New studies shed light on genetic factors in kidney disease
An international team of researchers, funded in part by the EU, has identified genetic variants that could explain why some individuals are more susceptible to chronic kidney disease than others. Two studies published in the journal Nature Genetics provide important new insights into the specific causes of chronic kidney disease. One of the studies was financed part by the GENECURE ('Applied genomic strategies for treatment and prevention of cardiovascular death in uraemia and end stage renal disease') project, which received EUR 2.25 million in funding under the 'Life sciences, genomics and biotechnology for health' Theme of the Sixth Framework Programme (FP6). GENECURE partners sought to systematically assess the role of genetic factors in cardiovascular risk in patients with renal failure. Reduced kidney function and kidney damage are problems that have been shown to increase the risk of cardiovascular diseases such as coronary heart disease and stroke. As such, chronic kidney disease represents a serious public health problem affecting around 11% of people in Europe and the US. Kidney disease tends to 'cluster' in families, but until recently the precise hereditary factors underlying the disease had been difficult to determine. Using the latest methods in genetic analysis, two teams of researchers from several countries conducted genome-wide association studies. One team examined common variations in DNA (deoxyribonucleic acid) sequences in approximately 24,000 people of European descent who were participating in 9 population-based studies. They looked specifically at genetic information associated with serum creatine levels and cystatin c, which are important measures of kidney function. 'Our findings of common genetic variants associated with creatine, cystatin c and chronic kidney disease provide insight into the metabolic, solute, and drug-transport mechanisms underlying kidney function and chronic kidney disease,' the authors wrote. Further studies of these pathways, they believe, may lead to the development of new strategies to protect kidney function and prevent the disease from materialising. According to an author of the second genome-wide association study, Dr Linda Kao of Johns Hopkins Bloomberg School of Public Health in the US, 'We've known for a long time that diabetes, hypertension and family history are strong risk factors for kidney disease, but we have not been able to fully understand why. These findings will ultimately shed light on how and why kidney disease clusters in families and why it occurs in some individuals but not others.' Dr Anna Köttgen of the same institution added, 'By studying the genes identified in this study, we can learn more about basic mechanisms underlying kidney function and disease. These novel insights can form a foundation to improve prevention and therapy of kidney diseases.' Commenting on the findings, research team member Dr Josef Coresh said: 'It is exciting to see research from around the world come together to collaborate and unlock the mysteries of kidney disease genetics. We learned that together we can do a lot more than apart.'