Trace Element Status in Hemodialysis Patients

Abstract

Patients with chronic kidney disease undergoing hemodialysis (HD) are potentially at risk of deficiency and excess of trace elements. HD exposes patients to large volumes of water (>120 l/week) in the form of dialysate. Although levels of certain ions (such as potassium and calcium) are carefully regulated in dialysate, many others are measured infrequently, if ever. As a result, substances in lower concentrations in the dialysis may be leached from the body. Conversely, toxic trace elements present in water but not in blood may accumulate and cause toxicity. Given that essential trace elements play key roles in multiple biological systems including immunological defense against oxidation and infection, it has been hypothesized that the increased morbidity and mortality seen in HD patients may in part be due to the imbalance of trace elements that has not been recognized. A recent systematic review has shown that compared with healthy controls, HD patients have significantly lower blood levels of zinc, manganese, and selenium, while blood levels of lead are likely to accumulate. Other trace elements, such as mercury and arsenic, are biologically plausible causes of excess mortality in dialysis patients, but available evidence is inconclusive as to whether they consistently accumulate in this population. Whether altered trace element levels are potentially reversible causes of adverse clinical outcomes in dialysis patients remains to be determined. This review highlights key issues related to this hypothesis, with special emphasis on zinc, manganese, selenium, lead, mercury, and arsenic.

Selenium supplementation improves the nutritional status of hemodialysis patients: a randomized, double-blind, placebo-controlled trial

“…A few cardiovascular deaths also occurred in both selenium and placebo groups; however, these deaths are probably due to higher prevalence of CVDs in HD population. The low incidence of adverse events in this study may be due to the administration of lower dose of selenium (200 µg/day) compared with its maximum allowance dose (400-450 µg/ day) [12]. Other trials which used similar doses of selenium in HD patients also did not report the adverse events of selenium toxicity [18,30,32].…”

“…Selenium has a low therapeutic index, and toxicity may occur with its high-dose supplementation; adverse effects of selenium toxicity include brittle hair and nails and their loss, dermatitis, pulmonary edema, neurotoxicity, nausea and vomiting [12,45]. Except for gastrointestinal disturbances in few patients, none of the other adverse effects of selenium toxicity was observed in this trial.…”

“…Among defense mechanisms against oxidative injury, selenium-dependent enzymes like glutathione peroxidase are the most important ones [5,8,25]. There are several reports on the deficiency of selenium and its dependent enzymes in HD patients [5,12,13,26]. Furthermore, low levels of selenium in HD patients have been reported to be associated with increased inflammatory markers [27].…”

Blood Arsenic and Cadmium Concentrations in End-Stage Renal Disease Patients who were on Maintenance Haemodialysis

“…Higher arsenic (As) concentrations have been reported in the blood and bone marrow of patients with renal failure [23,24]. In healthy subjects, arsenic is usually excreted in urine and it is removed to a certain extent by haemodialysis; however, the removal of arsenic by haemodialysis may not be sufficient, thus leading to its accumulation in the body of haemodialysis patients [25][26][27]. The correlations between lower serum selenium and arsenic toxicity, i.e., skin lesions have been reported [28][29][30].…”

Selenium for malnutrition in hemodialysis patients: have we considered all of the elements?

“…Antioxidant therapy is potentially harmful, and until more is known about its long-term effects, it should be reserved for those who might benefit the most. Selenium is no exception to this general rule and has the potential to be highly toxic in hemodialysis patients; it has a high level of bioavailability, is excreted in urine and has a narrow therapeutic window [28].…”