Contrast-induced acute kidney injury (CI-AKI) is a common cause of hospital-acquired acute kidney injury (AKI). We evaluated the evidence that uric acid (UA) plays a pathogenic role in CI-AKI. Ten studies were eligible for inclusion for meta-analysis. Hyperuricemia predicted risk for cases with AKI in prospective cohort studies. Higher levels of serum UA (SUA), as defined by the authors, were associated with a 2-fold increased risk to develop AKI (pooled odds ratio 2.03; 95% confidence interval [CI] 1.48-2.78). Significant heterogeneity was found in cohort studies ( P = .001, I = 85.7%). In 2 clinical trials, lowering of SUA with saline hydration was significantly associated with reduced risk for AKI compared with saline hydration alone or saline hydration with N-acetyl cysteine. An analysis of 2 randomized controlled trials found that allopurinol with saline hydration had a significant protective effect on renal function (assessed by serum creatinine values) compared with hydration alone (mean difference: -0.52 mg/dL; 95% CI: -0.81 to -0.22). Hyperuricemia independently predicts CI-AKI. Two clinical trials suggest lowering SUA may prevent CI-AKI. The mechanism by which UA induces CI-AKI is likely related to acute uricosuria.

The presumed superiority of renin-angiotensin-aldosterone system (RAAS)-blocking agents over other antihypertensive agents in patients with diabetes to delay development of end-stage kidney disease (ESKD) has recently been challenged. In addition, there is ongoing uncertainty whether RAAS-blocking agents reduce mortality and/or delay ESKD in patients with diabetes and chronic kidney disease (CKD) stages 3-5. In this subgroup, there might be an expedited need for renal replacement therapy (RRT) when RAAS-blocking agents are used. We conducted a meta-analysis of randomized controlled trials (RCTs) of at least 6-months duration in adult patients with diabetes who also have non-dialysis CKD stages 3-5. RCTs comparing single RAAS-blocking agents to placebo or alternative antihypertensive agents were included. Outcomes of interest were all-cause mortality, cardiovascular morbidity, progression of renal function, ESKD and adverse events. A total of nine trials (n = 9797 participants with CKD stages 3-5) fit our inclusion criteria. There was no difference between the RAAS group and control group regarding all-cause mortality {relative risk [RR] = 0.97 [95% confidence interval (CI) 0.85-1.10]}, cardiovascular mortality [RR = 1.03 (95% CI 0.75-1.41)] and adverse events [RR = 1.05 (95% CI 0.89-1.25)]. There was a trend for a favourable effect for non-fatal cardiovascular events [RR = 0.90 (95% CI 0.81-1.00)] and a lower risk of the composite endpoint need for RRT/doubling of serum creatinine [RR = 0.81 (95% CI 0.70-0.92)] in the RAAS-blocking agents group versus the control group. We found evidence that in patients with diabetes mellitus and CKD stages 3-5, treatment with RAAS-blocking agents did not result in a clear survival advantage. The effect on renal outcomes did depend on the selected outcome measure. However, we did not find evidence that the use of RAAS-blocking agents expedited the need for RRT in patients with CKD stages 3-5.

Introduction Cognitive impairment is a major, but underdiagnosed, risk factor for negative outcomes in patients with chronic kidney disease (CKD). The main goal of this study was to evaluate, for the first time, the relationship between arterial stiffness and cognitive impairment in a cohort of hemodialysis patients. Methods We prospectively analyzed the cognitive function and pulse wave velocity (PWV) of 72 hemodialysis patients, mean age 56.54 ± 13.96 y, from two Romanian dialysis centers. We administered to all patients the Mini Mental State Examination (MMSE), Trail Making Test Part-A (TMTA) and Part-B (TMTB), and Mini-Cog Test. Radial arterial waveforms during 40 cardiac cycles were recorded in each patient. Findings Mean MMSE score was 25.13 ± 3.47, mean MiniCog score was 3.51 ± 1.18, mean TMTA (sec) was 103.77 ± 53.13 and mean TMTB (sec) was 214.93 ± 112.25. In linear unadjusted regression, PWV values were associated with worse MMSE scores (β = -0.36, P = 0.001, 95% CI: -0.68 to -0.17), and MiniCog scores (β = -0.26, P = 0.02, 95% CI: -0.19 to -0.01). Also, PWV value was significant associated with TMTA test, but not with TMTB. After further adjustments, PWV remained a strong predictor for cognitive impairment measured by MMSE, TMTA, MiniCog, but not for TMTB. Discussion Cognitive impairment was associated with higher PWV values in our cohort. Further evidence is needed in order to support arterial stiffness as a long-term predictor for cognitive decline in ESRD patients.

Background: The effect of anemia correction on kidney function in chronic kidney disease (CKD) patients remains unclear. As 19-40% of patients with CKD receive an erythropoiesis-stimulating agent (ESA), this is a potentially important consideration. Summary: We conducted a systematic review and meta-analysis of randomized trials to January 1, 2014 in adult patients with CKD stages 1 to 4. Selection criteria for studies: randomized controlled trials of at least 2 months duration. Patients were allocated to ESA versus placebo, no treatment, or different ESA doses with the purpose of achieving a higher versus a lower hemoglobin target. The analyzed outcomes were the need for renal replacement therapy, doubling of serum creatinine, change in GFR (ml/min), mortality and withdrawal of treatment due to adverse events. A total of 19 trials (n = 8,129 participants with CKD stage 1-4) were reviewed. There was no difference in the risk of end-stage kidney disease (RR, 0.97 [CI 0.83-1.20], 17 trials, 8,104 participants), change in GFR (Mean Difference [MD] -0.45 [-2.21, 1.31], 9 trials, 1,848 participants) or withdrawal of treatment due to adverse events (RR, 1.18 [CI 0.77-1.81], 10 trials, n = 1,958 participants) for patients at higher hemoglobin (Hb) targets. Furthermore, no statistically significant differences in mortality (Risk Ratio [RR] 1.10 [CI 0.90-1.35], 16 trials, n = 8,082 participants) were observed. Key Messages: There is no evidence that ESA treatment affects renal function in patients with CKD. Use of these agents should not therefore be influenced by considerations about influencing CKD progression.

Vasopressin receptors antagonists may reduce body weight and increase Na but do not improve all-cause mortality, cardiovascular mortality or kidney function. In addition, acceptability of long-term treatment side effects and hospitalization appears problematic.

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In hemodialysis patients malnutrition-inflammation syndrome, evaluated by biochemical laboratory analysis and through bioimpedance spectroscopy, was associated to impaired quality of life and with an increased risk of mortality. The present study goal was to investigate, in a cross-sectional analysis, performed in 122 hemodialysis patients, the association between biochemical parameters and bioimpedance-derived measurements the association of undernutrition with quality of life and illness perception. The results showed that our cohort perceived an impaired quality of life and illness perception and that these psychometric evaluation was associated with malnutrition markers.