is an inherited condition characterized by the presence of multiple scattered cysts of biliary origin throughout the liver parenchyma (Fedeles et ah, Nature Genetics 2011, 43(7):639-648; Qian et ah, Hepatology 2003, 37, 164-171). PLD occurs frequently as an extra-renal manifestation of ADPKD, but it also exists as a distinct dominantly inherited genetic entity without kidney cysts (autosomal dominant PLD (ADPLD)). Mutations in PRKCSH or SEC63 may underlie isolated ADPLD (Reynolds et al., Am. J. Hum. Genet. 2000, 67, 1598-1604; Li et al., Am. J. Hum. Genet. 2003, 72, 691-703; Davila et al., Nat. Genet. 2004, 36, 575-577; Drenth et al, Nat. Genet. 2003, 33, 345-347).
[0005] PCI, PC2, and FPC, along with one Meckel syndrome gene product (MKS3) (Smith et ah, Nat. Genet. 2006, 38, 191-196), have been reported to be the only integral membrane proteins mutated in cilia-associated fibrocystic diseases (Sharma et ah, Curr. Top. Dev. Biol. 2008, 85, 371-427). ADPKD and ADPLD are also unique in that they may be the only dominantly inherited traits among the cilia-associated diseases (Menezes et ah, Methods Cell Biol. 2009, 94, 273-297).
[0006] Subjects with PKD {e.g., ADPKD) may be treated by hemodialysis, peritoneal dialysis, or renal transplantation. Treatment of PLD {e.g., ADPLD) may include cyst aspiration, cyst fenestration, liver resection, and liver transplantation. Currently, there are no FDA-approved therapeutic drugs that directly target PKD. Several clinical trials are underway testing the cAMP inhibitor (Tolvaptan) or excessive intake of water as means to slow down the progression of PKD. Certain mTOR inhibitors, such as rapamycin, have been studied in clinical trials, but those mTOR inhibitors have not shown significant clinical effectiveness. Therefore, there remains a need for improved treatment of PKD and PLD.
SUMMARY OF THE INVENTION
[0007] The present invention provides compounds of Formula (I) or (II), which are thought to be able to inhibit mTOR (mammalian target of rapamycin) signaling pathway, induce UPR (unfolded protein response), and/or perturb mitochondrial function of a cyst cell {e.g., a cyst cell causing polycystic kidney disease (PKD, e.g., autosomal dominant PKD (ADPKD) or autosomal recessive PKD (ARPKD)) or polycystic liver disease (PLD, e.g., autosomal dominant PLD (ADPLD) or autosomal recessive PLD (ARPLD)). The invention also provides pharmaceutical compositions, kits, and methods involving the compounds described herein for use in treating and/or preventing PKD or PLD, inhibiting the growth of a cyst cell, and/or killing a cyst cell. [Read more]
Scott and Chafian's 20th wedding anniversary is Jan. 25. One day earlier, he will donate a kidney to his wife. Photo from GoFundMe.com
A Virginia man is giving his wife something really big for their 20th wedding anniversary instead of traditional china: his kidney.
For six years, Scott Chafian had wanted to donate his kidney to his wife, Cindy, who suffers from polycystic kidney disease and has been on dialysis for almost two years.
She wouldn't take it until her condition deteriorated.
"I hit kind of rock bottom, and I looked at him and I said OK, I'm ready," Cindy Chafian told WTKR-TV.
The transplant surgery is scheduled for Jan. 24 -- the day before their 20th anniversary.
The Chafians learned the date five days before Christmas.
"He called me and he told me that everything was a go. He gave me a date and that was the first time I allowed myself any emotion and I actually cried," she said.
The family is accepting wedding gifts in the form of donations at GoFundMe.They need money for the surgery and while they are not working while recovering. Through Monday, a total of $1,835 of their $5,000 goal was raised.
The posting on the website says: "This is a beautiful milestone in marriage. Usually couples get to throw a big party or maybe renew their vows. But they won't be getting to do any of that. In fact they'll both be in separate hospital rooms recovering."
A doctor said Scott Chafian is the "cleanest donor" he has seen in five years, according to the website.
"To know that he's kind of giving me that ability is even more of an amazing gift," she told the TV station. He powers me in so many ways ... he is literally going to give me life. So it's an amazing gift."
Many of our cells are equipped with a hairlike "antenna" that relays information about the external environment to the cell, and scientists have already discovered that the appearance and disappearance of these so-called primary cilia are synchronized with the process of cellular duplication, called mitosis. Now, cell biologists at Johns Hopkins report the discovery of new information about how this "hair loss" and cell duplication are linked through the dramatic clipping of the tips of the cilia -- what the scientists dub decapitation -- that begins their disassembly.
The researchers say the new information is key to better understanding how cells decide to undergo mitosis, a process integral to the development of organisms, the maintenance of tissues and the formation of cancer. They also hope their work will shed light on cilia-related diseases, like polycystic kidney disease, and certain forms of intellectual disability.
"The decapitation of cilia had been observed before but never explored," says Dr. Takanari Inoue, associate professor of cell biology at the Johns Hopkins University School of Medicine, who led the study. "We now know that it's a normal process, not just something that happens under certain experimental conditions. And we have identified the molecular players that drive it."
A summary of his team's findings appears Jan. 12 in the journal Cell.
Like antennas on minivans, primary cilia are tiny structures that appear on cells within the kidney, brain, retina and inner ear, among other organs, and provide cells with information about the flow and chemistry of fluids outside.
When a cell is not dividing, a state called quiescence, most cellular structures are continuously changing, but primary cilia are relatively stable. Inoue and his group sought to understand what causes the "haircut" when a cell exits quiescence and begins mitosis, during which replicated chromosomes divide and populate two new "daughter" cells.
They started by comparing cells with more and less of an enzyme called Inpp5e, which previous studies had implicated in the stability of cilia. After adding a fluorescent tag to the membrane of cilia in quiescent mouse embryonic cells, the team videotaped cilia's tips. They were seemingly being severed and drifting away once every several hours.
The rate of decapitation was higher in cells missing the Inpp5e gene and when cells were given signals that stimulate mitosis. But when the scientists added a molecular code to the Inpp5e protein so that it would collect in the cilia, the rate of decapitation greatly slowed. Inoue says this suggests that the presence of Inpp5e in the cilia stalls the decapitation process and that mitotic signals expel Inpp5e from the cilia to promote decapitation.
"Because genetic mutations in Inpp5e are associated with Joubert syndrome, which is characterized by abnormal brain development and intellectual disability, we now suspect that Inpp5e affects brain development," says Inoue.
The function of Inpp5e is to deplete a fatlike molecule, called PIP2, from the membrane of cilia. A fluorescent tag that binds to PIP2 showed the researchers that the concentration of PIP2 in the cilia, especially near the tip, was synchronized too: PIP2 accumulated at the tips of cilia after cells received mitotic signals, and the cilia were clipped off at the site of PIP2 accumulation.
Because PIP2 plays a key role in the formation of wirelike structures made from the protein actin, the team used a fluorescent biosensor to measure and view the structures' formation in cilia. In cilia containing excess PIP2 due to a lack of Inpp5e, the researchers found a tenfold increase in wire formation. In addition, they saw that the wire formation happened right at the site of decapitation just a few minutes ahead of time.
"We think that wire formation is actually providing the force that decapitates the cilia," says Inoue.
To see how decapitation affected the rest of cilia disassembly, Siew Cheng Phua, a graduate student in Inoue's lab and the primary author of the paper, designed a way to stop wires from forming within cilia. She found that the wires are essential to cilia decapitation and that decapitation is required for the full disassembly of cilia.
Next, the team analyzed the timing of cilia decapitation. Using a rainbow of fluorescent tags, the researchers followed cells with cilia from quiescence through their transition to mitosis. The cilia were marked in blue, and the nuclei of the cells changed from yellow to red to dark as they progressed. In normal cells, cilia decapitation generally occurred while cells were still in the quiescent state (yellow nuclei), before transitioning into mitosis (dark nuclei). But in cells whose cilia were prevented from forming wires, the inability to decapitate cilia was associated with a slower transition from quiescence to mitosis.
"Somehow, decapitation triggers the shrinking of the cilia; they shrink by more than what is clipped off," says Inoue. "At the same time, that seems to signal to the cell that it's time to exit quiescence and begin division."
When they analyzed the contents of the decapitated cilia tips -- a collaborative project with researchers in Japan -- they mostly found molecules important for cell signalling and cilia growth, implying that decapitation adjusts the composition and function of cilia.
The clipped tips of cilia might also have clinical implications, according to Phua. Recent research shows that urine from patients with polycystic kidney disease contains tiny sacs enclosed in membrane. Inoue says it's possible they are cilia tips and that they play a role in disease development, but more research is needed to confirm this idea.
Phua adds that: "Abnormal sensory functions of cilia are associated with some cancers, like skin and brain cancer. The novel link between cilia decapitation and mitosis could help us understand how defects in primary cilia influence the abnormal cell divisions which underlie cancer formation.”
Article adapted from a Johns Hopkins Medicine news release.
Living with PKD From NIDDK (National Institute of Diabetes and Digestive and Kidney Diseases) of U.S. Department of Health and Human Services
Acquired cystic kidney disease happens when a person's kidneys develop fluid-filled sacs, called cysts, over time. Acquired cystic kidney disease is not the same as polycystic kidney disease (PKD), another disease that causes the kidneys to develop multiple cysts.
Acquired cystic kidney disease occurs in children and adults who have chronic kidney disease (CKD)—a condition that develops over many years and may lead to end-stage kidney disease, or ESRD. The kidneys of people with CKD gradually lose their ability to filter wastes, extra salt, and fluid from the blood properly. end-stage kidney disease—total and permanent kidney failure that requires a kidney transplant or blood-filtering treatments called dialysis.
The cysts are more likely to develop in people who are on kidney dialysis. The chance of developing acquired cystic kidney disease increases with the number of years a person is on dialysis. However, the cysts are caused by CKD or kidney failure, not dialysis treatments.
What are the differences between acquired cystic kidney disease and polycystic kidney disease?
Acquired cystic kidney disease differs from PKD in several ways. Unlike acquired cystic kidney disease, PKD is a genetic, or inherited, disorder that can cause complications such as high blood pressure and problems with blood vessels in the brain and heart.
The following chart lists the differences: People with Polycystic Kidney Disease are born with a gene that causes the disease have enlarged kidneys develop cysts in the liver and other parts of the body
People with Acquired Cystic Kidney Disease do not have a disease-causing gene have kidneys that are normal-sized or smaller do not form cysts in other parts of the body
In addition, for people with PKD, the presence of cysts marks the onset of their disease, while people with acquired cystic kidney disease already have CKD when they develop cysts.
Acquired cystic kidney disease becomes more common the longer a person has CKD. About 7 to 22 percent of people with CKD already have acquired cystic kidney disease before starting dialysis treatments. Almost 60 percent of people on dialysis for 2 to 4 years develop acquired cystic kidney disease.1 About 90 percent of people on dialysis for 8 years develop acquired cystic kidney disease.1 What causes acquired cystic kidney disease?
Researchers do not fully understand what causes cysts to grow in the kidneys of people with CKD. The fact that these cysts occur only in the kidneys and not in other parts of the body, as in PKD, indicates that the processes that lead to cyst formation take place primarily inside the kidneys.
What are the signs and symptoms of acquired cystic kidney disease?
A person with acquired cystic kidney disease often has no symptoms. However, the complications of acquired cystic kidney disease can have signs and symptoms.
What are the complications of acquired cystic kidney disease?
People with acquired cystic kidney disease may develop the following complications: an infected cyst, which can cause fever and back pain. blood in the urine, which can signal that a cyst in the kidney is bleeding. tumors in the kidneys. People with acquired cystic kidney disease are more likely than people in the general population to have cancerous kidney tumors. However, the chance of cancer spreading is lower in people with acquired cystic kidney disease than that of other kidney cancers not associated with acquired cystic kidney disease, and the long-term outlook is better.
How is acquired cystic kidney disease diagnosed?
A health care provider may diagnose a person with acquired cystic kidney disease based on medical history imaging tests Medical History
Taking a medical history may help a health care provider diagnose acquired cystic kidney disease. A health care provider may suspect acquired cystic kidney disease if a person who has been on dialysis for several years develops symptoms such as fever, back pain, or blood in the urine. Imaging Tests
To confirm the diagnosis, the health care provider may order one or more imaging tests. A radiologist—a doctor who specializes in medical imaging—interprets the images from these tests, and the patient does not need anesthesia.
Ultrasound uses a device, called a transducer, that bounces safe, painless sound waves off organs to create an image of their structure. A specially trained technician performs the procedure in a health care provider's office, an outpatient center, or a hospital. The images can show cysts in the kidneys as well as the kidneys' size and shape.
Computerized tomography (CT) scans use a combination of x-rays and computer technology to create images. For a CT scan, a nurse or technician may give the patient a solution to drink and an injection of a special dye, called contrast medium. CT scans require the patient to lie on a table that slides into a tunnel-shaped device where an x-ray technician takes the x-rays. An x-ray technician performs the procedure in an outpatient center or a hospital. CT scans can show cysts and tumors in the kidneys. Magnetic resonance imaging (MRI) is a test that takes pictures of the body's internal organs and soft tissues without using x-rays. A specially trained technician performs the procedure in an outpatient center or a hospital. Although the patient does not need anesthesia, a health care provider may give people with a fear of confined spaces light sedation, taken by mouth. An MRI may include the injection of contrast medium. With most MRI machines, the patient will lie on a table that slides into a tunnel-shaped device that may be open-ended or closed at one end. Some machines allow the patient to lie in a more open space. During an MRI, the patient, although usually awake, must remain perfectly still while the technician takes the images, which usually takes only a few minutes. The technician will take a sequence of images from different angles to create a detailed picture of the kidneys. During the test, the patient will hear loud mechanical knocking and humming noises from the machine.
Sometimes a health care provider may discover acquired cystic kidney disease during an imaging exam for another condition. Images of the kidneys may help the health care provider distinguish acquired cystic kidney disease from PKD.
How is acquired cystic kidney disease treated?
If acquired cystic kidney disease is not causing complications, a person does not need treatment. A health care provider will treat infections with antibiotics—medications that kill bacteria. If large cysts are causing pain, a health care provider may drain the cyst using a long needle inserted into the cyst through the skin.
When a surgeon transplants a new kidney into a patient's body to treat kidney failure, acquired cystic kidney disease in the damaged kidneys, which usually remain in place after a transplant, often disappears.
A surgeon may perform an operation to remove tumors or suspected tumors. In rare cases, a surgeon performs an operation to stop cysts from bleeding.
Have Regular Screenings to Look for Cyst or Tumor Growth
Some health care providers recommend all people with end-stage kidney disease get screened for kidney cancer using CT scans or MRIs after 3 years of dialysis. People with acquired cystic kidney disease should talk with their health care provider about when to begin screening. Eating, Diet, and Nutrition
No specific diet will prevent or delay acquired cystic kidney disease. In general, a diet designed for people on hemodialysis or peritoneal dialysis reduces the amount of wastes that accumulate in the body between dialysis sessions.
Acquired cystic kidney disease happens when a person's kidneys develop fluid-filled sacs, called cysts, over time. Acquired cystic kidney disease occurs in children and adults who have chronic kidney disease (CKD) end-stage kidney disease (ESRD) People with acquired cystic kidney disease may develop the following complications: an infected cyst, which can cause fever and back pain blood in the urine, which can signal that a cyst in the kidney is bleeding tumors in the kidneys
To confirm the diagnosis, the health care provider may order one or more imaging tests: Ultrasound Computerized tomography (CT) scan Magnetic resonance imaging (MRI) If acquired cystic kidney disease is not causing complications, a person does not need treatment. A health care provider will treat infections with antibiotics—medications that kill bacteria. If large cysts are causing pain, a health care provider may drain the cyst using a long needle inserted into the cyst through the skin. A surgeon may perform an operation to remove tumors or suspected tumors. In rare cases, a surgeon performs an operation to stop cysts from bleeding. References
[1] Torres VE, Grantham JJ. Cystic diseases of the kidney. In: Taal MW, ed. Brenner & Rector's The Kidney. 9th ed. Philadelphia: W.B. Saunders; 2011: 1626–1667.
[2] Chapman AB, Rahbari-Ouskoui FF, Bennett WM. Acquired cystic disease of the kidneys in adults. UpToDate website. www.uptodate.com. Updated January 14, 2014. Accessed August 8, 2014. Clinical Trials
The National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) and other components of the National Institutes of Health (NIH) conduct and support research into many diseases and conditions.
What are clinical trials, and are they right for you?
Clinical trials are part of clinical research and at the heart of all medical advances. Clinical trials look at new ways to prevent, detect, or treat disease. Researchers also use clinical trials to look at other aspects of care, such as improving the quality of life for people with chronic illnesses. Find out if clinical trials are right for you . What clinical trials are open?
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SIOUX CITY -- Sitting next to his wife in a cramped exam room at Renal Associates, Richard Jeffs remarked that she probably wouldn't have had the strength to finish this interview five years ago.
JoAnne Jeffs, 71, started receiving hemodialysis in July 2011. This treatment for kidney failure, which uses a machine to send a patient's blood through a filter to clean it, left the Hinton, Iowa, woman feeling weak, tired and dehydrated. She didn't think she'd make it to Christmas that year.
"I slept a lot," said Jeffs, who has polycystic kidney disease, a condition which causes clusters of cysts to develop in the kidneys.
At age 60, Jeffs' body began to shut down. Her skin took on a gray tone and she lost her appetite. The diagnosis was kidney failure.
A prior bout with breast cancer took Jeffs out of the running for a kidney transplant. She partially regained her kidney function only to begin hemodialysis a couple years later.
Today, Jeffs isn't sure she would even want a donor kidney. She said switching from hemodialysis to peritoneal dialysis gave her back her life. This treatment, which can be done in the comfort of a kidney patient's home, has grown in popularity over the last decade.
According to the U.S. Renal Data System, peritoneal dialysis is less expensive than hemodialysis. One year of hemodialysis can cost up to $72,000, while a year of peritoneal dialysis costs about $53,000.
Renal Associates will begin offering a home peritoneal dialysis training program for patients and their loved ones in March in Dakota Dunes. Learning the process takes about six weeks.
"We are going to be pushing toward this modality because of the fact that we feel that it is going to be better for our patients in the long run," said Ashar Luqman, Jeffs' nephrologist.
"Patients will be much more well-versed in dealing with all the problems which come with dialysis if they are doing it themselves."
Luqman said a young patient recently diagnosed with kidney failure due to polycystic kidney disease, lupus or high blood pressure could survive for years on dialysis if the patient has no other medical problems. He said many patients who are afraid of dialysis say they would rather die than undergo the rigorous treatment.
"I cannot tell you how many times I've had patients when they initially see me they say, 'Absolutely no dialysis,'" Luqman said. "But when they start getting sick and the kidneys shut down, at that time it's too little, too late because they've already gotten to a point where even if we start doing dialysis they're not going to feel a lot better."
Two types of dialysis
Any form of dialysis is better than no dialysis, according to Jeffs. While hemodialysis didn't work well for her, she acknowledged that some people have success with it.
Patients undergoing hemodialysis visit a hospital or dialysis center three days a week. They sit in a chair for 4 1/2 hours as a filter or dialyzer used in conjunction with a dialysis machine removes toxins and extra fluid from their blood. If a patient is late for an appointment, Luqman said they go without dialysis that day.
With peritoneal dialysis, Jeffs has more flexibility. If she wakes up at 8:30 a.m. instead of 7 a.m., she can still do an exchange at that time.
Jeffs fills her abdomen with a dialysis solution through a catheter. The solution, dextrose (sugar), salt and other minerals dissolved in water, sits in the belly half an hour to two hours, depending on the patient. The toxins and extra fluid are then drained into an empty bag. On average, Luqman said patients performing manual peritoneal dialysis average four to five exchanges a day.
"It kind of gives you that lifestyle where you can still work, go to college or spend time with your family rather than being stuck in the chair for half the week," he said.
Peritoneal dialysis patients can also connect themselves to a small computerized cycler machine that performs the exchanges while they sleep. When they wake up in the morning, the treatments are complete. Jeffs said the cycler machine wasn't a good fit for her because of the placement of her catheter.
Peritoneal dialysis might be uncomfortable at first, but Luqman said patients get used to it. He said some worry about others seeing the catheter, but he said the plastic tube is easily hidden underneath clothing.
More than half of all hemodialysis patients use an arteriovenous fistula, a surgically created vein in the arm, to remove and return blood during hemodialysis. If the fistula isn't strong enough or the technician doesn't put the needles in the right places, patients experience extreme swelling and pain in their arm.
Luqman said many patients who've run into problems with fistulas would rather have hemodialysis through a catheter placed in a vein in their neck, but this technique puts them at risk for developing a life-threatening infection.
Keeping her dialysis equipment free of contaminants, Jeffs said, is the biggest challenge she's faced doing peritoneal dialysis. Luqman said developing an infection in the belly is much less serious than contracting an infection in the bloodstream -- a potential consequence of hemodialysis.
24 hours after receiving the call, Worland woman awakes with a new kidney
WORLAND - It's a call you hope and pray will come someday, sooner rather than later, but when it does, it sends a flood of emotions through you - fear, joy and shock.
Those were the emotions that Karen Surat of Worland felt Nov. 9, when she got a call from her transplant coordinator at the University of Colorado Hospital in Denver. Surat had been on the kidney transplant list at the University of Colorado Hospital in Denver for about five years
Surat was born with a defective gene which causes polycystic kidney disease (PKD). According to mayoclinic.org, "Polycystic kidney disease (PKD) is an inherited disorder in which clusters of cysts develop primarily within your kidneys. Cysts are noncancerous round sacs containing water-like fluid. The cysts vary in size and, as they accumulate more fluid, they can grow very large." The most common effects of PKD are kidney failure and high blood pressure.
While Surat was born with the gene that caused polycystic kidney disease, she didn't become aware of the disease until 2008 when x-rays were taken of her lungs during a bout with pneumonia. The x-rays captured part of her kidneys, revealing the cysts.
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On Nov. 9, 2016, Surat was working on finishing the final pages of layout at the Northern Wyoming Daily News. She gets a call about 5 p.m. from her kidney transplant coordinator. They had a possible match for a kidney and they would call her back.
"I wasn't expecting it. The average wait time for that type of donor is so much longer. I figured I would end up on dialysis before getting that type of transplant. It was kind of a shock. I was happy, but I was scared [at the thought of facing major surgery]," Surat said.
She went home after the initial call and her coordinator called her back and wanted Surat to start heading to Denver. They had a virtual match in the computer, the donor matched her antibodies.
They wanted to run the blood work to see if it was a match that would allow for the surgery. Testing would take about six hours. Surat, and her sister Lisa Monroney, headed to Denver knowing that they might get a call that the blood work wasn't a match and she'd be turning around heading home.
About the time they reached Cheyenne, they got the call that it was a good match and they'd be waiting for her.
They arrived at the hospital about 3 a.m. and they immediately began prepping Surat for surgery, including doing more blood work. They had to wait for her new kidney to arrive. Surgery began about 1 p.m. She was out of recovery and in her hospital room about 24 hours after getting the initial call.
Following the surgery, Surat found herself again dealing with a wide range of emotions, including sadness and sympathy for the donor's family. She said, I feel bad that they had to lose a family member in order for my life to be saved." [Read more]
Judy Stanwick began to cry when she heard a kidney was available.
Her tears welled up not from joy, but from fear.
On that April evening in 1998, Stanwick was performing peritoneal dialysis at her home when the phone rang. This treatment for kidney failure uses the lining of a patient's belly to filter their blood inside their body. Stanwick, who was diagnosed with kidney failure two years earlier, was comfortable with the process.
"I didn't want to go. I wasn't going to do it," Stanwick said of the kidney transplant. She immediately called her brother, Doug.
Polycystic kidney disease runs in Stanwick's family. Her mother, her brother and her daughter have all been diagnosed with the disease, which causes clusters of cysts to develop in the kidneys. Stanwick's brother received a kidney transplant, while her 37-year-old daughter's kidney function is normal.
"(Doug) basically told me if I didn't get in the car and go he was going to kick my butt," recalled Stanwick, who began the five-hour drive to the University of Iowa Transplant Center in Iowa City knowing there were two patients ahead of her on the transplant list. "As we pulled into the parking lot, they called and said, 'You are a go. Where are you?'"
A few hours later, Stanwick was lying on the operating room table watching medical personnel unpack her new kidney from a small cooler. The organ came from a 39-year-old man who was killed in a motorcycle crash. Stanwick spent five days in the hospital.
"It was weird for me because they brought a cart for the flowers and I walked all the way through and out," she said.
More than 18 years later, the 57-year-old's transplanted kidney is functioning normally in spite of a battle with breast cancer and the rapid onset of Guillain-Barre syndrome two years ago. Guillain-Barre is a potentially life-threatening condition that causes the immune system to attack the nerves resulting in paralysis. [Read more]
From Westerly News, British Columbia, Canada, NORA O’MALLEY
Three months ago, Deb Kelleher donated one of her kidneys to someone on the B.C. transplant waitlist. In 2009, Dave McIntosh received a new kidney from a live donor. — Image Credit: Nora O'Malley
On Sept. 26, 2016, just four days after celebrating her 60th birthday, Ucluelet local Deb Kelleher donated her left kidney to a complete and utter stranger.
Her friends hosted a going away party for “Sidney the Kidney”; the name Kelleher lovingly dubbed her organ. They brought her gifts of love, joy and canned kidney beans.
It was a whimsical sendoff to be sure, but in all sincerity, Kelleher’s altruistic gesture triggered a domino chain of kidney transplants that saved seven lives, all on the same day.
“My mom was diagnosed with kidney cancer [in 2013] and I just immediately thought I’d give her one of mine. I didn’t know anything about it. I knew that I have O negative blood so I can give blood to anybody so I figured I can give my kidney to anybody,” Kelleher told the Westerly News over coffee.
“But it turned out my mom didn’t need my kidney. They just took her bad one out. I didn’t take my name off the offering list. Then I was on the internet one day and I just stumbled on this article about the live organ donor program that I went on to. The last little blurb at the end of the article said this dedicated team of surgeons most treasured find is an O type person who will give a kidney and doesn’t need a kidney,” she said.
“I thought well that kind of sounds like me. I have O blood. I have a kidney. I don’t need two. So I phoned them and they sent me a package. That was in March of 2015.”
By Sept. 1, the doctors heading up the Kidney Paired Donation (KPD) program had found a match.
Kelleher said the scariest part of the whole process was navigating Vancouver.
“That was the biggest stress. Getting around in the city. Giving the organ was minor compared to that,” said Kelleher. “I have no regrets. If I had three [kidneys] I would do it again.”
She didn’t care to know who got her kidney. She said she didn’t want to feel obliged to someone and she didn’t want someone to feel obliged to her.
“If you’ve decided to give, that’s as far as you can go as far as thinking,” she said.
Kelleher realizes that organ donation is a very personal decision. While she would never coax someone into donating an organ, she did encourage people to check-in with B.C. Transplant to see if they have registered their decision on the official donor registry.
According to the Kidney Foundation of Canada, the median wait time for British Columbians in line for a kidney transplant is 4.8 years. Ucluetian Dave McIntosh, who suffered from polycystic kidney disease, had to wait six years before receiving his new organ in 2009.
“It was like a having a fog in front of you. You don’t think very well,” said McIntosh of his ailment.
Now in his early seventies, the fog has lifted. McIntosh’s health is revived and he is free from the shackles of routine kidney dialysis.
“It’s a miracle,” he said. “The transplant changed my life.”
Kelleher feels different as well.
“My being, my essence has shifted. But a good shift,” she said.
Kelleher bought a special post organ donation bracelet for herself, which she clasp on her left wrist.
The piece of jewellery weighs roughly five-ounces... The same weight as a healthy kidney.
From Belfast Telegraph, Northern Ireland, By Allan Preston
A Ballymena mother donating two vital organs to save her four-year-old boy's life has promised him: "This is going to be your year."
Sarah Lamont (36) said she hasn't doubted for a second her decision to donate both a kidney and part of her liver to her son Joe.
Born with a rare condition - autosomal recessive polycystic kidney disease - Joe was forced to have his kidneys removed and has depended on constant dialysis ever since.
He has also developed advanced liver disease, which could prove life threatening without a transplant.
His mother told the Belfast Telegraph she could wait no longer to get him the help he needs.
"In June, Joe had been on the transplant list for over a year and there was no sign of him getting a call," she said.
"Meanwhile, we saw other wee kids getting kidneys from their mum or dad. It's life changing for them."
Needing dialysis three times a week, Sarah said Joe "just wasn't getting a chance to do what wee boys do."
Sarah said she wants nothing more than to take Joe on holiday to Disneyland and to attend mainstream school, but is worried that delays caused by his illness will make it too hard for him to catch up with other children his own age.
After having a "brainwave" to contact Birmingham's Children's Hospital last year, Sarah is feeling optimistic.
The liver transplant is planned for January 25, with the kidney operation in the following months when both mother and son have recovered.
"I'll be all right, I'm a very optimistic person. If I could do it today I would, the sooner the better," said Sarah.
"I would never have doubts. Joe's been through so much, there's been a few times where I've been told he's not going to make it and he always does."
Despite the health problems Joe has had to suffer, his mum said she was inspired by his happy personality. [Read more]
A husband is preparing to give his wife the gift of life the day before their 20th wedding anniversary. Scott Chafian is donating his kidney to his wife Cindy.
Simple actions such as cooking dinner or going out to Busch Gardens are hard or impossible for Cindy because she was diagnosed with polycystic kidney disease in her 20s. It’s a disease where excessive cyst growth will shut down her kidneys.
“It is very difficult,” Cindy told WTKR. “When I started out I wanted to do home dialysis. Peritoneal, where I had a little bit more control. I’ve been through two years of one surgery after another.”
Scott said watching his wife get increasingly sicker as she grew older was tough. “It’s devastating because of course you always see your spouse before you and to not have anything, it was just a feeling of helplessness.”
So Scott took action to help his wife the only way he knew he could by donating his kidney. He remembers when their doctor told him it would work.
“Did you just say I’m a match to my wife and this is going to work? And it was and for me such a wonderful experience to have this opportunity to something for the person I love more than anybody,” said Scott.
That was six years ago. But Cindy wasn’t ready. She told Scott she was not going to take his kidney. Then, in 2016, Cindy’s health took a turn for the worse.
“I hit kind of rock bottom and I looked at him and I said okay, I’m ready,” said Cindy.
The Chafians learned the date of their transplant surgery five days before Christmas. [Read more]
Dorilyn Harrison of Modesto has an unorthodox way of searching for an organ donation needed to save her life.
When her friends and family members are out on the roads and freeways, magnetic signs on their automobiles make an appeal to potential donors.
The signs read: “Wanted – Kidney donor. Young mother needs a kidney.” Any potential donors are invited to contact Harrison by phone or email.
Harrison said a couple of people have responded and passed an initial organ donor screening, although they apparently were not a match. She received another text Wednesday.
Harrison, 47, is on the list for a kidney transplant using a cadaver organ but faces a waiting time of four to seven years. Many patients with kidney failure don’t survive that long, so the Modesto mom has taken unusual measures to find an altruistic live donor.
The former assistant principal at Grace Davis High School began searching three years ago when her kidney function dropped to 20 percent. Her kidney function has since declined to 9 percent, beyond the level at which most patients are on dialysis.
Harrison has polycystic kidney disease. She has extremely enlarged kidneys, the size of footballs, that are painful and make it hard for her to breathe. Along with receiving a new kidney, a transplant surgery would remove her enlarged kidneys.
“I can’t get sick with the flu, because it could put me in complete kidney failure,” she said.
Harrison learned she had the hereditary disease when she was 18 years old, after her father came down with kidney problems. An uncle and aunt have the same disease.
Her father lived for 14 years with a kidney donated by his son’s girlfriend but died from complications in September 2015. Harrison’s kidneys began failing when she was 40, forcing her to stop working at Davis High in 2010.
More than a year ago, her mother came up with the idea for the magnetic signs, which were ordered from a business online. About 25 signs are on vehicles in the Modesto area, the Bay Area and Southern California.
Her husband, Thor Harrison, said other motorists slow down to take pictures of the sign stuck to the tailgate of his pickup, and a few have asked him to pull over to talk. A producer for a San Francisco news station saw one of the signs in traffic in the Bay Area, and Harrison’s story ran on television this month.
“The hard part is she does not want to ask people for a kidney,” Thor Harrison said. “If there is an altruistic person who wants to donate, here is a great candidate.”
Dorilyn Harrison also has summoned her courage to contact people who put donor profiles on www.matchingdonors.com, a nonprofit organization that helps find altruistic living donors for patients who need transplants.
“I have a real hard time asking for help, especially for something that would affect another person’s life so dramatically,” she said. “I know I have to do it, but at the same time it is very difficult.”
Candidates are screened
People who respond to the signs are referred to an online screening done by University of California, San Francisco, Medical Center, where Harrison would undergo transplant surgery. The screening determines if they are healthy enough to serve as a donor, then tests are run on good candidates to see if they are a match. [Read more]
A grassroots effort to find a kidney has made a Colerain Township woman’s name known across the city.
She’s Ann.
You see signs emblazoned with her message: “A Kidney for Ann” at many major intersections in Kenwood, College Hill, Western Hills, Colerain Township... wherever she thinks they will catch the eye of a motorist idling at a red light or driving by. She’s hoping one of them has a kidney they are willing to donate to keep her alive.
Veronica Ann Mills has polycystic kidney disease, which is genetic. Fluid-filled sacs form in the kidneys and interfere with filtration. Her grandmother lived into her 90s before she saw any evidence of the problem, and Mills, 53, says she expected the same kind of timeline. So the diagnosis in October that her PKD had kicked in with a vengeance and she was facing kidney failure came as a real shock. For now, the most frustrating symptom of her disease is exhaustion.
“I see changes, and I can’t keep going as long as I used to,” she said. And there is nausea, as well. “My body is trying to adjust,” she said.
She has limited options: dialysis or a transplant. Both have drawbacks. Both can keep her alive. She says only about 2.5 percent of people, once they know they need a transplant, are able to find a kidney donor before dialysis, and Mills is determined to be part of that 2.5 percent.
Because her disease is genetic, her blood relatives are not eligible donors. Her husband has been medically excluded.
Not content to sit on a list and wait, she did what she usually does: came up with a plan.
“It’s up to me to find a donor,” she said.
“I am not a person who asks for help easily,” she said. “And I am not a person to share personal details about my health. But I want to be here for my children. I am going to do whatever I can to do that. To be here. I am not ready to die. I had my pity party, and now I am going to figure out what to do.”
First, she and her family handed out fliers at their parish, St. John Church Dry Ridge. They felt they needed to reach more people and the fliers were expensive.
She’s had unwitting help from a lot of politicians. From both sides of the political aisle, at grassroots and national political levels, candidates have unknowingly aided her campaign for a donor. She has, in fact, turned a part of that political world inside out. Literally.
She uses their discarded political signs.
When her family decided to mount a sign campaign, they began recycling all the election signs they could find. The family turns the signs inside out and Ann hand letters her simple message on the blank flip sides of the sign and then reuses the wires that support those signs as she posts her placards for kidney donors. [Read more]
Read more here: http://www.modbee.com/living/health-fitness/article123693869.html#storylink=cpy
