Researchers Uncover Mechanism for Vitamin D-Mediated Cardio-Protection in Kidney Insufficiency

Abnormal vitamin D status and elevated levels of the hormone FGF23 contribute to cardiac hypertrophy — a thickening of the heart muscle that may result in a decrease in size of the chamber of the heart and affect cardiac performance — in patients with chronic kidney disease.

During an oral platform session at the 50th annual meeting of the American Society of Nephrology in Chicago, UM investigators Michael Freundlich, M.D., professor of clinical pediatrics in the Division of Pediatric Nephrology, and Christian Faul, Ph.D., research associate professor of medicine and cell biology, presented findings demonstrating that the activated vitamin D analog paricalcitol improves cardiac hypertrophy by interfering with previously unrecognized molecular mechanisms.

The study demonstrated that the administration of paricalcitol to rats with renal insufficiency, in addition to its known repressive effects on the renin-angiotensin system, also downregulates the calcineurin/NFAT signaling cascade in the myocardium, and the effects were amplified when it was administered together with a FGF23 receptor blocker improving further the myocardial hypertrophy.

“These findings help explain the cardio-protective effects of vitamin D analogs in chronic kidney disease and open opportunities for possible therapeutic trials targeting these upregulated molecular mechanisms,” said Freundlich.

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