AIMS: We evaluated the relationship between elevated serum uric acid (SUA) and mortality as well as cardiac allograft vasculopathy (CAV) among 184 heart transplant (HTx) recipients. We also measured inflammatory, neurohormonal, and oxidative stress markers to explore pathophysiological mechanisms. METHODS AND RESULTS: There were 28 (15%) deaths, patients with SUA > or = 502 micromol/L (upper quartile) at 1 year post-HTx had an increased risk of total mortality (adjusted HR 2.21, P = 0.03) and cardiac mortality (adjusted HR 4.38, P = 0.03). Elevated SUA was a significant risk factor for development of moderate/severe angiographic CAV (adjusted HR 4.79, P = 0.01). A smaller decline in SUA (<97 micromol/L) during the first year post-HTx was also associated with an increased risk of mortality (P = 0.02). Patients with elevated SUA had significantly higher levels of high-sensitivity C-reactive protein (P = 0.008) and N-terminal probrain natriuretic peptide (P = 0.022), but there was no significant difference in oxidative stress parameters. CONCLUSION: Elevated SUA at 1 year post-HTx, or a modest rather than a marked decline in SUA levels during the first year post-HTx, is associated with an increased risk of mortality. Although the pathophysiological mechanism is unclear, our data indicate a potential relationship between SUA and inflammation which should be explored further.
AIMS: We evaluated the relationship between elevated serum uric acid (SUA) and mortality as well as cardiac allograft vasculopathy (CAV) among 184 heart transplant (HTx) recipients. We also measured inflammatory, neurohormonal, and oxidative stress markers to explore pathophysiological mechanisms. METHODS AND RESULTS: There were 28 (15%) deaths, patients with SUA > or = 502 micromol/L (upper quartile) at 1 year post-HTx had an increased risk of total mortality (adjusted HR 2.21, P = 0.03) and cardiac mortality (adjusted HR 4.38, P = 0.03). Elevated SUA was a significant risk factor for development of moderate/severe angiographic CAV (adjusted HR 4.79, P = 0.01). A smaller decline in SUA (<97 micromol/L) during the first year post-HTx was also associated with an increased risk of mortality (P = 0.02). Patients with elevated SUA had significantly higher levels of high-sensitivity C-reactive protein (P = 0.008) and N-terminal probrain natriuretic peptide (P = 0.022), but there was no significant difference in oxidative stress parameters. CONCLUSION: Elevated SUA at 1 year post-HTx, or a modest rather than a marked decline in SUA levels during the first year post-HTx, is associated with an increased risk of mortality. Although the pathophysiological mechanism is unclear, our data indicate a potential relationship between SUA and inflammation which should be explored further.
Authors: Joseph C Longenecker; Sana Waheed; Ghassan Bandak; Christine A Murakami; Blaithin A McMahon; Allan C Gelber; Mohamed G Atta Journal: BMC Nephrol Date: 2017-03-27 Impact factor: 2.388
Authors: Martina Bona; Rahel K Wyss; Maria Arnold; Natalia Méndez-Carmona; Maria N Sanz; Dominik Günsch; Lucio Barile; Thierry P Carrel; Sarah L Longnus Journal: J Am Heart Assoc Date: 2021-01-30 Impact factor: 5.501