Why does pneumonia cause siadh

She is febrile Physical examination suggests euvolemia. The association of hyponatremia with respiratory illness has been recognized for more than 70 years.

The underlying nature of these associations, however, remains obscure. The mechanism of hyponatremia in pneumonia is incompletely understood. Her vital signs have normalized and she is now saturating well on ambient air. She remains euvolemic. A trial of increased dietary salt is offered, but she refuses, stating that her primary care physician has advised her for years to avoid salt due to her blood pressure.

At this point, the nephrology service is consulted for consideration of a vasopressin receptor antagonist. Download citation. Published : 20 March Anyone you share the following link with will be able to read this content:.

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View Metrics. Citing articles via Google Scholar. Email alerts Article Activity Alert. Latest Issue Alert. News Latest News Archive. Close Modal. This site uses cookies. Based on our analysis, we believe that in severe disease the stress response per se is the dominant stimulus for the upregulation of ADH, and overrules the osmotic stimulation. Still, as evidenced by the positive correlation between sodium levels and ADH-precursors, the physiological osmoregulatory stimulus to ADH secretions seems to be intact in this patient population.

First, studies have shown direct effects of cytokines on the kidney leading to renal salt loss [ 49 — 51 ]. Haines et al. Also, other natriuretic hormones may be important in this regard. Different studies have reported increased levels of atrial natriuretic peptide ANP , as well as B-type-natriuretic peptide BNP in patients with pneumonia [ 52 — 54 ].

These hormones may contribute to low sodium levels via increased natriuresis. The strengths of our study are the systematic assessment of sodium and CT-ProVasopressin in a large prospective study of patients with CAP of different etiologies.

Yet, this study also has limitations. First, we did not measure mature ADH directly. However, clinical evidence suggests that CT-ProVasopressin is a good surrogate for ADH, and may thus be used instead in clinical routine [ 55 ].

Second, we were not able to assess sodium and osmolarity measurements in urine limiting our model to the measurement of CT-ProVasopressin and correlating blood sodium levels. Our observations were rather on the population level and not on a patient level [ 16 , 37 , 56 ]. Last, there may have been unmeasured confounders in our study population such as the use of diuretics and aldosterone antagonist, which were not recorded.

Rather, ADH was upregulated in response to the stress of severe infection, which seemed to have overruled the osmoregulatory stimulus. As a consequence, free water restriction should not be pursued in this patient population, but rather replacement of salt losses by hydration and salt repletion.

Cunha BA: The clinical diagnosis of Legionnaires' disease: the diagnostic value of combining non-specific laboratory tests.

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