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. 2020 Sep 25;8(3):165-176.
doi: 10.2478/jtim-2020-0026. eCollection 2020 Sep.

Renal Function is a Major Determinant of ICU-acquired Hypernatremia: A Balance Study on Sodium Handling

Marjolein van IJzendoorn  1 , Linda de Vries  1 , Jacob van den Born  2 , Hanneke Buter  1 , Gerjan Navis  2 , Christiaan Boerma  1
Affiliations

Renal Function is a Major Determinant of ICU-acquired Hypernatremia: A Balance Study on Sodium Handling

Marjolein van IJzendoorn et al. J Transl Int Med. .

Abstract

Background and objectives: The development of ICU-acquired hypernatremia (IAH) is almost exclusively attributed to 'too much salt and too little water'. However, intrinsic mechanisms also have been suggested to play a role. To identify the determinants of IAH, we designed a prospective controlled study.

Methods: Patients with an anticipated length of stay ICU > 48 hours were included. Patients with hypernatremia on admission and/or on renal replacement therapy were excluded. Patients without IAH were compared with patients with borderline hypernatremia (≥ 143 mmol/L, IAH 143) and more severe hypernatremia (≥ 145 mmol/L, IAH 145).

Results: We included 89 patients, of which 51% developed IAH 143 and 29% IAH 145. Sodium intake was high in all patients. Fluid balances were slightly positive and comparable between the groups. Patients with IAH 145 were more severely ill on admission, and during admission, their sodium intake, cumulative sodium balances, serum creatinine and copeptin levels were higher. According to the free water clearance, all the patients conserved water. On multivariate analysis, the baseline serum creatinine was an independent risk factor for the development of IAH 143 and IAH 145. Also, the copeptin levels remained significant for IAH 143 and IAH 145. Sodium intake remained only significant for patients with IAH 145.

Conclusions: Our data support the hypothesis that IAH is due to the combination of higher sodium intake and a urinary concentration deficit, as a manifestation of the renal impairment elicited by severe illness.

Keywords: ICU-patients; balance study; critically ill; electrolytes; hypernatremia; sodium handling.

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Conflict of interest statement

Conflict of Interest None of the authors have a conflict of interest.

Figures

Figure 1
Figure 1
Inclusion flowchart. LOS: length of stay; RRT: Renal replacement therapy.
Figure 2
Figure 2
Course of mean serum sodium concentration in mmol/L. White box: no IAH; Dark grey box: IAH 143; Light gray box: IAH 145; Green dots: no IAH; Yellow dots: IAH 143; Red dots: IAH 145; IAH: ICU-acquired hypernatremia.
Figure 3
Figure 3
Cumulative sodium intake over time in mmol/L. White box: no IAH; Dark grey box: IAH 143; Light gray box: IAH 145; Green dots: no IAH; Yellow dots: IAH 143; Red dots: IAH 145; IAH: ICU-acquired hypernatremia. *P < 0.05, **P < 0.01.
Figure 4
Figure 4
Cumulative renal sodium excretion (A), sodium balance (B) and serum creatinine concentration (C) over time. White box: no IAH; Dark grey box: IAH 143; Light gray box: IAH 145; Green dots: no IAH; Yellow dots: IAH 143; Red dots: IAH 145; IAH: ICU-acquired hypernatremia. *P < 0.05, **P < 0.01.
Figure 5
Figure 5
Correlation between decrease in serum creatinine and increase in urine sodium excretion.
Figure 6
Figure 6
Serum sodium, serum copeptin and urine osmolality over time. Green: serum sodium concentration; Red: serum copeptin concentration; Purple: urine osmolality. ● = patients without IAH; □ = patients with IAH 143; = patients with IAH 145.
Figure 7
Figure 7
Fluid intake (A), diuresis (B), fluid balance (C) and body weight in kg (D) over time. White box: no IAH; Dark grey box: IAH 143; Light gray box: IAH 145; Green dots: no IAH; Yellow dots: IAH 143; Red dots: IAH 145; IAH: ICU-acquired hypernatremia; * P < 0.05.
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