Despite the favorable effects of kidney transplantation on cardiac function and structure, de novo heart failure develops in approximately 18% of kidney transplant recipients within 3 years.1 Now new research shows that post-transplantation anemia, persistent secondary hyperparathyroidism (SHPT), and adiposity all independently associate with impaired diastolic function underlying heart failure with preserved ejection fraction (HFpEF).

In a study of 43 stable kidney transplant recipients, low hemoglobin and high parathyroid hormone (PTH) concentrations were both significantly associated with increased E/e’, an index of left ventricular filling pressure, Patrick H Dessein, MD, of the University of the Witwatersrand in Johannesburg, South Africa, and colleagues reported in the International Journal of Nephrology and Renovascular Disease. Likewise, adiposity indicated by waist-to-height ratio and body mass index displayed significant relationships with worse diastolic function. These associations were independent of left ventricular mass index and cardiac preload and afterload measures.

Post-transplantation anemia may mediate diastolic dysfunction through myocyte hypoxia and consequent cardiac fibrosis, the investigators suggested. Parathyroid hormone can lead to oxidative stress, necrotic cell death, and fibrosis.

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“Whether adequate management of post transplantation anaemia, persistent secondary hyperparathyroidism and excess adiposity can prevent the development of heart failure with preserved ejection fraction in kidney transplant recipients merits further investigation,” according to Dr Dessein’s team wrote. The investigators noted that HFpEF is common in chronic kidney disease, and it is associated with mortality.


  1. Hsu H-C, Norton GR, Peters F, et al. Association of post transplantation anaemia and persistent secondary hyperparathyroidism with diastolic function in stable kidney transplant recipients. Int J Nephrol Renovasc Dis. 2021 Jul 2;14:211-223. doi:10.2147/IJNRD.S314313