Thiazide-Induced Hyponatremia

Friedman, Eitan; Shadel, Mordechai; Halkin, Hillel; Farfel, Zvi

doi:10.7326/0003-4819-110-1-24

Cited by 168 publications

(41 citation statements)

References 20 publications

(13 reference statements)

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“…The traditional explanation is that renal sodium loss leads to volume contraction with subsequent release of vasopressin. However, this would require a substantial loss of sodium and body weight, while patients with thiazide-induced hyponatraemia often have increased body weight (38). It might be reasonable to assume that thiazides directly induce the release of vasopressin or increase the response of the collecting duct to circulatory vasopressin.…”

Section: Renal Sodium Lossmentioning

confidence: 99%

“…It might be reasonable to assume that thiazides directly induce the release of vasopressin or increase the response of the collecting duct to circulatory vasopressin. In any case, there appears to be an individual susceptibility to these effects, as hyponatraemia only occurs in certain patients and usually reoccurs if thiazides are reintroduced (38). Despite the potential for causing more urinary sodium loss, loop diuretics only rarely cause hyponatraemia because they reduce osmolality in the renal medulla and thus limit the kidney's ability to concentrate urine (39).…”

Section: Renal Sodium Lossmentioning

confidence: 99%

“…The natriuresis induced by diuretics may cause 'appropriate' vasopressin release and subsequently hyponatraemia because of a decrease in circulating volume. Finally, diuretics may cause a SIAD-like state characterised by normal or mildly increased extracellular fluid volume (38,111). Urine sodium concentration can also be low in patients with heart failure or liver cirrhosis, due to reduced effective circulating arterial volume, even when they are taking diuretics (diuretic resistance) (112) (Appendix 6.…”

Section: Diagnostic Difficulty With Diureticsmentioning

confidence: 99%

See 2 more Smart Citations

Clinical practice guideline on diagnosis and treatment of hyponatraemia

Spasovski

Vanholder

Allolio

et al. 2014

European Journal of Endocrinology

612

671

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Hyponatraemia, defined as a serum sodium concentration !135 mmol/l, is the most common disorder of body fluid and electrolyte balance encountered in clinical practice. It can lead to a wide spectrum of clinical symptoms, from subtle to severe or even life threatening, and is associated with increased mortality, morbidity and length of hospital stay in patients presenting with a range of conditions. Despite this, the management of patients remains problematic. The prevalence of hyponatraemia in widely different conditions and the fact that hyponatraemia is managed by clinicians with a broad variety of backgrounds have fostered diverse institution-and speciality-based approaches to diagnosis and treatment. To obtain a common and holistic view, the European Society of Intensive Care Medicine (ESICM), the European Society of Endocrinology (ESE) and the European Renal Association -European Dialysis and Transplant Association (ERA-EDTA), represented by European Renal Best Practice (ERBP), have developed the Clinical Practice Guideline on the diagnostic approach and treatment of hyponatraemia as a joint venture of three societies representing specialists with a natural interest in hyponatraemia. In addition to a rigorous approach to methodology and evaluation, we were keen to ensure that the document focused on patient-important outcomes and included utility for clinicians involved in everyday practice.

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Section: Renal Sodium Lossmentioning

confidence: 99%

Section: Renal Sodium Lossmentioning

confidence: 99%

Section: Diagnostic Difficulty With Diureticsmentioning

confidence: 99%

See 1 more Smart Citation

Clinical practice guideline on diagnosis and treatment of hyponatraemia

Spasovski

Vanholder

Allolio

et al. 2014

European Journal of Endocrinology

612

671

View full text Add to dashboard Cite

show abstract

“…Additional factors that predispose to hyponatremia are chronic natriuresis and bodily potassium deficit. Older women are known to be at higher risk of thiazide-induced hyponatremia [18]and to have a tendency to increased water intake [19]. …”

Section: Discussionmentioning

confidence: 99%

Hyponatremia-Associated Rhabdomyolysis

Trimarchi

González

Olivero

1999

Nephron

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Background: Hyponatremia is the most frequent electrolyte disorder. However, hyponatremia rarely results from excessive water intake, unless the kidney is unable to excrete free water, such as in patients on thiazide diuretics; in addition, hyponatremia is an uncommon cause of rhabdomyolysis. Methods: We present a 51-year-old hypertensive woman on chronic hydrochlorothiazide therapy who developed acute water intoxication and severe myalgias. Results: The patient developed acute hypotonic hyponatremia and subsequent rhabdomyolysis. We discuss the mechanisms responsible for the development of hyponatremia and its association with rhabdomyolysis. Conclusion: Muscle enzymes should be monitored in patients with acute hyponatremia who develop muscle pain, and hyponatremia-induced rhabdomyolysis must be considered in patients with myalgias receiving thiazide diuretics.

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“…Risk factors for thiazide-induced hyponatremia are age (although not a risk factor according to Sonnenblick et al [44]), gender, hypokalemia, and a low lean body mass, while the concomitant use of loop diuretics, angiotensin-converting enzyme inhibitors, or non-steroidal anti-inflammatory drugs were not identified as risk factors [44, 45]. Interestingly, Friedman et al [46] showed that a single dose of a thiazide diuretic may predict the development of hyponatremia because it produced a 5.5-mmol/l fall in serum sodium associated with weight gain in patients with thiazide-induced hyponatremia compared to a 1.2- and 1.8-mmol/l fall in serum sodium and weight loss in healthy controls or elderly hypertensive patients.…”

Section: The Hyponatremias: Overview Of Hyponatremic Disordersmentioning

confidence: 99%

Hyponatremia Revisited: Translating Physiology to Practice

Hoorn

Zietse²

2008

Nephron Physiol

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The complexity of hyponatremia as a clinical problem is likely caused by the opposite scenarios that accompany this electrolyte disorder regarding pathophysiology (depletional versus dilutional hyponatremia, high versus low vasopressin levels) and therapy (rapid correction to treat cerebral edema versus slow correction to prevent osmotic demyelination, fluid restriction versus fluid resuscitation). For a balanced differentiation between these opposites, an understanding of the pathophysiology of hyponatremia is required. Therefore, in this review an attempt is made to translate the physiology of water balance regulation to strategies that improve the clinical management of hyponatremia. A physiology-based approach to the patient with hyponatremia is presented, first addressing the possibility of acute hyponatremia, and then asking if and if so why vasopressin is secreted non-osmotically. Additional diagnostic recommendations are not to rely too heavily of the assessment of the extracellular fluid volume, to regard the syndrome of inappropriate antidiuresis as a diagnosis of exclusion, and to rationally investigate the pathophysiology of hyponatremia rather than to rely on isolated laboratory values with arbitrary cutoff values. The features of the major hyponatremic disorders are discussed, including diuretic-induced hyponatremia, adrenal and pituitary insufficiency, the syndrome of inappropriate antidiuresis, cerebral salt wasting, and exercise-associated hyponatremia. The treatment of hyponatremia is reviewed from simple saline solutions to the recently introduced vasopressin receptor antagonists, including their promises and limitations. Given the persistently high rates of hospital-acquired hyponatremia, the importance of improving the management of hyponatremia seems both necessary and achievable.

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Thiazide-Induced Hyponatremia

Abstract: Use of a single-dose of a thiazide diuretic may predict the development of hyponatremia. Increased body weight apparently due to polydipsia may play a major role in the pathogenesis of thiazide-induced hyponatremia.

Cited by 168 publications

References 20 publications

Clinical practice guideline on diagnosis and treatment of hyponatraemia

Clinical practice guideline on diagnosis and treatment of hyponatraemia

Hyponatremia-Associated Rhabdomyolysis

Hyponatremia Revisited: Translating Physiology to Practice

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