Conflicting results have been reported from studies evaluating serum uric acid (SUA) levels as an independent risk factor for cardiovascular mortality in patients with chronic kidney disease (CKD). We systematically searched MEDLINE, Web of Science, and bibliographies of retrieved articles to identify studies reporting on the association between SUA levels and cardiovascular mortality in patients with CKD. Random-effects models were used to calculate the pooled hazard ratios (HR) and corresponding 95% confidence intervals (CI). We included 11 studies with an overall sample of 27,081 patients with CKD in this meta-analysis. By meta-analysis, restricted to 7 studies (n = 11,050), patients with the highest SUA were associated with an increased risk of cardiovascular mortality (HR 1.47, 95% CI 1.11–1.96) compared with patients with the lowest SUA. There was no indication of publication bias or significant heterogeneity (I2 = 40.4%; P = 0.109). Meta-analysis of 10 studies (n = 26,660) indicated that every 1 mg/dl increase in SUA levels increased a 12% risk in cardiovascular mortality (HR 1.12, 95% CI 1.02–1.24), with significant heterogeneity (I2 = 79.2%, P < 0.001). Higher SUA levels are associated with significantly increased risk of cardiovascular mortality in patients with CKD. More designed studies, especially randomized controlled trials, should be conducted to determine whether high SUA levels is a potentially modifiable risk factor for cardiovascular mortality in patients with CKD.

Background: The association between homocysteine (Hcy) and IgA nephropathy (IgAN) is not well understood. We aimed to investigate the relationship between Hcy and clinicopathologic features in IgAN patients.Methods: A total of 337 IgAN patients and 150 sex- and age- matched healthy controls were enrolled in this single-center retrospective study. According to Hcy ≤ 10 μmol/L or > 10 μmol/L, patients were divided into low and high Hcy groups. Multivariate logistic regression was performed to explore the risk factors for elevated Hcy.Results: Serum Hcy was higher in IgAN patients than in healthy controls [11.6 (9.1,15.3) vs. 8.8 (7.5,10.6) μmol/L,P < 0.001], unanimously in the subgroup of 156 patients with a normal estimated glomerular filtration rate (eGFR) (≥ 90 ml/min/1.73 m²) [9.9 (7.6,12.4) vs. 8.8 (7.5,10.6) μmol/L,P < 0.001]. Compared to the low Hcy group, serum creatinine (Scr), blood urine nitrogen (BUN), uric acid (UA), endocapillary hypercellularity (E) and tubular atrophy/interstitial fibrosis lesion (T) were higher in the high Hcy group. Hcy levels were positively correlated with Scr, BUN, UA, 24-h urine protein, and E and T lesions, but negatively correlated with eGFR and superoxide dismutase (SOD). In the subgroup with normal eGFR, patients with higher Hcy were persistent with higher Scr, BUN and T lesions. A multivariate logistic regression model showed that the risk of elevated Hcy in patients with pathological T increased by 2.87-fold. T lesions could better predict high Hcy, with an odds ratio (OR) of 14.20 in the subgroup with normal eGFR.Conclusions: Pathologic T was an independent risk factor associated with elevated Hcy, especially at the early stage of IgAN.

Few data has been available on the effect of serum HDL-C levels on the prognosis of lupus nephritis (LN) patients. The present study therefore aimed to explore the effect of serum HDL-C levels on LN patients. We included 775 patients with follow-up information registered in an LN database between 1 January 2006 and 31 December 2011. The patients were divided into groups with low, intermediate and high HDL-C, according to NCEP ATPIII criteria. Cox regression analyses were used to explore the effects of HDL-C levels on end-stage renal disease (ESRD), all-cause mortality and cardiovascular disease (CVD) mortality. During a median follow-up of 56 months (3–206 months), 71 (9.2%) had ESRD. 84 (10.8%) deaths occurred, 17 (20.2%) of which were due to CVD. There was no statistically significant association of HDL-C category or continuous HDL-C levels with ESRD in the total cohort, but in subgroup analyses by eGFR, with each 0.1 mmol/L increase in HDL-C level, adjusted HRs for ESRD were 0.92 (95% CI: 0.83–1.04, P = 0.173) for eGFR ≥60 ml/min/1.73m2 and 1.11 (95% CI: 1.01–1.23, P = 0.036) for eGFR <60 ml/min/1.73m2. The effect of the interaction between eGFR category and serum HDL-C level on ESRD was statistically significant (β = −1.738, P = 0.005). Low HDL-C was associated with all-cause mortality (HR = 2.16, 95% CI: 1.06–4.40, P = 0.033) with intermediate HDL-C as reference category after adjusting for several variables. Our results demonstrate that high HDL-C levels were associated with increased risk of ESRD in LN patients with advanced renal dysfunction. While low HDL-C levels were associated with increased risk of all-cause mortality in LN patients. ClinicalTrials.gov Identifier: NCT03001973 , 22 December 2016 retrospectively registered.