Dr. Tsuneo Ishida
Zinc (Ⅱ) supplementation (30 mg/day) should become likely therapeutic chronic kidney disease (CKD) prevention implications with immense importance of CKD-associated immunological and neurological complications of central nervous system (CNS) disorder and peripheral nervous system (PNS) condition.
Zinc induced neuro immunological inhibitive CKD progression with Stage 2～3A, 3B, zinc supplementation may be beneficial for nutritional status in CKD children and adolescents, and zinc could reduce urinary protein excretion composed of albumin and/or minimize proteinuria excretion in proteinuric CKD. In CKD 4～5 stage, risk of cardiovascular disease (CVD) become higher that zinc supplementation of 25 mg/day in zinc homeostasis has a beneficial effect for CVD in vascular dysfunction, in which zinc induced CKD Stage 5 (eGFR < 15) is involved that zinc is actively bound to several proteins that the decrease of circulating zinc levels in CKD is becoming zinc-deficiency with advanced stage CKD and ESRD in CKD. Zinc 15 mg/day and Selenium 50–70 μg/day that are recommended may be thought to prevent ESRD stage.
Zinc induced NAD (P)H oxidase (Nox) activation occurring ROS generation in CKD cell involves assembly that ROS include the superoxide anion (O2•–), hydrogen peroxide (H2O2), and hydroxyl radicals (OH•) in the kidney.
Zinc(Ⅱ) ions-binding protein molecular mechanism is involved that Zn2+ ions induced binding ligands of such as albumin, a-macroglobulin and transferrin in several proteins had been found on the binding specificity by Zn2+ ions-centered tetrahedral geometric coordination, in which causing zinc-activated serine, histidine and aspartate hydrogen residues enhance renal function activity and resulting inhibition of CKD progression proceeds.
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