THU0528 How Kidneys, Heart and Liver Change When Tophi Are Present?
Authors: R.N. Gancheva, A. Kundurdjiev, M. Ivanova, T. Kundurzhiev, Z. Kolarov
Journal: Annals of the Rheumatic Diseases (2016)

<h3>Background</h3> Gout is related to metabolic, cardiovascular and renal disorders. Whether pathological changes in the main substrate – kidneys, heart and liver are more pronounced in the presence of tophi is still unknown. <h3>Objectives</h3> To determine ultrasonographic parameters of the kidneys, heart and liver echogenicity. <h3>Methods</h3> A total of 132 gout patients (pts) were examined cross-sectionally and were divided into two groups: 78 gouty arthritis without tophi, 63 males and 15 females aged 56.46±12.38 years and 54 gouty tophi, 53 males and 1 female aged 58.83±11.46 years. All pts underwent a complex multimodal ultrasonography done by one investigator, who was unaware with clinical data. The following parameters were measured: renal length and resistive index (RRI) – an indicator of renal blood flow, thickness of the interventricular septum (IVS) and posterior wall (PW) of the left ventricle in end-diastolic phase, left ventricular muscle mass (LVMM), left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume (LVESV), stroke volume (SV), ejection fraction (EF), fraction of shortening (FS), left atrium (LA), aortic (Ao) root and liver echogenicity. Data were analyzed by Kolmogorov-Smirnov, t-test, chi-square tests and multiple logistic regression. <h3>Results</h3> Pts were age matched (p=0.267) and had similar mean serum levels of uric acid (p=0.078). Also, in the groups no significant difference in the proportion of pts with flare was estimated – 20 (25.6%) of gouty arthritis without tophi and 22 (40.7%) of gouty tophi (p=0.067), but gouty tophi were with higher CRP (mean±SD; 24.35±34.86 vs 12.11±20.43 mg/l, p=0.002), lower Hb (p=0.001), Hct (p=0.015) and serum albumin (p&lt;0.001). Further, we did not establish difference in renal length (p=0.553), but gouty tophi were with higher RRI (mean±SD; 0.68±0.06 vs 0.65±0.05, p=0.003). Comparing gouty tophi to gout without no difference was found in IVS (mean±SD; 12.57±1.84 vs 12.27±1.84 mm, p=0.366), PW (mean±SD; 12.49±1.90 vs 12.13±1.84 mm, p=0.277), LVMM (p=0.292), Ao root (p=0.786) and SV (p=0.070), but a tendency of significantly reduced FS was observed (mean±SD; 37.22±4.26 vs 38.61±3.52%, p=0.050). Gouty tophi were with larger LA (mean±SD; 40.84±5.93 vs 37.96±4.90 mm, p=0.003), higher LVEDV (mean±SD; 55.77±22.40 vs 44.76±24.83 ml/m<sup>2</sup>, p=0.012), higher LVESV (mean±SD; 17.69±9.98 vs 13.78±8.33 ml/m<sup>2</sup>, p=0.018) and lower EF (mean±SD; 66.93±5.85 vs 68.94±4.16%, p=0.024). In both groups the proportion of pts with hepatic steatosis was large – 55 (74.3%) of gouty arthritis without tophi and 38 (76%) of gouty tophi (p=0.832). We conducted a multiple logistic regression in which LA, LVEDV, LVESV and EF were included. The factor for development of tophi was LA. Its increase by 1 mm raised the subject9s risk of having tophi with an OR=1.102 (95% CI; 1.026–1.184, p=0.008). <h3>Conclusions</h3> When tophi were present renal blood flow was reduced and LA was larger. Furthermore, LA was independently associated with the development of tophi. In gouty tophi higher LVEDV and LVESV with the lack of significant difference in SV can be explained with the activation of compensatory mechanisms. Probably, chronic inflammation is one of the causes for the pathological alterations. <h3>Disclosure of Interest</h3> None declared