AI Article Synopsis
- Thiazide-associated hyponatremia (TAH) is a significant side effect of thiazide diuretics, leading to lower sodium levels and distinct symptom profiles among patients.
- A retrospective study compared patients on thiazides to those not on thiazides, revealing significant differences in various biochemical markers and demographic factors.
- The findings indicate that thiazide use can result in more severe hyponatremia and volume depletion, although there was no increase in in-hospital mortality rates among affected patients.
Article Abstract
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.
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| http://dx.doi.org/10.1080/00325481.2022.2063634 | DOI Listing |
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