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. 2019 Mar 7;14(3):432-434.
doi: 10.2215/CJN.12141018. Epub 2019 Feb 6.

Hypernatremia

Qi Qian  1
Affiliations

Hypernatremia

Qi Qian. Clin J Am Soc Nephrol. .
No abstract available

Keywords: Acids; Dehydration; Ions; Noncarboxylic; Potassium; Sodium; diabetes insipidus; diagnosis; hypernatremia; pathophysiology; sodium regulation; treatment; water regulation.

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Figures

Figure 1.
Figure 1.
Cellular adaptation and relations of serum and urine osmolality. (A) Hypernatremia causes a rapid osmotic water efflux, which activates regulatory volume increase. The latter counters the cell shrinkage force by initially gathering ionic osmolytes (within minutes) and subsequently, through a transcriptional process, replacing the ionic osmolytes with more compatible organic osmolytes (within hours to days). The accumulation of intracellular organic osmolytes, although less toxic, can cause multiple cellular dysfunctions as evidenced by continued DNA breakdown and oxidative stress. Tissue can buffer extracellular fluid Na+ and constitutes another potential aspect of Na+ concentration regulation. Until hyperosmolality is corrected, these abnormalities persist. (B) The relationship between plasma and urine osmolality during the (a) genesis, (b) adaptation, and (c) correction (resolution) phases of a hypernatremia episode is depicted. Our first patient had an adequate kidney response to antidiuretic hormone, arginine vasopressin. Her urine became concentrated (solid yellow line) before the elevation of serum osmolality. During resolution (fluid administration), the serum osmolality returned to normal before urine dilution. The dotted yellow line represents our second patient. Her urine concentration would be minimally increased despite elevation of serum osmolality, consistent with lithium-induced nephrogenic diabetes insipidus.
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