Dopamine, an important neurotransmitter that helps to control the brain’s reward and pleasure centers, is often studied in connection with neurological disorders like Parkinson’s disease.  Now researchers at Vanderbilt University Medical Center have discovered that dopamine produced within the kidneys, rather than the brain, is critical to maintaining normal blood pressure and salt and water balance. They showed that mice with impaired kidney dopamine production developed hypertension and died sooner than ordinary mice, despite having normal brain and plasma dopamine levels. Although dopamine has previously been associated with hypertension, this study pinpoints the important role of dopamine made in the kidneys.

Sources:

Long Live Dopamine Production by the Kidneys, Vanderbilt University Medical Center, June 23, 2011

Intrarenal Dopamine Deficiency Leads to Hypertension and Decreased Longevity in Mice, Journal of Clinical Investigation, June 23, 2011

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Last week was an exciting one for diabetes news. In addition to our recent post about a new drug that can improve kidney function in Type 2 diabetics, there have been many other interesting discoveries.

Newcastle University researchers in England have found that a very extreme diet can reverse Type 2 diabetes in newly diagnosed patients. The diet reduced fat levels in the pancreas and liver, helping insulin production to return to normal. It isn’t known whether results will be permanent. – Type 2 Diabetes in Newly Diagnosed “Can Be Reversed”

Researchers from Massachusetts General Hospital have shown that a generic vaccine for tuberculosis that transiently reversed Type 1 diabetes in mice could work in humans as well. – Research Shows Promise in Reversing Type 1 Diabetes and Massachusetts General Hospital, Iacocca Foundation Announce Promising Results of Phase I Diabetes Trial

According to a new study, young adults with Type 1 diabetes have thicker, stiffer carotid arteries, a risk factor for heart disease. – Young People with Type 1 Diabetes at Risk for Heart Disease, Research Shows Another study found that Type 1 diabetic girls show signs of risk factors for heart disease at an early age. – Diabetic Girls May Have Heart Risk Factors

Researchers at the Karolinska Institute in Sweden have conducted two studies that may impact future treatment for diabetes. In the first study, the scientists discovered a signalling pathway that makes insulin-releasing beta cells more sensitive to high blood glucose levels. The second study found that blood levels of a lipoprotein rise prior to the onset of Type 1 diabetes. They theorize that inhibiting the lipoprotein known as ApoCIII could delay onset of the disease. – New Discoveries in Diabetes Suggest Novel Ways to Treat, Delay the Disease

Researchers from the Institute for Aging Research of Hebrew SeniorLife have identified a gene linked to having low body fat as well as an increased risk for Type 2 diabetes and heart disease. – Genetic Study Shows That Low Body Fat May Not Lower Risk for Heart Disease & Diabetes

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Results of a year-long drug trial conducted by researchers from UT Southwestern Medical Center show that the experimental drug bardoxolone methyl improves estimated glomerular filtration rates in Type 2 diabetic patients with moderate to severe CKD. Lab tests for those patients revealed decreased blood urea nitrogen, serum phosphorus, uric acid, and magnesium. The new phase 3 trial of bardoxolone is expected to be complete in 2013.

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Drug Shows Improved Kidney Function for Patients with Type 2 Diabetes, UT Southwestern Researchers Report, UT Southwestern Medical Center, June 24, 2011

Bardoxolone Improves eGFR Out to One Year in Advanced CKD, By Daniel M. Keller, Ph.D., Renal and Urology News, June 24, 2011

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Researchers from UC San Diego, the National Institutes of Health, and the Mayo Clinic have shown that an experimental drug called pirfenidone can stop damage and improve kidney function in diabetic patients. Study participants treated with a small amount of the drug for one year showed improved glomerular filtration rates.

Pirfenidone, an anti-inflammatory and anti-fibrotic or anti-scarring drug, targets transforming growth factor beta (TGF-ß), a protein that contributes to kidney scarring.  Prolonged, elevated blood sugar levels lead to over-expression of TGF-ß, but pirfenidone appears to block the protein. The drug has already been used to slow the progression of FSGS and may be an option for treating other fibrotic conditions, such as pulmonary fibrosis.

Source:

Drug Effective in Treating Kidney Disease in Diabetic Patients, By Debra Kain, UC San Diego, April 21, 2011

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We’re excited to announce that UKRO will be sponsoring a rider on the 2012 Donate Life Rose Parade float. Next year’s parade theme, “Just Imagine…” pairs perfectly with the Donate Life float theme of “…One More Day,” envisioning a dream day when past moments are recaptured and new memories are made – “when donor families are reunited with loved ones, transplant recipients thrive, and living and registered donors step forward so that a life-saving transplant is available to everyone in need.”  Research undoubtedly plays a part in making “one more day” possible for kidney patients, transplant recipients, and their families, and we’re proud to be a part of this inspiring float.

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Researchers at St. Michael’s Hospital in Toronto have discovered that special cells found in bone marrow and blood do a better job of promoting blood vessel growth in nocturnal home hemodialysis patients than in patients undergoing dialysis in a hospital setting. Longer and more frequent nightly dialysis sessions greatly reduce the amount of toxins in the blood and this may explain why these EPLC cells (short for “early-outgrowth endolethial progenitor-like” cells) work better. The researchers believe that nocturnal home hemo may help patients with blood vessel damage avoid complications such as amputation and decreased mobility.

Source:

New Evidence of the Benefits of Home Dialysis for Kidney Patients, St. Michael’s Hospital, July 21, 2011

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Yale School of Medicine researchers have discovered that the PKD1 gene not only causes cysts to grow on the kidneys, but on the liver as well.  Their studies of families with liver-only polycystic disease led them to explore the relationship between that liver condition and the most common form of Polycystic Kidney Disease, ADPKD. They have determined that low expression of PKD1 leads to cysts and theorize that increased expression could slow cyst formation. They believe that targeting the activity of PKD1 could benefit those with liver-only polycystic disease, as well as children with recessive PKD and some adults with ADPKD.

Source:

Single Gene Controls Development of Many Forms of Polycystic Disease, Yale University, July 19, 2011

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Researchers at the University of Miami Miller School of Medicine have linked elevated levels of a hormone known as FGF23 to an increased risk of kidney failure and death in patients with early stages of chronic kidney disease. FGF23 regulates phosphorus, which is vital to bone health and cellular function, but potentially harmful to patients whose kidneys are no longer able to remove the excess mineral from the blood. High phosphate levels in CKD patients can cause serious bone and heart problems and may make kidney disease worse. “Since FGF23 rises before phosphate in people with early or intermediate-stage chronic kidney disease, this hormone could be an early marker – like a road sign – pointing to patients who may benefit from early management of phosphate levels, which may help preserve kidney function and reduce deaths,” said senior study author Myles Wolf, M.D., M.M.Sc. Further study is needed to determine whether FGF23 is more than a marker and whether reducing levels of the hormone might actually improve patient outcomes.

Source:

NIH Researchers Identify New Marker to Predict Progressive Kidney Failure, Death, NIH, June 14, 2011

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Researchers from the University of Freiberg in Germany have identified a metabolic enzyme called mTOR as a target for preventing diabetic kidney disease. They showed that while mTOR is important to early glomerular development, it becomes overactive in diabetics, causing damage to the filtering units of the kidney. Using a mouse model, the scientists inhibited mTOR activation genetically to stop the progression of kidney damage. The discovery may one day result in a viable therapy for diabetic nephropathy and other glomerular diseases.

Source:

When Sugar Damages Kidneys: New Hope for Diabetes Patients with Kidney Disease, University of Freiberg, June 15, 2011

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Researchers from Fox Chase Cancer Center in Philadelphia have found that Aurora A kinase, an enzyme linked to tumor growth in cancer, may contribute to polycystic kidney disease. They discovered that Aurora A is over-expressed in the cells lining PKD cysts. It likely contributes to the disease by disrupting the activity of polycystin-2, a protein produced by the PKD-2 gene, which is often mutated in patients. Polycystin-2 acts as a calcium channel, allowing the flow of calcium ions into kidney cells and triggering functions important to kidney development. The scientists theorize that inhibiting Aurora A may restore polycystin-2 activity in some PKD patients. They hope continued research will explain why Aurora A is over-expressed in PKD and plan to conduct experiments to determine if inhibiting Aurora A slows the growth of cysts.

Sources:

Aurora A May Contribute to Kidney Disease, Rockefeller University Press, June 13, 2011

Research Abstract: Aurora A Kinase Activity Influences Calcium Signaling in Kidney Cells

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