Inflammation and oxidative stress are two etiologies that may contribute to poor nutritional status and ultimately increased mortality rates in patients with chronic kidney disease (CKD). Interventions that can blunt or ameliorate inflammation and oxidative stress are relevant to these patients. Nutrients with antioxidant properties may be used as such a treatment, especially if the patients are deficient in the nutrients.

Zinc is an interesting trace element with antioxidant properties. Furthermore, zinc deficiency has been documented in patients with CKD. In a recent editorial, the authors reported zinc deficiency in 40%-78% of hemodialysis (HD) patients (Ren Fail 2011;33:466-467).

Zinc concentrations in patients with CKD may vary between body compartments and individuals depending on diet, environment, and medications or supplements prescribed or obtained over the counter. Smythe et al (Ann Intern Med 1982;96:302-310) found no significant difference in tissue concentrations of zinc between healthy controls and patients with CKD. In contrast, McGregor et al (Kidney Int 2001;59:2267-2272) found decreased plasma zinc in CKD patients and Yilmaz et al (Am J Kidney Dis 2006;47:42-50) observed a step-wise reduction in erythrocyte zinc concentrations with advancing stages of the disease.

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Lower concentrations of plasma zinc also may be associated with atherosclerotic status and depression in CKD patients. A 2011 study from Turkey, demonstrated that serum zinc concentrations were lower in HD patients when compared with healthy controls and serum zinc was inversely and significantly associated with carotid artery intima-media thickness: The lower the zinc concentration, the higher the carotid artery intima-media thickness (Biol Trace Elem Res 2011; published online ahead of print).

Similarly, in a 2011 study from Iran, depressed HD patients (Beck Depression Index score higher than 14) had significantly lower plasma zinc concentrations than non-depressed patients (67.5 vs. 85.3 µg/dL) (J Renal Nutr 2011;21:184-187).

Insufficient intake of dietary zinc may contribute to inadequate zinc status in CKD patients. A study in peritoneal dialysis (PD) patients showed that more than half of the patients consumed inadequate quantities of dietary zinc. This study had 73 PD patients that were assessed using the subjective global assessment, 24-hour recalls, and markers of inflammation. The patients who were malnourished had an average zinc intake of 5 mg/day and the well-nourished patients had an average intake of 7 mg/day (Perit Dial Int 2011; published online ahead of print). Both of these intakes are below the dietary reference intake for healthy adults at 8 mg/day.

Foods with higher protein content, such as beef, liver, poultry, and whole grains, tend to be richer in zinc. Patients in later stages of CKD, prior to dialysis, may be instructed on keeping to low phosphorus and protein diets, whereas patients on dialysis are instructed on low phosphorus and high protein diets. These diets may result in reduced intake of whole grain foods and possibly foods containing animal protein. Additionally, while a patient should be placed on a vitamin supplement, the supplements may not contain minerals. In a study with 211 HD patients at an inner city university hospital dialysis center, only 12.9% of the patients were prescribed oral or intravenous trace element supplementation (Nephrol Dial Transplant 2011;26:1006-1010).

Zinc supplementation has been shown to be effective in increasing serum zinc concentrations, although conclusive effects on inflammation parameters have not been demonstrated. In a small clinical trial, zinc sulfate at 220 mg was given to 28 HD patients. C-reactive protein (CRP) and serum zinc were measured at days 0 and 42 and the values were compared to a control group of 27 subjects. At day 42, mean serum zinc levels significantly increased in the treatment group (from 57.4 to 88.4 µg/dL). However, CRP levels did not significantly differ between the treatment and control groups at day 42 (J Ren Nutr 2009;19:475-478). Finally, in a small trial discussed in the 2011 editorial mentioned previously, 38 patients with serum zinc concentrations below 70 µg/dL were supplemented with zinc sulfate at a dosage of 250 mg/day. At day 42, the serum zinc values had increased significantly and CRP had decreased significantly.

In conclusion, patients with CKD are at risk for zinc deficiency that may impact their inflammatory, atherosclerotic, and mental status. Supplementation with zinc sulfate will increase serum values but whether it will improve outcomes is controversial.