Thiazide-associated hyponatremia in internal medicine patients: analysis of epidemiological and biochemical profiles.

OBJECTIVES: Thiazide-associated hyponatremia (TAH) is a clinically important side effect of the therapy with thiazide and thiazide-like diuretics. This study aims to analyze epidemiological, biochemical, and symptomatological profiles (including volume status) of patients admitted with TAH. METHODS: A retrospective hospital record study was performed. Epidemiological and biochemical parameters and symptoms were compared between the thiazide (n = 143) and non-thiazide (n = 282) groups. Patients in the thiazide group were classified as hypo-, normo-, or hypervolemic. Furthermore, the comparison of epidemiological, biochemical, partially pharmacotherapeutical, and symptomatological parameters between the hypovolemic and normovolemic TAH groups was performed. RESULTS: The thiazide group showed lower s-Na (p = 0.008), s-K (p < 0.001), s-Cl (p < 0.001), measured s-osmolality (p = 0.021), and eGFR (p < 0.001); higher s-urea (p < 0.001), s-creatinine (p = 0.023), s-glucose (p < 0.001), u-osmolality (p = 0.012), u-Na (p < 0.001), u-K (p = 0.023), and u-Cl (p < 0.001). Patients using thiazide were older (p < 0.001), more likely to be female (p = 0.011), and with symptoms corresponding more to chronic hyponatremia. Compared to the normovolemic group (n = 93; 65%), the hypovolemic patients (n = 47; 32.9%) showed higher s-urea (p = 0.005), s-creatinine (p = 0.045), and s-UA (p = 0.010); lower eGFR (p = 0.032), u-Na (p = 0.015), u-Cl (p = 0.016), anorexia (p < 0.001), and a higher frequency of furosemide use (p < 0.001). CONCLUSIONS: Thiazide use is a crucial etiological cause of hypotonic hyponatremia among internal medicine inpatients, associated with more severe hyponatremia, but with no difference in the in-hospital mortality. Even in hypo-osmolar conditions of TAH, 32.9% of patients exhibited signs of volume depletion. FE-UA did not differ between the hypovolemic and the normovolemic patients in TAH conditions. Anorexia and the combination of thiazide together with furosemide, rather than thiazide use alone, were risk factors for hypovolemic hyponatremia without affecting FE-UA.

The role of angiotensin-converting enzyme 2 in the pathogenesis of COVID-19: the villain or the hero?

Angiotensin-converting enzyme 2 (ACE 2) is the entry receptor for the novel coronavirus SARS-CoV-2, the aetiological agent of COVID-19. At the same time, ACE 2 expression decreases during COVID-19. Two seemingly contradictory relationships between the expression of ACE 2 and COVID-19 have been reported. Increased level of expression of ACE 2 may be a risk factor for the development of COVID-19 infection, while reduced ACE 2 expression during COVID-19 leads to acute respiratory distress syndrome. This article provides a comprehensive overview of available scientific knowledge about the role of ACE 2 in the pathogenesis of COVID-19, which is available up to current day. Also, it discusses unknown factors that we will have to reveal in order to understand the whole role of ACE 2 in the pathogenesis of COVID-19.