Many Kidney Diseases Caused by Single-Gene Defects

And causes of death in chronic kidney disease patients found to vary amongst rich, poor countries
By Beth Gilbert
HealthDay Reporter

FRIDAY, April 9 (HealthDay News) -- Many genetic kidney diseases are caused by single-gene defects, which means those defects can be targeted in disease treatments, according to an article published in the April 10 kidney medicine special issue of The Lancet. According to another article in the same issue, in low- and middle-income countries, most patients with chronic kidney disease (CKD) die without receiving dialysis or transplantation because of limited availability.

In one article, Friedhelm Hildebrandt, M.D., of the University of Michigan in Ann Arbor, writes that, recently, many genetic kidney diseases have been shown to be caused by single-gene defects. Having knowledge of a disease-causing mutation in such a disorder is an important diagnostic example of personalized medicine, he writes, since this type of mutation is associated with a nearly 100 percent chance of developing the disease.

In the other article, Matthew T. James, M.D., of the University of Calgary in Canada, and colleagues write that, because of aging populations and the growing prevalence of diabetes and other diseases, rates of CKD and kidney failure have increased worldwide. Although in developed countries, many more people die of cardiovascular causes than progress to kidney failure, in low- and middle-income countries, most CKD patients die of kidney failure because they do not have access to dialysis or organ transplantation. Early recognition and prevention of CKD is vital in both developed and developing countries because it may be possible to prevent cardiovascular events or progression to kidney failure, the authors write.

"Novel clinical methods to better identify patients at risk of progression to later stages of CKD, including kidney failure, are needed to target management to high-risk subgroups," James and colleagues write.

Abstract - Hildebrandt
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Abstract - James
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