Kidney Transplants
June 25, 2019 | 7 p.m. CDT
Preparing for a kidney transplant can be overwhelming. Once you get through the evaluation process and are ready for surgery, you may be thinking of questions about what to expect after your transplant. Join us to get answers to some of the most common questions transplant recipients have about what to expect when it is time to leave the hospital, recover from surgery and get used to the new normal of living with a kidney transplant.
Mandy Riester, RN BSN
Renal/Pancreas Transplant Nurse Coordinator | University of Kansas Health System
Mandy Riester has worked with transplant patients for almost 7 years. For the last 4 years she’s been the inpatient kidney nurse coordinator at University of Kansas Health System, teaching new kidney and pancreas patients how to care for themselves immediately following transplant. Mandy has a passion for transplant and for PKD patients.
From Forbes, by Robert Pearl, M.D., Contributor
Should The US Government Pay People For Their Kidneys?
These are trying times for healthcare optimists. Despite all the hype surrounding breakthroughs in clinical practice and technology, American medicine is stuck in in neutral. Though the engine is revving loudly, little progress is being made.
This unfortunate truth came into clearer light last week when I was preparing lesson plans for the healthcare strategy course I teach at the Stanford Graduate School of Business. During the first class of the semester, I offer a summary of healthcare-system successes over the previous year. This year, the pickings were slim: New developments in
artificial intelligence and progress with
Haven, the much-discussed Amazon-Berkshire-Chase venture, offered some glimmers.
The bulk of industry movement, however, was heading in the wrong direction. Dozens of scandals, from
generic-drug price fixing to
gross conflicts of interest, plagued some of healthcare’s biggest players. Even more discouraging, there was no concrete evidence that U.S. medical care has become more affordable, more accessible, more convenient or better (as measured in quality outcomes) since this time last year.
Life expectancy in the United States fell for an unprecedented third year in a row.
Americans still spend 50% more on healthcare than any other nation (as a percentage of GPD). And, to rub salt in the wound, the United States slipped again in
the latest global health rankings.
Wanting to introduce a ray of optimism, and to stoke the possibility of positive change, I thought about the following question.
What could our nation realistically do to improve patient health and reduce medical costs in the next year?
With the operative word being “realistically,” this query proved difficult to answer.
Congress could cap drug prices or legalize the importation of effective biosimilars like insulin. But how likely is either action, given that the pharmaceutical industry spends
hundreds of millions each year to influence legislation?
What about healthcare’s outdated information technology platforms?
Six in 10 physicians think electronic health records (EHR) need a complete overhaul. That could achieved if the leading manufacturers were forced to open their application processing interfaces (APIs) to third party developers. But, once again, how likely is that? EHR vendors are just as protective of their profits as drug industry reps.
One solution: Pay people for their kidneys
The idea of paying people for their organs is not new but it is currently illegal. Back in 1984, the National Organ Transplant Act (NOTA) outlawed the buying and selling of human organs.
Prior to the U.S. government’s involvement in the transfer and transplantation of organs, one doctor in Virginia had attempted to
establish a company for the express purpose of buying and selling kidneys commercially. And because there were no laws in place to stop him, NOTA made sense. Today, it doesn’t.
We should let the government purchase kidneys and continue to use an independent agency to decide exactly which individuals should receive these organs.
To understand why this solution makes sense now, it’s helpful to look at how far we’ve come in the past 35 years. In the 1980s, transplantation was an inexact science and often dangerous. At the time NOTA was signed into law, only 80% of kidney transplant recipients survived the operation and the associated immunosuppression. Today, transplant success rates exceed 95% among experienced surgeons and transplant teams.
Back in the ‘80s, the lack of diagnostic tests for infectious diseases like AIDS and hepatitis stoked fears that people might lie about their health status to sell an organ, thus increasing the risk of disease transmission for organ recipients.
Finally, proponents of NOTA felt an ethical obligation to uphold the goodwill of organ donation. They didn’t want to see it tainted by those seeking personal, financial gain. In 1983, Dr. David A. Ogden, president of the National Kidney Foundation, told The New York Times, “It is immoral and unethical to place a living person at risk of surgical complication and even death for a cash payment to that person.”
With advances in both science and society, NOTA needs to be modernized for the 21st century. We can realistically save tens of thousands of lives and billions of dollars if Medicare were allowed to purchase kidneys for appropriate recipients and if it paid for transplantation, rather than dialysis.
To highlight the benefits of this approach, two sets of numbers are worth considering. The first set pertains to the discrepancy between kidney need and availability, courtesy of “
The Kidney Project” at the University of California in San Francisco (UCSF):
More than 100,000 patients in the United States are currently waiting on the kidney transplant list.
Just over 21,000 donor organs were available for transplant last year.
The need for donor kidneys in the United States is rising at 8% per year.
The other important set of numbers, also from UCSF, are financial:
Americans living with end-stage renal disease (ESRD) comprise 1% of the U.S. Medicare population but account for 7% of the Medicare budget.
Dialysis comes with an average treatment cost of $89,000 per patient annually.
The average cost of a kidney transplant is $32,000 for the surgery and $25,000 per year in post-surgery care.Armed with these numbers, let’s calculate how much money would be saved by providing 100,000 people on the kidney transplant list with new kidneys, versus keeping approximately 100,000 people on dialysis.
Knowing the annual dialysis expense for this population is $89,000 per patient, the total expense for all 100,000 people over the next five years would be $44.5 billion.
The expense for this same population to receive new kidneys would be $32,000 for the procedure itself, plus $25,000 for post-op care annually, which over the same five-year period would equal $15.7 billion.
That’s a savings of nearly $25 billion.
Of course, these latter calculations assume we can find 100,000 new kidneys donors. Finding living donors would be best for a couple of reasons. First, kidney transplantations that involve “living” donors are more successful than when organs are harvested from the deceased. And second, there are millions of Americans who could contribute.
To find 100,000 donors, the United States government could offer to pay $50,000 for a kidney (plus all surgical costs and follow-up care expenses) for about $5 billion. Doing so would not only improve the health and life-expectancy of the recipients, it would still result in a total healthcare savings of $20 billion over the next five years.
The savings could then be used to fund programs that improve medical prevention, help manage the nation’s high blood pressure problem and lower the rates of adult-onset diabetes—all of which would go a long way toward preventing kidney disease and lowering future healthcare costs.
So, if the proposal has the potential to improve American health, lower medical costs and fund future programs to help more Americans avoid kidney failure, what are the potential pitfalls?
Legalizing the sale of organs, some say, would lead to the wealthy taking advantage of the poor. This concern, however, isn’t based in fact. According to UCSF data, kidney disease disproportionately affects the nation’s minority and low-income patients. Therefore, a government-run kidney purchasing program would disproportionately benefit the poor, not the rich.
Others fear that amending NOTA would create a black market. In fact, implementing this proposal would eliminate the need for a black market, since organs would be readily available and controlled by a federal agency.
There’s also the concern that low-income individuals would be coerced by economic factors to donate kidneys at the expense of their personal health. Here too, the argument is specious. Science has proven that a donor’s remaining organ compensates for the loss. Following removal, the twin kidney enlarges and becomes just effective as when there were two.
Furthermore, science has mastered screening for communicable diseases, rendering historical concerns that poor people might lie about their existing diseases for the donor money both outdated and culturally insensitive.
Finally, what about the risk of the donor losing the remaining kidney from trauma or cancer? Currently, people who anonymously donate kidneys are automatically placed at the top of the transplant list should they need one in the future. By making this same promise to the paid donors, the small risk associated with having a single kidney would be offset by the certainty of receiving immediate access to transplantation should it prove necessary.
There is no silver bullet for solving our nation’s healthcare crisis, and every solution has its risks and downsides.
Using money to incentivize kidney donations carries certain dangers, but also tremendous upside. Those willing to donate would earn $50,000, which would go a long way toward a college education, a home or other family expenses. And those receiving the organs would have a better and more productive life. This solution is realistic. And, done well, the program’s biggest problem might be having to turn away potential donors due to popular demand.
I look forward to hearing what the students think of this idea come September. And please share your thoughts with me on
Twitter and
LinkedIn.
Dr. Robert Pearl is a former healthcare CEO who teaches at Stanford. More than 10,000 people subscribe to his "Monthly Musings on American Healthcare." Follow him @RobertPearlMD
Dialysis Issues
From Los Angeles Times, By DUC DANG
Assembly bill could make it harder for some dialysis patients to receive treatment
The California Assembly recently voted on a matter of life and death for me and thousands of other Californians living with failed kidneys.
If it sounds dramatic, it is because it is.
At age 50, I depend on a charitable financial grant from the nonprofit American Kidney Fund to help pay for my daily at-home dialysis. Without the grant, I cannot afford the treatment. Without the treatment, I will die. Assembly Bill 290, supported by California’s health insurance companies, will force AKF to cease operating its program in California, hurting me and the more than 3,700 Californians who rely on its financial assistance.
This is because provisions in AB 290 conflict with the strict federal guidelines under which AKF operates and, rather than risk its operations nationwide, AKF will simply stop offering assistance in California. The bill recently passed the Assembly and is headed to the Senate.
When I was 30 and first suffered kidney failure as a result of hypertension, my brother gave me one of his kidneys. I lived a healthy life for 19 years after the successful transplant, working in the mortgage business. But that kidney failed in 2017, forcing me back on dialysis. I lost 30 pounds and was so sick for six months I could not work. Even after returning to work, I soon got laid off because my illness prevented me from bringing in business.
Today the AKF’s charitable premium assistance, along with COBRA from my previous job, combine to pay for expensive dialysis treatment that cleans my blood and removes toxins from my body. This treatment keeps me alive.
AB 290, as the insurance companies designed it, means I will lose my financial assistance and I will be unable to pay my insurance premiums. I will be forced on to Medicare which I don’t want. It will not provide the medical coverage that is best for me.
I’m not alone. There are more than 3,700 dialysis patients in California who will lose financial assistance if AB 290 passes and AKF is forced to stop offering its services in California.
By forcing dialysis patients on to government-funded health care plans, AB 290 will threaten the long-term viability of dialysis clinics since government reimbursements don’t cover the cost of care. If dialysis clinics are forced to cut back services or close because they can’t cover their costs, patients will end up in emergency rooms where care is up to eight times more expensive. The health care system as a whole, and taxpayers, will bear the burden of higher costs.
Not surprisingly, AB 290 also allows insurance companies to pay less to dialysis providers as reimbursement for dialysis treatments. Of course that’s why the insurance industry is supporting the bill. But it doesn’t force insurers to pass any of their savings to consumers. A win-win for insurance companies, but not for patients.
I am trying to do my part to contribute to my health care; working part time and awaiting a kidney transplant on the UC Irvine Medical Center donor list. But it will be years, most likely, before I can get another kidney.
If AB 290 passes, it would cruelly revoke my insurance, right when I need it the most. Dialysis that keeps me alive might be pulled away from me before I even get a chance for my name to come up on the transplant list. I will be forced to either live so far in debt I won’t be able to afford food or shelter, or I will die.
This bill, quite literally, is targeting some of California’s poorest and sickest residents.
It is that simple, and that sad.
PKD Research
From Science Signaling, by Isotta Lorenzi and Luca Scorrano
Too close not to encyst: Polycystic kidney disease and interorganellar contact sites
Abstract
Mitofusin 2 (MFN2) tethers mitochondria to the endoplasmic reticulum (ER). In the 7 May 2019 issue of Science Signaling, Kuo et al. report that polycystin 2 (PC2), encoded by a gene mutated in type 2 autosomal dominant polycystic kidney disease (ADPKD), contributes to cystogenesis by affecting MFN2, thus extending the role of mitochondria-ER contact sites to a common genetic disorder.
Fig. 1The connection between PC2 and mitochondria-ER tethering.
In normal cells, endogenous PC2 resides in the ER and associates with VDAC, an ion channel localized to the outer mitochondrial membrane. In PC2-depleted cells, MFN2 abundance is increased, resulting in greater ER-mitochondria apposition, increased mitochondrial Ca2+ flux, and enhanced mitochondrial metabolism. IP3R [IP3 (inositol 1,4,5-trisphosphate) receptor] and the MCU (mitochondrial Ca2+uniporter) complex are located in the ER and in the inner mitochondrial membrane, respectively. TCA, tricarboxylic acid; WT, wild type.CREDIT: A. KITTERMAN/SCIENCE SIGNALINGWithin the cell, interorganelle communication is often mediated at membrane contact sites, where two heterotypic membranes are in close proximity but do not fuse. The endoplasmic reticulum (ER)–mitochondria contact sites (MERCs) are one of the best-characterized examples of such contacts. MERCs, also known as mitochondria-associated membranes (MAMs), are patches of ER associated with mitochondria. They are crucial for the regulation of several cellular processes, including Ca2+ homeostasis, the transfer of lipids, ER stress, apoptosis, and autophagy. Alteration of the ER-mitochondria juxtaposition indeed impacts on mitochondrial metabolism and cellular response to Ca2+-mediated cell apoptosis (
1). Despite the importance of such interface, only a handful of different proteins have been placed at MERCs and unambiguously identified to play a role in tethering or modulating ER-mitochondria proximity in mammalian cells. These include the mitochondrial fusion protein mitofusin 2 (MFN2) (
2,
3) and its modulator trichoplein (also known as mitostatin) (
4); the phosphofurin acidic cluster sorting protein (PACS-2) (
5); the functional complex composed of the inositol 1,4,5-trisphosphate receptor (IP3R), the glucose-regulated protein 75 (Grp75), and the voltage-dependent anion channel (VDAC) (
6); and the interaction between the vesicle-associated membrane protein–associated protein B (VAPB) and the protein tyrosine phosphatase–interacting protein 51 (PTPIP51) (
7). Most of these genes are mutated in genetic disorders: MFN2 is associated with Charcot-Marie-Tooth disease, type 2a, VAPB is associated with amyotrophic lateral sclerosis type 8, and PACS-2 is associated with early infantile epileptic encephalopathy-66. These disease-associated mutations further substantiate the importance of MERCs in cell physiology. In the 7 May 2019 issue of Science Signaling, Kuo et al.nominate type 2 autosomal dominant polycystic kidney disease (ADPKD) as another MERC disorder.
ADPKD is an autosomal dominant form of polycystic kidney disease characterized by renal and liver cysts and intracranial aneurysms and often leads to end-stage renal disease. Type 2 ADPKD is caused by mutations in PKD2, which encodes polycystin 2 (PC2), a transient receptor potential (TRP) superfamily of large-conductance, nonselective cation channels involved in Ca2+ signaling. Classically, PC2 has been localized in cilia, but the PC2-PC1 (which is encoded by PKD1) complex has been placed in MERCs, and loss of PKD1 results in lower mitochondrial Ca2+ uptake and impaired mitochondrial respiration (
8). The connection between PC2 and mitochondria is poorly characterized. Kuo and colleagues (
9) determine a novel functional role of PC2 in the modulation of MERCs. They showed that endogenous PC2 was located at the MAM and it associated with VDAC, which helps to transfer Ca2+ between ER and mitochondria (
6). Loss of PKD2 indeed led to enhanced mitochondrial Ca2+ influx and altered mitochondrial metabolism (
Fig. 1). To rationalize these physiological findings, Kuo and colleagues explored the extent of ER-mitochondrial tethering in PKD2-depleted cells, where they found increased MFN2 protein levels. Accordingly, they reported, using various approaches, that in cells lacking PKD2, ER-mitochondria tethering was increased. They therefore propose a model in which increased MFN2 levels sustain MERCs formation and higher mitochondrial Ca2+ uptake. To test this possibility, Kuo and colleagues turned to an in vivo cystic mouse model in which they modulated MFN2 levels. Several studies on animal models have proposed a role for dysregulated Ca2+, and cyclic adenosine 3′,5′-monophosphate (cAMP) signaling in ADPKD cystogenesis and treatment strategies lowering cAMP levels in cystic tissues have proven beneficial. However, treatments of ADPKD cysts by restoring intracellular contact site levels had not been previously attempted. Cyst formation was strikingly dependent on the amount of MFN2 and hence on mitochondria-ER contacts. Tissue-specific deletion of MFN2 in cystic cells decreased cell proliferation and curtailed the increased mitochondrial Ca2+ uptake, ultimately blunting cyst formation and expansion. Because of the causal relationship between MFN2 levels and cyst formation in this ADPKD model, the study of Kuo et al. (
9) opens to the exciting possibility that cyst formation in ADPKD patients harboring PKD2 mutations might be prevented by treatments that target MFN2, for example, by using small-molecule or peptide MFN2 inhibitors (
10). Although these MFN2 inhibitors primarily affect MFN2 fusion, tethering function remains to be addressed, calling for the development of small-molecule inhibitors that can differentially target the two different functions of this pleiotropic molecule.
The catalog of diseases associated with changes in ER-mitochondria contact sites is long. Most of them, however, can be classified as diseases of reduced juxtaposition. The Kuo et al. paper raises the possibility that increased tethering between these two organelles can be regarded as a crucial pathogenic event at least in one disease, with the exciting corollary that specific MFN2 inhibition can curtail cyst formation. Besides the therapeutic possibility, another implication of the Kuo et al.work is to nominate MERCs as sites also for cAMP signaling. Although they did not specifically measure the influence of MFN2 deletion on cAMP levels in PKD2-deleted cells, it is tempting to speculate that correction of the exaggerated tethering might also affect local cAMP concentrations. Future research will be needed to decode local cAMP sensors at MERCs and their role in cell biology and signaling to other cellular components and to the nucleus to orchestrate complex processes such as cyst formation and maintenance.
PKD Awareness
From WNKY TV
Jackrabbit Jog returns to raise awareness for polycystic kidney disease
BOWLING GREEN, Ky. – Several Kentuckians kicked off their Memorial Day with a morning run.
A run that supports and raises awareness of individuals with polycystic kidney disease and to also raise money for an undeveloped cure.
This was all during the 4th annual Jackrabbit Jog 5K run/walk at Kerieakes Park.
People of all ages endured the heat to participate in a variety of events.
Including the 5-mile solo run and the 1-mile kids race called the “Bunny Hop.”
All of the proceeds from the running events go directly to the Polycystic Kidney Disease Foundation (PKD).
The PKD Foundation is still working to find a cure for polycystic kidney disease.
The Jackrabbit Jog 5K has raised over $10,000 so far in its three years running.
Even though event coordinator Ryan Dearbone lost his mother to the disease, he hasn’t lost hope.
Hope that one day the run won’t be needed anymore, but wanted to celebrate the disease being cured for good.
Dearbone anticipates that Monday’s run raised around $3,000 alone towards finding the cure.
