Affiliations: University of Ferrara, Ferrara, Italy
General Hospital of Rovigo, Rovigo, Italy,
*Erasme University Hospital, Brussels, Belgium
Correspondence to: Annalisa Cogo, MD, Department of Clinical and Experimental Medicine, Section of Respiratory Diseases, University Via Savonarola 9, 44100 Ferrara, Italy; e-mail: firstname.lastname@example.org
We read with great interest the article by Abid et al (December 2001),1demonstrating the predictive value of microalbuminuria in the identification of more severe ICU patients. Microalbuminuria is reported to be an early feature of acute inflammatory conditions due to the rapid increase in renal permeability induced by inflammatory mediators and oxygen free radicals. In our opinion, hypoxemia also could play a role on capillary endothelial permeability as shown by much research, both in vivo and in vitro. In fact, studies at high altitude2 suggest that systemic hypoxemia may cause a generalized increase in capillary permeability, while in vitro studies have shown that cultured endothelial cells exposed to low oxygen concentrations4 become larger, and small intercellular gaps appear. These phenomena are reversible.
We therefore aimed to investigate the presence and degree of proteinuria in a group of patients with chronic lung diseases with or without respiratory failure by retrospectively examining the clinical records of all patients with chronic lung diseases admitted to our department (January 1998 to January 1999) due to a worsening of their respiratory conditions. Data from 177 patients were examined. Seventy-five patients were excluded due to the presence of other factors potentially inducing proteinuria (acidosis, renal failure, infections, systemic hypertension, diabetes, hypokalemia). Data from 102 patients (65 male and 37 female) are reported (Table 1
). A significant correlation was found between urinary proteins and Pao2 (p < 0.01). When the patients were classified into two groups, normoxemic and hypoxemic, using the value of 60 mm Hg (8 kPa) of Pao2 as cut-off, we didn’t find any significant difference, except for the degree of proteinuria.
Patients with respiratory failure seem to have a significantly increased proteinuria as compared to a similar group of patients without respiratory failure. As serum levels of proteins were similar in the two groups, we suppose that the observed proteinuria is an acute phenomenon, yet prolonged hypoxemia could lead to a reduction in serum total proteins that could contribute to a poor outcome.5 Monitoring urinary and serum levels of proteins should therefore be recommended in all patients with respiratory failure.
Data expressed as mean ± SE. NS = not significant.
We appreciate the comments by Dr. Cogo and colleagues, raising the hypothesis that hypoxemia in itself could play a role in the development of hypoalbuminemia. However, as in many areas of medicine, is this a cause-effect relationship or simply an association, ie, the inflammatory response is responsible for permeability alterations in the kidney (resulting in hypoalbuminuria) and in the lung (resulting in hypoxemia)?
Moreover, some of our patients required a high fraction of inspired oxygen (sometimes in addition to positive end-expiratory pressure), but we never allow hypoxemia (Pao2 < 60 mm Hg) to persist in critically ill patients. Hence, we do not believe a low Pao2, by itself, could have contributed to our findings.
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