Elevated Antidiuretic Hormone Does Not Cause Hyponatremia in Legionnaires' Disease

In patients with Legionnaires’ disease, the prevalence of antidiuretic hormones (ADH) is not associated with hyponatremia, according to research published online in BMC Infectious Disease.

Philipp Schuetz and colleagues from the Medical University Clinic in Switzerland observed data on 873 patients with confirmed community-acquired pneumonia (CAP), 27 of whom tested positive for Legionella pneumophila. Upon hospital admission, all of the patients’ sodium levels were measured via urine samples and subsequent blood samples were received to detect the presence of the ADH known as CT-ProVasopressin.

To absolutely verify whether the subjects had Legionnaires’ disease, the study authors also performed a combination of clinical diagnoses and X-ray examinations, though some patients also underwent blood bacterial culture and polymerase chain reaction (PCR) testing as a supplementary measure.

Although the investigators discovered a link between Legionnaires’ disease and hyponatremia, they denied that ADH was the cause.

“When comparing CT-ProVasopressin levels with sodium levels, we found no negative correlation in patients with Legionnaires’ disease,” they explained. “In contrast, ADH precursors showed a positive correlation with sodium levels, arguing against this hypothesis” that elevated ADH levels are the causal pathway to hyponatremia.

Ironically, among patients with CAPs unrelated to Legionnaires’ disease, there was “a slight positive correlation of CT-ProVasopressin and sodium levels without reaching statistical significance.”

“ADH was unregulated in response to the stress of severe infection, which seemed to have overruled the osmoregulatory stimulus,” the researchers said. They asserted that other factors unrelated to ADH could result in sodium loss for people with Legionnaires’ disease, including “direct renal effects of cytokines or toxins, as well as natriuretic hormones.”

In light of the findings and the importance of rectifying low sodium levels, the researchers recommended “free water restriction should not be pursued in this patient population, but rather replacement of salt losses by hydration and salt repletion.”