Estimation of extracellular fluid volume in children

Peters, A. M.

doi:10.1007/s00467-012-2117-9

Cited by 1 publication

(1 citation statement)

References 13 publications

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“…As copeptin and aldosterone V d and t 1/2 are unidentifiable with the current study design, they were fixed to the literature values. Copeptin V d was set to the extracellular fluid volume (ECF), 41 calculated as the following 42,43 :

\begin{matrix} left ECF goodbreak= 0.0215 \cdot {weight}^{0.647} \cdot {height}^{0.724} \end{matrix}

One individual's missing height was imputed from the World Health Organization growth charts using known weight and age 44 . Because copeptin is a peptide, which generally are considered to have fast turnover t 1/2 (≤10 min), 41 its t 1/2 was fixed to 0.1 h. Aldosterone V d and t 1/2 were fixed to values reported for fludrocortisone, an aldosterone analog, of 1.11 L/kg and 1.4 h, respectively 45 …”

Section: Methodsmentioning

confidence: 99%

Semimechanistic modeling of copeptin and aldosterone kinetics and dynamics in response to rehydration treatment for diabetic ketoacidosis in children

Otto

Burckhardt

Szinnai

et al. 2022

CPT Pharmacom & Syst Pharma

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Diabetic ketoacidosis (DKA), a frequent complication of type 1 diabetes (T1D), is characterized by hyperosmolar hypovolemia. The response of water-regulating hormones arginine vasopressin (AVP; antidiuretic hormone) and aldosterone to DKA treatment in children is not well understood, although they may have potential as future diagnostic, prognostic, and/or treatment monitoring markers in diabetic patients. We aimed to characterize the dynamics of the response in copeptin (marker for AVP) and aldosterone secretion to rehydration treatment in pediatric patients with DKA. Data originated from a prospective, observational, multicenter study including 28 pediatric T1D patients treated for DKA (median age, 11.5 years; weight, 35 kg). Serial measurements of hormone levels were obtained during 72 h following rehydration start. Semimechanistic pharmacometric modeling was used to analyze the kinetic/dynamic relationship of copeptin and aldosterone secretion in response to the correction of hyperosmolality and hypovolemia, respectively. Modeling revealed different sensitivities for osmolality-dependent copeptin secretion during the first 72 h of rehydration, possibly explained by an osmotic shift introduced by hypovolemia. Response in aldosterone secretion to the correction of hypovolemia seemed to be delayed, which was well described by an extra upstream turnover compartment, possibly representing chronic upregulation of aldosterone synthase (cytochrome P450 11B2). In conclusion, semimechanistic modeling provided novel physiological insights in hormonal water regulation in pediatric patients during DKA treatment, providing rationale to further evaluate the potential of monitoring copeptin, but not aldosterone due to its delayed response, for future optimization of rehydration treatment to reduce the risk of acute complications such as cerebral edema.

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