POS1144 SERUM URIC ACID TO CREATININE RATIO IS ASSOCIATED WITH URINARY URIC ACID EXCRETION IN PATIENTS WITH GOUT

Background:Underexcretion of uric acid is the dominant mechanism leading to hyperuricemia [1] and the 24-hour urinary uric acid excretion is an important measurement. However, it is inconvenient due to accurate timing and complete collection of the specimen.Objectives:The aim of this study was to investigate the relationship between serum uric acid to creatinine ratio (sUACR) and 24-hour urinary uric acid excretion in gout patients.Methods:A total of 110 gout patients fulfilling 2015 ACR/EULAR classification criteria from Guangdong Second Provincial General Hospital from January 2019 to January 2021 were retrospectively enrolled in this study. Patients were divided into underexcretion group (<3600 μmol/24h) and non-underexcretion group (≥3600 μmol/24h). The correlation between sUACR and 24-hour urinary uric acid excretion was analyzed by the Pearson’s correlations analysis. Receiver operation characteristic (ROC) curves were performed to assess the utility of sUACR for discriminating between underexcretion group and non-underexcretion group. Furthermore, the risk factors of uric acid underexcretion were evaluated using binary logistic regression analysis.Results:sUACR in the underexcretion group was significantly lower than the non-underexcretion group (p=0.0001). Besides, sUACR was positively correlated with 24-hour urinary uric acid excretion (r=0.4833, p<0.0001). Furthermore, ROC suggested that the area under the curve (AUC) of sUACR was 0.728, which was higher that of serum uric acid and creatinine. The optimal cutoff point of sUACR was 5.2312, with a sensitivity and specificity of 71.9% and 67.9%. Logistic analysis results revealed that decreased sUACR (<5.2312) was an independent risk factor of underexcretion of uric acid (OR =5.510, 95% CI: 1.952-15.550, P=0.001).Conclusion:sUACR is lower in gout patients with underexcretion of uric acid and may serve as a useful and convenient marker of assessing underexcretion of uric acid in gout patients.References:[1]Perez-Ruiz F, Calabozo M, Erauskin GG, Ruibal A, Herrero-Beites AM. Renal underexcretion of uric acid is present in patients with apparent high urinary uric acid output. Arthritis Rheum 2002; 47: 610–13.Figure 1.A. Comparison of serum uric acid to creatinine ratio between underexcretion group and non-underexcretion group. B. Correlation between serum uric acid to creatinine ratio and 24h uric acid excretion.Disclosure of Interests:None declared.

Anti-hyperuricemic effect of Polydatin in model mice: promoting uric acid excretion and inhibiting XOD

Objective The aim of this study was to understand the role of anti-hyperuricemic mechanism and nephro-protective effects of polydatin. Methods The oxonate-induced hyperuricemia mice model was established and uric acids in serum were observed. Kidney tissues were used to detect gene contents of URAT1, OAT1 and OAT3 by real-time-PCR. and to detect pathological features .The activity of XOD in liver tissues of mice was detected . Results Polydatin significantly reduced serum urate levels in hyperuricemic mice. Polydatin significantly inhibited increasing tendency of the mRNA and the protein levels of OAT1 and OAT3 ,and decreasing tendency of the mRNA and the protein level of URAT1 in hyperuricemic mice. Polydatin significantly inhibited the level of XOD in liver tissues of mice in a concentration-dependent manner in hyperuricemic mice. Polydatin showed a protective effect on the pathological injury of kidney in hyperuricemic mice. Conclusion The anti-hyperuricemic effect of polydatin was related to the down-regulation of renal URAT1, up-regulated renal OAT1 and OAT3 and inhibition XOD in the hyperuricemic mice.

Expression and phylogeny of multidrug resistance protein 2 and 4 in African white backed vulture (Gyps africanus)

Diclofenac toxicity in old world vultures is well described in the literature by both the severity of the toxicity induced and the speed of death. While the mechanism of toxicity remains unknown at present, the necropsy signs of gout suggests primary renal involvement at the level of the uric acid excretory pathways. From information in the chicken and man, uric acid excretion is known to be a complex process that involves a combination of glomerular filtration and active tubular excretion. For the proximal convoluted tubules excretion occurs as a two-step process with the basolateral cell membrane using the organic anion transporters and the apical membrane using the multidrug resistant protein to transport uric acid from the blood into the tubular fluid. With uric acid excretion seemingly inhibited by diclofenac, it becomes important to characterize these transporter mechanism at the species level. With no information being available on the molecular characterization/expression of MRPs of Gyps africanus, for this study we used next generation sequencing, and Sanger sequencing on the renal tissue of African white backed vulture (AWB), as the first step to establish if the MRPs gene are expressed in AWB. In silico analysis was conducted using different software to ascertain the function of the latter genes. The sequencing results revealed that the MRP2 and MRP4 are expressed in AWB vultures. Phylogeny of avian MRPs genes confirms that vultures and eagles are closely related, which could be attributed to having the same ancestral genes and foraging behavior. In silico analysis confirmed the transcribed proteins would transports anionic compounds and glucose.