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Review
. 2023 Mar 1;4(3):398-404.
doi: 10.34067/KID.0007812021.

Zinc Deficiency: A Potential Hidden Driver of the Detrimental Cycle of Chronic Kidney Disease and Hypertension

Affiliations
Review

Zinc Deficiency: A Potential Hidden Driver of the Detrimental Cycle of Chronic Kidney Disease and Hypertension

Adaku C Ume et al. Kidney360. .

Abstract

Globally, over 103 million individuals are afflicted by CKD, a silent killer claiming the lives of 1.2 million people annually. CKD is characterized by five progressive stages, in which dialysis and kidney transplant are life-saving routes for patients with end stage kidney failure. While kidney damage impairs kidney function and derails BP regulation, uncontrolled hypertension accelerates the development and progression of CKD. Zinc (Zn) deficiency has emerged as a potential hidden driver within this detrimental cycle of CKD and hypertension. This review article will (1) highlight mechanisms of Zn procurement and trafficking, (2) provide evidence that urinary Zn wasting can fuel Zn deficiency in CKD, (3) discuss how Zn deficiency can accelerate the progression of hypertension and kidney damage in CKD, and (4) consider Zn supplementation as an exit strategy with the potential to rectify the course of hypertension and CKD progression.

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Conflict of interest statement

The authors have nothing to disclose.

Figures

Figure 1
Figure 1
Zinc distribution in organs (clockwise). Brain (11 μgZn/gram, 0.6%), lungs (17 μg Zn/gram, 0.5%), heart (27 μg Zn/gram, 0.3%), spleen (15 μg Zn/gram, 0.1%), kidneys (55 μg Zn/gram, 0.6%), skeletal muscles (51 μg Zn/gram, 50%), hair/skin/nails (279 μg Zn/gram, 4.7%), bone (100 μg Zn/gram, 37%), blood vessels (6.81 μg Zn/gram, 1.5%), pancreas (33.3 μg Zn/gram, 0.2%), liver (58 μg Zn/gram, 3.4%), stomach (13.4 μg Zn/gram, 0.5%), and eyes (1.3 μg Zn/gram, <0.01%).
Figure 2
Figure 2
Normal zinc handling. MTs, metallothioneins; ZIPs, Zrt-, Irt-like proteins; ZnTs, Zn transporters.
Figure 3
Figure 3
Zinc deficiency can accelerate the detrimental cycle of hypertension and kidney damage in CKD. Zn deficiency is partially fueled by a newly uncovered phenomenon—urinary Zn wasting. Zn deficiency alone causes kidney damage and is also sufficient to induce hypertension. This overlooked culprit drives renal Na+ retention and can consequently promote the self-perpetuating cycle of hypertension and kidney damage that accelerates CKD progression to end stage kidney failure.
Figure 4
Figure 4
Zinc supplementation: A possible offramp from the road to end stage kidney failure.

References

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