One of the many, many drawbacks to a life-sustaining dialysis is the energy-draining side effects that plaque the patients. But Dr. Van Geertruyden thinks he has found the answer in a very unlikely place . . . ceramic.

William Van Geertruyden, who holds three degrees in materials science and engineering from Lehigh, has developed a new type of dialysis filter that, he says, represents the first major breakthrough in 30 years for dialysis patients.
Van Geertruyden, who earned a Ph.D. from Lehigh in 2004, has filed a patent application on a ceramic filter that he believes is dramatically superior to the traditional polymer, or rubber-like, filter used in dialysis.
Last September, his company, EMV Technologies, LLC, received a $195,000 Small Business Technology Transfer grant from the National Institutes of Health (NIH) to verify the feasibility of the new filter. EMV, which is located in Bethlehem, has received smaller grants from the Pennsylvania Keystone Innovation Zone (KIZ) program and the Ben Franklin Technology Partners.
The new ceramic filter has the potential to make kidney dialysis much more efficient, says Van Geertruyden, and to reduce by 30 minutes to one hour the time required for a dialysis treatment.
Specifically, the new filter promises to double the amount of toxins removed during dialysis and to double the glomulellar filtration rate (GFR), or rate of toxin removal. GFR is 100 percent in a normal person but only 15 percent at best for a dialysis patient, a rate that has changed little in the past 30 years.
The ceramic filter’s secret, says Van Geertruyden, lies in its pores, which are organized in orderly rows and columns and which measure mere nanometers in diameter.
These nanopores, says Van Geertruyden, correspond more closely to the nano-sized toxins in the blood than do the larger pores of the standard dialysis filter. These polymeric pores vary in size and, when viewed with a microscope, appear in random arrangements of ovals, circles, slits and other shapes.
“Our goal is to double the amount of toxins removed during dialysis and to double GFR,” says Van Geertruyden. “We base our confidence on the superior porosity of our medium.
“If we can improve the efficiency of filtration, we can improve mortality rate and quality of life.”

Press release: A new, nanoporous ceramic filter offers hope to kidney-dialysis patients …

Neurobiologist Katerina Akassoglou, at the University of California, has made a breakthrough in understanding the regenerative properties of the human liver. Cirrhotic livers everywhere raise their glasses to her in appreciation.

Researchers may have identified a master switch that activates the liver’s ability to heal itself, suggesting a route to better treatments for liver diseases such as hepatitis and cirrhosis. Mice that lacked the gene showed a marked deterioration in their livers and lived shorter lives than normal mice.
Damage to the liver activates a group of specialized wound-healers called hepatic stellate cells (HSCs), which churn out scaffoldlike collagen fibers that support the growth of new liver cells. “You want the cells to get activated but you don’t want them to stay activated for too long,” says neurobiologist Katerina Akassoglou of the University of California, San Diego, because the fibers begin substituting for healthy liver tissue, leading to liver failure in people with chronic cirrhosis, for example. But researchers do not know which genes control the process.
Akassoglou and her colleagues thought they had a good candidate in the gene for the p75 neurotrophin receptor (p75NTR), a regulator of cell death in the brain that also switches on soon after liver injuries. Using mice that had a propensity for liver disease, her team created a strain of rodents that lacked the p75NTR gene. The livers of the engineered mice were covered in lesions after 10 weeks, and only half of the animals lived longer than that, compared with more than six months for the unmodified rodents.
The p75NTR protein sits on the surface of HSCs. The group believes that when activated by a still-unknown agent after liver damage, it stimulates a cascade of signals inside the cells that trigger them to begin the healing process, according to results presented in this week’s Science. The next step, Akassoglou says, is to determine the role p75NTR plays in later stages of liver disease, to see if shutting it down will stop the harmful production of collagen.
“If you know what the switch is,” she says, “and if you know how these cells become quiescent again … then you can start interfering with this process.”

Scientific American . . .