Decreased blood levels of a kidney-derived protein called Klotho increases the risk of heart disease in mice with kidney disease, according to a study from UT Southwestern Medical Center. If the findings are confirmed in humans, Klotho replacement therapy may help protect the heart health of patients with poor kidney function.
Heart disease is the leading cause of death in patients with chronic kidney disease (CKD). Also, cardiac hypertrophy (thickening of the heart muscle) occurs in up to 95% of patients with CKD and increases their risk for cardiovascular death. Through decades of research, investigators have found several risk factors for CKD-associated cardiac hypertrophy, which is also called uremic cardiomyopathy. Despite correction of all these known factors, however, many patients with CKD still develop uremic cardiomyopathy.
The team designed a study to investigate whether a decrease in levels of circulating soluble Klotho, a protein that is produced by the kidneys and is known to have anti-aging and heart-protective effects, is a missing link to the cause of uremic cardiomyopathy.
The researchers found that levels of soluble Klotho circulating in the blood are reduced in mice with CKD. Also, mice with a genetic deficiency in soluble Klotho develop much more severe uremic cardiomyopathy, and replacing soluble Klotho can protect mice against developing uremic cardiomyopathy.
More than 20 million people in the United States have chronic kidney disease, and heart disease is the leading cause of death in these patients.
The team state that the study showed that a decrease in circulating soluble Klotho in CKD is an important cause of uremic cardiomyopathy and opens new avenues for treatment of the disease. If confirmed in humans, increasing Klotho levels may help protect the hearts of patients with chronic kidney disease.
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