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Patients with chronic kidney disease (CKD) are susceptible to changes in zinc homeostasis through anorexia and dietary restrictions, as well as hemodialysis (HD). Changes in zinc homeostasis might predispose CKD and HD patients to specific adverse effects, including erythropoietin-resistant anemia, oxidative stress, atherosclerosis, and cardiovascular disease. Because serum zinc levels are rarely measured in CKD and HD patients, zinc supplementations do not represent a routine therapy for CKD and dialysis patients. Therefore, in this meta-analysis, we aimed to assess serum zinc levels in CKD and HD patients compared with healthy controls (HC). In addition, we investigated whether HD affects serum zinc levels by comparing serum zinc levels in HD versus CKD patients and comparing serum zinc pre- versus post-HD.A comprehensive search of databases was conducted to identify either observational studies or randomized trials that assessed serum zinc levels in either CKD and/or HD patients in comparison to HC. We conducted a random-effects meta-analysis.Our meta-analysis included 42 studies with a total of 4,161 participants, of whom 460 were CKD patients, 2,047 were HD patients, and 1,654 were HCs. Both CKD and HD patients showed lower serum zinc levels compared with HC (mean difference = -22.86 μg/dL, 95% CI -33.25 to -12.46; mean difference = -13.64 μg/dL, 95% CI -21.47 to -53.80, respectively). CKD and HD patients showed no significant difference in serum zinc levels (mean difference = 15.39, 95% CI -8.91 to 39.68). Pre-HD serum zinc levels were significantly lower than those post-HD (mean difference = -7.51 μg/dL, 95% CI -14.24 to -0.78).In the current study, the serum zinc levels were lower in CKD and HD patients compared to HCs and appears to be more common than reported in daily clinical practice. It may be beneficial to assess serum zinc levels in CKD and HD patients. More research on zinc in kidney disease is encouraged.

Background and objective There is currently no FDA-approved medical therapy for delayed graft function (DGF). Dexmedetomidine (DEX) has multiple reno-protective effects preventing ischemic reperfusion injury, DGF, and acute kidney injury. Therefore, we aimed to evaluate the reno-protective effects of perioperative DEX during renal transplantation. Methods A systematic review and meta-analysis synthesizing randomized controlled trials (RCTs) from WOS, SCOPUS, EMBASE, PubMed, and CENTRAL until June 8th, 2022. We used the risk ratio (RR) for dichotomous outcomes and the mean difference for continuous outcomes; both presented with the corresponding 95% confidence interval (CI). We registered our protocol in PROSPERO with ID: CRD42022338898. Results We included four RCTs with 339 patients. Pooled risk ratio found no difference between DEX and placebo in reducing DGF (RR: 0.58 with 95% CI [0.34, 1.01], p = 0.05) and acute rejection (RR: 0.88 with 95% CI [0.52, 1.49], p = 0.63). However, DEX improved short-term creatinine on day 1 (MD: − 0.76 with 95% CI [− 1.23, − 0.3], p = 0.001) and day 2 (MD: − 0.28 with 95% CI [− 0.5, − 0.07], p = 0.01); and blood urea nitrogen on day 2 (MD: − 10.16 with 95% CI [− 17.21, − 3.10], p = 0.005) and day 3 (MD: − 6.72 with 95% CI [− 12.85, − 0.58], p = 0.03). Conclusion Although there is no difference between DEX and placebo regarding reducing DGF and acute rejection after kidney transplantation, there may be some evidence that it has reno-protective benefits because we found statistically significant improvement in the short-term serum creatinine and blood urea nitrogen levels. More trials are required to investigate the long-term reno-protective effects of DEX.