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Archive for May, 2011

Tuesday, May 31st, 2011

Scientists at UT Southwestern Medical Center have discovered that the anti-aging hormone Klotho inhibits renal fibrosis by blocking signaling pathways that can cause tissue damage. Klotho works in a similar way to stop the spread of cancer.  In addition to its potential uses in the treatment of chronic kidney disease and acute kidney injury, Klotho may provide researchers with valuable insight into tumor suppression.

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Anti-Aging Hormone Klotho Inhibits Renal Fibrosis, Cancer Growth, UT Southwestern Medical Center, April 14, 2011

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Monday, May 30th, 2011

Researchers from the United States, Italy, and China have joined together to unravel the mysteries of IgA nephropathy, a disease that is the leading cause of kidney failure in Asia and Southern Europe. Scientists studying a group of IgA nephropathy patients of Chinese and European heritage uncovered five regions of the human genome associated with the disease. Now they want to find out if these genetic differences occur in other populations affected by the disorder. And they hope to discover why some patients experience a benign form of the disease and others progress to kidney failure. These findings may also pave the way for improved diagnosis with genetic testing, eliminating the need for today’s invasive kidney biopsies.

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NIH Study Finds Genetic Clues to Major Cause of Kidney Disease Worldwide, National Institutes of Health, April 4, 2011

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Friday, May 27th, 2011

Researchers at Wake Forest Baptist Medical Center have discovered that variations in a gene called APOL1 explain why transplanted kidneys from some African American donors don’t last as long as others. The study showed that 2 copies of the recessive gene hindered kidney survival. The genetic anomaly, affecting 10 to 12 percent of African Americans, is linked with an increased risk of kidney disease. Researchers hope that these findings will result in better transplant outcomes and improved screening to protect living kidney donors who might develop chronic kidney disease later in life.

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Genes, Not Race, Determine Donor Kidney Survival, Wake Forest Baptist Medical Center, May 10, 2011

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Thursday, May 26th, 2011

Some interesting kidney-related research stories came out of last week’s American Urological Association Meeting in Washington, D.C.

Researchers have found that what’s good for the heart is also good for preventing kidney stones. And they believe that kidney stones may be an indicator of possible heart disease. – What Protects the Heart May Also Protect the Kidneys

Millions of American men suffer from enlarged prostate, but this study shows that many of them aren’t getting the help they need. Untreated enlarged prostate can lead to serious complications including kidney failure. - Fewer Men Having Surgery to Treat Enlarged Prostate: Study

Researchers from Duke University Medical Center have discovered that current and former smokers are 1.5 to 1.6 times more likely to have advanced kidney cancer than nonsmokers. – Heavy Smoking Tied to Advanced Kidney Cancer

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Wednesday, May 25th, 2011

Australian researchers have discovered how to turn specialized human kidney cells back into generalized cells known as induced pluripotent stem cells or iPS cells. This type of cell reprogramming is a useful tool for studying genetic kidney diseases.  The scientists hope to generate iPS cells from patients with Polycystic Kidney Disease and Alport syndrome; the transformed cells would retain the genetic information that causes these diseases, providing scientists with greater insight into how these disorders work and how to develop stem cell therapies to treat them.

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Stem Cell Tool in Kidney Disease, The Australian, May 18, 2011

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Tuesday, May 24th, 2011

Researchers at the University of Louisville have used a mouse model to show how human kidney genes change as diabetic nephropathy progresses. By studying gene expression, they discovered that inflammatory genes underwent the most changes. Paul Epstein, Ph.D., acting director of the Kosair Children’s Hospital Research Institute said, “In future studies, we can use this mouse model to explore whether inflammation causes disease progression or if the progression of the disease causes further inflammation. If it turns out that inflammation is causal, the next step would be to test the effectiveness of anti-inflammatory drugs.”

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UofL Researchers Replicate Human Kidney Gene Changes in Mouse Model, University of Louisville, May 23, 2011

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Monday, May 23rd, 2011

Scientists from the University of Oxford, University College London, and the Karolinska Institute in Sweden have discovered a way to manipulate and grow regulatory T cells that will stop organ rejection in mice. The technique involves extracting T cells from the subject as well as cells from the donor organ and culturing them in a lab dish with a drug that causes new T cells to grow. The T cells learn to recognize the foreign cells and turn off rejection. The cell therapy proved successful in a mouse with an immune system similar to a human’s.

Although testing in humans is 3 to 5 years away, the discovery has huge implications for transplant patients. A treatment of this kind would eliminate the life-long need for costly, harmful immune-suppressing drugs and may mean that donor organs could last indefinitely.

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Cell Therapy Aims to Prevent Transplant Rejection, University of Oxford, May 19, 2011

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Thursday, May 12th, 2011

Researchers at UC Santa Barbara have discovered that the same molecular mechanism that causes cancer cells to multiply also causes cysts to grow in patients with ADPKD, the most common form of Polycystic Kidney Disease. They found that the transcription factor STAT3 is activated by a mutated protein present in ADPKD patients. UCSB researchers are now investigating whether experimental cancer drugs to inhibit STAT3 could one day prove an effective therapy for PKD.

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UCSB Scientists Discover New Drug Target for Kidney Disease, UC Santa Barbara, April 26, 2011

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Wednesday, May 11th, 2011

Researchers at the Translational Genomics Research Institute (TGen) in Phoenix, Arizona are shedding new light on the role of the PVT1 gene in reducing kidney filtration and causing diabetic kidney disease. They discovered that high blood sugar increases the rate of PVT1 gene expression, unleashing proteins associated with damage to the mesangial cells of the glomerulus. Using RNA interference, they were able to curb the gene’s expression and reduce protein production.

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TGen Findings Contribute to Understanding of Diabetic Kidney Disease, The Translational Genomics Research Institute, April 22, 2011

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