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Introduction: It is considered that many factors may play a role in urolithiasis. Experimental and clinical studies have shown that zinc has an inhibitory effect on urolithiasis. Materials and Methods: In this study, urinary zinc and copper were measured in 27 healthy controls and 30 calcium oxalate stone formers. Results: Urinary zinc excretion was significantly higher (p < 0.001) in stone formers than healthy controls (2,575 ± 274 and 960 ± 80 mg/day, respectively). There was no significant difference in urinary copper excretion between healthy controls and stone formers (32.3 ± 3.5 and 33.3 ± 3.2 µg/day, respectively). Conclusions: According to our results, the potent inhibitory effect of urinary zinc excretion on urolithiasis could be reviewed.

The microcirculation is regulated by oxygen gradients and by endothelial release of nitric oxide, which can react with hemoglobin to form S-nitroso derivatives. Here we induced flow-mediated dilatation of the brachial artery in response to ischemia in 141 non-diabetic patients with stage 3-4 chronic kidney disease who had no history of smoking, cardiovascular events or use of erythropoietin-based agents. Patients with hemoglobin concentrations above the cohort median of 11.6 g/dl were found to have significant reductions in flow-mediated dilatation compared to those below the median. This inverse relationship remained significant after adjustment for potential confounders, including insulin sensitivity, glomerular filtration rate, proteinuria, body mass index, serum urate, etiology of underlying renal disease, treatment with anti-hypertensive drugs, and traditional Framingham risk factors. Given that hemoglobin can act as an important nitric oxide carrier and buffer, our studies suggest that the mechanism by which hemoglobin influences the endothelium-dependent microcirculation requires its nitrosylation; however, more direct studies need to be performed.