Researchers led by the University of Washington have identified two blood markers strongly linked with the development of heart failure in individuals with mild to severe kidney disease. Elevations in these markers may indicate subclinical cardiovascular changes that subsequently contribute to the development of heart failure.
Chronic kidney disease (CKD) is a long-term condition where the kidneys do not work effectively. This is most often caused by the strain placed on the kidneys by other conditions, most commonly diabetes and high blood pressure. 60 million people globally have chronic kidney disease for which there is no cure, although treatment can slow or halt the progression of the disease and can prevent other serious conditions developing. Patients with chronic kidney disease (CKD) are at increased risk of developing heart failure and other cardiovascular diseases.
The team conducted a study to see if certain blood tests might help identify patients at especially high risk of heart failure. These tests, which measure proteins called high-sensitivity troponin T (hsTnT) and N-terminal pro-B-type natriuretic peptide (NT-proBNP), strongly predict heart failure in the general population, but their predictive utility in patients with CKD is unknown.
The researchers studied 3483 patients with CKD in the Chronic Renal Insufficiency Cohort (CRIC) Study who were recruited from June 2003 to August 2008 and were free of heart failure when they enrolled. Patients were followed for a median of nearly 6 years.
Compared with participants with the lowest levels of hsTnT at the start of the study, those with the highest hsTnT levels had a nearly 5-fold higher risk of developing heart failure. Those with the highest NT-proBNP levels had a nearly 10-fold higher risk of developing heart failure compared with those with the lowest levels.
This research is important in that it may advance the application of widely available cardiac biomarkers to identify CKD patients at the highest risk of developing heart failure, the most common cardiovascular complication in this patient population. These findings suggest that hsTnT and NT-proBNP may represent distinct biological pathways that likely involve subclinical changes in the structure and function of the heart.
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