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Revista Brasileira de Terapia Intensiva

Print version ISSN 0103-507X

Rev. bras. ter. intensiva vol.25 no.3 São Paulo July/Sept. 2013

https://doi.org/10.5935/0103-507X.20130032 

EDITORIAL

Urine assessment in the critically ill: a matter of both quantity and quality

Alexandre Toledo Maciel1 

Marcelo Park2 

1Intensimed Research Group, Intensive Care Unit, Hospital São Camilo Pompéia - São Paulo (SP), Brazil.

2Intensive Care Unit, Department of Medical Emergencies, Hospital das Clínicas, Universidade de São Paulo - USP - São Paulo (SP), Brazil.


In this issue of Revista Brasileira de Terapia Intensiva, Masevicius et al.( 1 ) reported on the behavior of the plasma chloride concentration ([Cl-]plasma) of 148 consecutive postoperative patients in the first 24 hours after their intensive care unit (ICU) admission. The authors' major finding was that, at the end of the first day in the ICU, the [Cl-]plasmawas primarily dependent upon the [Cl-]plasma on ICU admission and on the urinary strong ion difference ([SID]urine), also called the urinary anion gap. There were 3 patient groups: (1) increased, (2) decreased or (3) unaltered [Cl-]plasma during the 24 hours period. The increased [Cl-]plasma group had the lower [Cl-]plasma on ICU admission and the higher strong ion gap (SIG), i.e., the higher concentration of unmeasured anions. The opposite was observed in this same group after 24 hours: the higher [Cl-]plasma and the lower SIG. The volume of infused fluids and the SID of these fluids (only crystalloids) on the first ICU day were similar between groups, which led the authors to conclude that the fluids received during this period were not responsible for the distinct between-group [Cl-]plasma behaviors.

These results must be carefully interpreted. First, it is intuitive that the [Cl-]plasma on ICU admission is a determinant of the [Cl-]plasma after 24 hours because the latter greatly depends on the former (which was different between groups) and the amount of [Cl-] received during this 24 hours period (which was similar between groups). Normal saline, which has a high [Cl-] content (154mEq/L, well above the initial [Cl-]plasma in the 3 groups), was the primary fluid used; therefore, a decreased or even an unchanged [Cl-]plasma would not be expected. On the contrary, an increase in the [Cl-]plasma would be expected in all groups, particularly in the group with the lower initial [Cl-]plasma. At this point, the [SID]urine and the total urine volume play crucial roles. Because the kidneys are the major organs responsible for the SID regulation in plasma, it is expected that both the urine volume and [SID]urine are determinants of the final [Cl-]plasma. Diuresis volume in the 24 hours period was similar between groups, which directed our attention to the [SID]urine. The urine is the main fluid by which we excrete [Cl-]. Urinary [Cl-] excretion is of paramount relevance in acid-base equilibrium because it is usually the anion that follows ammonium (NH4 +) excretion, the main form of acid excretion by the organism. In the Masevicius et al. study,( 1 ) the increased [Cl-]plasma group had the higher [SID]urine, suggesting less capacity to excrete [Cl-] and manage saline-induced hyperchloremia. This finding could be an indirect sign of renal impairment,( 2 - 4 ) although in the present study, few patients met an AKIN( 5 ) stage 1 criterion for acute kidney injury (AKI), and the incidence of AKI was similar between groups.

Another between-group difference was the SIG value upon ICU admission. It is difficult to explain the reasons why SIG had distinct values based solely on the information provided by the authors. In addition, in terms of prognosis and therapeutic management of critically ill patients, the SIG utility remains to be determined. The opposite behaviors of [Cl-] and unmeasured anions (one increases, the other decreases and vice-versa) may be a physiological phenomenon, which has been suggested as an explanation for hypochloremia in untreated diabetic ketoacidosis( 6 ) or for an increased SIG in the presence of hypoalbuminemia.( 7 ) However, it may just be a mathematical coupling because until now, the SIG has been a calculated variable and not a directly measured variable. The fact that the increased [Cl-]plasma group had the higher SIG upon admission may also influence our interpretation of [SID]urine in the present study. In the presence of a predominantly SIG acidosis, it is possible that unmeasured anions, not [Cl-], follow urinary NH4 + excretion, which results in less [Cl-] excretion and higher [SID]urine values.

In conclusion, this important paper by Masevicius et al.( 1 ) brings some uncertainty about how to interpret the data: [SID]urine determines the changes in plasma [Cl-] or initial [Cl-] and SIG determine [SID]urine? Anyway, one certainty this study brings: we must evaluate the electrolyte composition of urine for a full understanding of the acid-base equilibrium, and intensivists should perform this evaluation daily. The relevance of urine in the ICU extends well beyond its volume and flow.

REFERÊNCIAS

1. Masevicius FD, Vazquez AR, Enrico C, Dubin A. Urinary strong-ion difference is a major determinant of the changes in plasma chloride concentration in postoperative patients. Rev Bras Ter Intensiva. 2013;25(3):197-204. [ Links ]

2. Masevicius FD, Tuhay G, Pein MC, Ventrice E, Dubin A. Alterations in urinary strong ion difference in critically ill patients with metabolic acidosis: a prospective observational study. Crit Care Resusc. 2010;12(4):248-54. [ Links ]

3. Maciel AT, Park M, Macedo E. Urinary electrolyte monitoring in critically ill patients: a preliminary observational study. Rev Bras Ter Intensiva. 2012;24(3):236-45. [ Links ]

4. Moviat M, Terpstra AM, van der Hoeven JG, Pickkers P. Impaired renal function is associated with greater urinary strong ion differences in critically ill patients with metabolic acidosis. J Crit Care. 2012;27(3):255-60. [ Links ]

5. Mehta RL, Kellum JA, Shah SV, Molitoris BA, Ronco C, Warnock DG, Levin A; Acute Kidney Injury Network. Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury. Crit Care. 2007;11(2):R31. [ Links ]

6. Funk GC, Zauner C, Bauer E, Oschatz E, Schneeweiss B. Compensatory hypochloraemic alkalosis in diabetic ketoacidosis. Diabetologia. 2003;46(6):871-3. [ Links ]

7. Gómez JL, Gunnerson KJ, Song M, Li J, Kellum JA. Effects of hypercapnia on BP in hypoalbuminemic and Nagase analbuminemic rats. Chest. 2007;131(5):1295-300. [ Links ]

Corresponding author: Alexandre Toledo Maciel Hospital São Camilo Unidade de Terapia Intensiva - 4º andar Avenida Pompéia, 1.178 Zip code: 05024-000 - São Paulo (SP), Brazil E-mail: alexandre.toledo@intensimed.com

Conflicts of interest: None.

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