Uric acid and clinical correlates of endothelial function in kidney transplant recipients

2014 ◽  
Vol 28 (10) ◽  
pp. 1167-1176 ◽  
Author(s):  
Dag Olav Dahle ◽  
Trond Jenssen ◽  
Hallvard Holdaas ◽  
Anders Åsberg ◽  
Inga Soveri ◽  
...  
Author(s):  
Elisabetta Bussalino ◽  
Laura Panaro ◽  
Luigina Marsano ◽  
Diego Bellino ◽  
Maura Ravera ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Thomas Duflot ◽  
Charlotte Laurent ◽  
Anne Soudey ◽  
Xavier Fonrose ◽  
Mouad Hamzaoui ◽  
...  

AbstractThis study addressed the hypothesis that epoxyeicosatrienoic acids (EETs) synthesized by CYP450 and catabolized by soluble epoxide hydrolase (sEH) are involved in the maintenance of renal allograft function, either directly or through modulation of cardiovascular function. The impact of single nucleotide polymorphisms (SNPs) in the sEH gene EPHX2 and CYP450 on renal and vascular function, plasma levels of EETs and peripheral blood monuclear cell sEH activity was assessed in 79 kidney transplant recipients explored at least one year after transplantation. Additional experiments in a mouse model mimicking the ischemia–reperfusion (I/R) injury suffered by the transplanted kidney evaluated the cardiovascular and renal effects of the sEH inhibitor t-AUCB administered in drinking water (10 mg/l) during 28 days after surgery. There was a long-term protective effect of the sEH SNP rs6558004, which increased EET plasma levels, on renal allograft function and a deleterious effect of K55R, which increased sEH activity. Surprisingly, the loss-of-function CYP2C9*3 was associated with a better renal function without affecting EET levels. R287Q SNP, which decreased sEH activity, was protective against vascular dysfunction while CYP2C8*3 and 2C9*2 loss-of-function SNP, altered endothelial function by reducing flow-induced EET release. In I/R mice, sEH inhibition reduced kidney lesions, prevented cardiac fibrosis and dysfunction as well as preserved endothelial function. The preservation of EET bioavailability may prevent allograft dysfunction and improve cardiovascular disease in kidney transplant recipients. Inhibition of sEH appears thus as a novel therapeutic option but its impact on other epoxyfatty acids should be carefully evaluated.


2021 ◽  
pp. 152692482110648
Author(s):  
Layna Cristine Brito Rocha ◽  
Danila Lorena Nunes-dos-Santos ◽  
Elisa Miranda Costa ◽  
Samira Vasconcelos Gomes ◽  
Vandilson Pinheiro Rodrigues ◽  
...  

Introduction Poor oral health can negatively affect general health and quality of life of kidney transplant recipients. The study aimed to investigate the association between chronic oral disease burden, serum biomarkers, and comorbidities in kidney transplant recipients. Design A cross-sectional comparative study was conducted with 44 patients after kidney transplant. The burden of chronic oral disease was composed of the following observable variables: moderate periodontitis and presence of dental caries. Serum biomarkers and comorbidities data were collected. The chi-square or Fisher's exact tests for categorical variables and Student's t-test or Mann–Whitney test for continuous variables were used. Robust Poisson regression was used to model the association. Results Higher levels of mean uric acid ( P = .01) and creatinine ( P = .03) were observed in the group of patients with oral disease burden, while the highest level of high-density lipoprotein was observed in the group without oral disease. Higher values of uric acid were associated with the occurrence of chronic oral disease burden (Adjusted PR = 1.24, 95% CI: 1.03-1.48, P = .019). There was no statistical difference between the groups with and without oral disease burden in comorbidities present. Conclusion The findings suggest that chronic oral diseases burden can be associated with uric acid and creatinine levels in kidney transplant recipients.


2005 ◽  
Vol 37 (7) ◽  
pp. 3119-3120 ◽  
Author(s):  
M. Kanbay ◽  
A. Akcay ◽  
B. Huddam ◽  
C.A. Usluogullari ◽  
Z. Arat ◽  
...  

2008 ◽  
Vol 86 (Supplement) ◽  
pp. 79
Author(s):  
P Randhawa ◽  
D Bohl ◽  
D Brennan ◽  
K Ruppert ◽  
G Storch ◽  
...  

2009 ◽  
Vol 41 (1) ◽  
pp. 188-191 ◽  
Author(s):  
A. Zawiasa ◽  
M. Szklarek-Kubicka ◽  
J. Fijałkowska-Morawska ◽  
D. Nowak ◽  
J. Rysz ◽  
...  

Author(s):  
Ersin Nazlican ◽  
Neshat Yucel ◽  
Saime Paydas ◽  
Ilker Unal

OBJECTİVE: Kidney transplant recipients (KTRs) may have increased serum uric acid (SUA) level due to presence of existing greft dysfunction and used immunosuppressives. In this retrospective study, we evaluated effect of high SUA levels and allopurinol therapy in KTRs on renal functions. PATIENTS and METHODS: 113 KTRs of 233 KTRs included, had elevated SUA level (G1). Fiftyseven of G1 received allopurinol treatment (G1A+) and 56 patients (G1A-) did not. 56 of 118 patients who were followed for five years (G5) were hyperuricemic (G5-1) and 26 of G5-1 treated with allopurinol (G5-1A+) and 30 of them did not (G5-1A-). 62 patients were normourisemic (G5-2). RESULTS: Of the 233 patients included the mean age was 42.8±11.6 (17-76), 164 were male (70.0%). In 2. year graft loss developed in 9 (7.5 %) and 18 (15.9%) of G2 and G1 respectively (p = 0.045). According to allopurinol therapy 10 of the graft loss occurred in the G1A+ and 8 in the G1A- (p=0,330). Graft loss occurred in 12 (21%) and 9 (14%) in G5-1 and G5-2 respectively (p = 0.62). Graft loss occurred in 7 (23 %) and 5 (19%) in G5-1A+ and G5-1A- respectively P = 0.71). Considering the first 2 in G5; in G5-1 graft loss was higher than in the G5-2 (p = 0.023), and higher SUA levels increased the graft loss by 3.6 times compared to normal SUA levels (95% confidence interval: 1,2-12.70). CONCLUSION: There was a significant relationship between high SUA levels and graf loss in kidney transplant recipients in 2 years and 5 years. Treatment of high SUA with alIopurinol therapy had protective effect on renal functions. So that hyperuricemia should be treated and low dose allopurinol can be option for treatment of hyperuricemia therefore prevention of loss of kidney function in kidney transplant recipients.


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