Effect of hyperuricemia on endothelium in kidney transplant patients
Lourdes Roca-Argente, Julio Hernández Jaras, Isabel Beneyto Castelló and Celia Bañuls Morant
Background: Uric acid has been historically regarded as both a beneficial molecule and evolutionary
factor for Homo sapiens and as a pathogenic molecule involved in the pathophysiology of some
diseases. Nowadays, there is not any evidence-based explanation to justify the apparently causal role
of serum uric acid in certain cardiovascular diseases such as hypertension in adults, chronic kidney
disease, type II diabetes or metabolic syndrome. One pathophysiological mechanism proposed to
explain the role of uric acid in cardiovascular diseases is the endothelial dysfunction.
Methods: We proposed an observational and prospective study of 38 first post-transplant patients to
analyze the relationship between serum uric acid levels and markers of endothelial dysfunction and
inflammation, such as VCAM, ICAM, IL10, CD40, TNFα, E-selectin, P-selectin and PCR.
Results: We observed an improvement in the endothelial markers VCAM and ICAM during the first
year of transplant. Indeed, diabetic patients had higher levels of TNFα and serum uric acid one year
after kidney transplant. Patients with cytomegalovirus infection presented higher levels of TNFα on
the third month and serum uric acid at the twelfth month after kidney transplant. However, we were
not able to demonstrate a positive correlation between serum uric acid and markers of endothelial
dysfunction and inflammation within our sample.
Conclusions: Results show a relationship between uric acid and markers of endothelial dysfunction
and inflammation in kidney transplant patients, although we were not able to identify whether uric
acid was the cause.
