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Uric acid (UA) is associated with renal disease and patient survival, but the causal associations remain unclear. Also, the longitudinal UA control (trajectory) is not well understood. We enrolled 808 subjects diagnosed with stage 3 chronic kidney disease from 2007 to 2017. We plotted the mean UA over a period of 6 months with a minimum requirement of 3 samples of UA. From the sampled points, we generated an interpolated line for each patient by joining mean values of UA levels over time. Using lines from all patients, we classified them into 3 groups of trajectories (low, medium, and high) through group-based trajectory modeling, and then we further separated them into either treatment or nontreatment subgroups. Due to multiple comparisons, we performed post hoc analysis by Bonferroni adjustment. Using univariate competing-risks regression, we calculated the competing risk analysis with subdistribution hazard ratio of possible confounders. All of the 6 trajectories appeared showed a gradual decline in function over time without any of the curves crossing over one another. For all-cause mortality risk, none of the variables (including age, gender, coronary arterial disease, cerebrovascular disease, diabetes mellitus, renin-angiotensin-aldosterone system inhibitors, trajectories of UA, and treatment of UA) were statistically significant. All 6 trajectories appeared as steady curves without crossovers among them over the entire period of follow-up. Patients with diabetes mellitus were statistically more likely to undergo dialysis. The only trend was seen in the on-treatment trajectories, which showed lower risks for dialysis compared to their nontreatment trajectories. There was no effect of UA control on survival. Initial treatment of UA is crucially important for UA control. However, the long-term effects on patients and renal survival appeared to be minor and without statistical significance., Competing Interests: The authors have no conflicts of interest to disclose., (Copyright © 2022 the Author(s). Published by Wolters Kluwer Health, Inc.)

The relationship between serum uric acid (SUA) and cardiovascular (CV) mortality in patients with chronic kidney disease (CKD) has been described as either a J- or U-shaped function. However, its effect in non-diabetic CKD (and varying severities of CKD) remains unclear. We analyzed the database of the National Health and Nutrition Examination Survey, USA, from the years 1999 to 2010. We then grouped the subjects into 4 categories according to their SUA levels: (a) < 5 mg/dl, (b) 5-7 mg/dl, (c) 7-9 mg/dl and (d) ≥ 9 mg/dl. For mortality comparison purposes (CV related, cancer related and all-cause mortality), we set the SUA group of 5-7 mg/dl as the reference. We also separated this population into moderate (stage 3) and severe (stages 4 and 5) CKD. A total of 1860 participants were included in this study. Results showed that the group with the lowest SUA levels (< 5 mg/dl), were the least male gender (19.25%), had the lowest body mass index (26.41(95% CI = 25.66-27.16) kg/m 2 ), highest systolic blood pressure (139.02 (95% CI 135.72-142.32) mmHg), highest high-density cholesterol (59.55 (95% CI 57.37-61.74) mg/dl), lowest blood glucose (95.46 (95% CI 93.16-97.76) mg/dl), highest total cholesterol (210.31 (95% CI 203.36-217.25) mg/dl), lowest serum albumin (4.09 (95% CI 4.04-4.14) g/dl), highest estimated glomerular filtration rate (eGFR) (47.91 (95% CI 45.45-50.49) ml/min/1.732m 2 ), least history of hypertension (54.4%), and least total energy intake (1643.7 (95% CI 1536.13-1751.27) kcal/day). In the group with SUA ≥ 9 mg/dl, patients had higher all-cause mortality (HR = 2.15) whatever their baseline CVD status. In non-DM CKD patients with a CVD history, the group with SUA ≥ 9 mg/dl had the highest all-cause mortality (HR = 5.39), CVD mortality (HR = 8.18) and CVD or cancer (HR = 8.25) related mortality. In non-DM patients with severe CKD (eGFR < 30 ml/min/1.732m 2 ), the group with SUA < 5 had a significantly increased all-cause mortality. On the contrary, in non-DM patients with moderate CKD (eGFR = 30-60 ml/min/1.832m 2 ), the group with SUA ≥ 9 had a significantly increased all-cause mortality. In moderate non-DM CKD, SUA ≥ 9 mg/dl is associated with higher all-cause mortality. However, once progressing to severe non-DM CKD, SUA < 5 mg/dl is associated with higher all-cause mortality (even though it has the least risk factors for metabolic syndrome).

The aim of this study was to determine whether elevated serum level of uric acid (sUA) could predict renal outcome after contrast-enhanced computerized tomography (CCT). We used a historical cohort of 58,106 non-dialysis adult patients who received non-ionic iso-osmolar CCT from 1 June 2008 to 31 March 2015 to evaluate the association of sUA and renal outcome. The exclusion criteria were patients with pre-existing acute kidney injury (AKI), multiple exposure, non-standard volume of contrast, and missing data for analysis. A total of 1440 patients were enrolled. Post-contrast-AKI (PC-AKI), defined by the increase in serum creatinine ≥ 0.3 mg/dL within 48 h or ≥50% within seven days after CCT, occurred in 180 (12.5%) patients and the need of hemodialysis within 30 days developed in 90 (6.3%) patients, both incidences were increased in patients with higher sUA. sUA ≥ 8.0 mg/dL was associated with an increased risk of PC-AKI (odds ratio (OR) of 2.62; 95% confidence interval (CI), 1.27~5.38, p = 0.009) and the need of hemodialysis (OR, 5.40; 95% CI, 1.39~21.04, p = 0.015). Comparing with sUA < 8.0 mg/dL, patients with sUA ≥ 8.0 mg/dL had higher incidence of PC-AKI (16.7% vs. 11.1%, p = 0.012) and higher incidence of hemodialysis (12.1% vs. 4.3%, p < 0.001). We concluded that sUA ≥ 8.0 mg/dL is associated with worse renal outcome after CCT. We suggest that hyperuricemia may have potential as an independent risk factor for PC-AKI in patients receiving contrast-enhanced image study. [ABSTRACT FROM AUTHOR]