BOSTON - January 15, 2013 - About 33 percent of people with type 2 diabetes suffer kidney damage that progresses to end stage renal disease (ESRD), at which point they require either dialysis or kidney transplantation. Scientists have thought that this kidney disease is driven by damage to the glomeruli, blood vessels in the kidney, which spill the protein albumin into the urine. Current treatments targeting the resulting "albuminuria" do not prevent kidney failure.
However, a new study by Joslin Diabetes Center researchers that compares the metabolic fingerprints of patients who develop ESRD versus those who don't has furnished new clues to the disease.
Published in Kidney International, the study is distinctive in examining the metabolism of patients while they were still healthy or in very early stages of the disease, and in the breadth of metabolic factors analyzed, says lead author Monika Niewczas, M.D., Ph.D. Dr. Niewczas is an instructor in medicine at Harvard Medical School and a research associate in the laboratory of Andrzej Krolewski, M.D., Ph.D., head of Joslin's Section on Genetics and Epidemiology and senior author on the paper.
The analysis drew on the Joslin Kidney Study, selecting 40 patients from that study who progressed to ESRD and 40 patients who remained alive without ESRD during 8-12 years of follow-up. The Joslin researchers used global mass spectrometry to look for levels of approximately 2,400 metabolites (molecules produced during metabolism) in plasma samples from the patients.
Among the results, the scientists found 16 "uremic solute" molecules present in much higher levels in those who would go on to develop ESRD than those who would not develop the condition.
Uremic solutes are known to accumulate in plasma in the presence of kidney failure. Dr. Niewczas stresses that at the time of the sample collection kidney function was normal in the vast majority of the study subjects,
|Contact: Jeffrey Bright|
Joslin Diabetes Center