Efficacy and Tolerance of Urea Compared with Vaptans for Long-Term Treatment of Patients with SIADH

Soupart, Alain; Coffernils, Michel; Couturier, Bruno; Gankam-Kengne, Fabrice; Decaux, Guy

doi:10.2215/cjn.06990711

Cited by 130 publications

(63 citation statements)

References 48 publications

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“…We found several case series demonstrating an increase in serum sodium concentration after 2-7 days for urea (202,203,204,205,206), demeclocycline (207), loop diuretics in combination with oral NaCl (123,125,208), phenytoin (209) and fluid restriction (210). We also identified case series of patients experiencing an increase in serum sodium over a longer time period of up to 12 months for urea (211,212,213), up to 3 weeks for demeclocycline (214,215,216,217,218,219), up to 20 weeks for lithium (220), up to 150 days for furosemide with oral NaCl (221) and up to 30 days in phenytoin (220).…”

Section: Rationale † Why This Question?mentioning

confidence: 89%

Clinical practice guideline on diagnosis and treatment of hyponatraemia

Spasovski

Vanholder

Allolio

et al. 2014

European Journal of Endocrinology

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627

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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: Rationale † Why This Question?mentioning

confidence: 89%

Clinical practice guideline on diagnosis and treatment of hyponatraemia

Spasovski

Vanholder

Allolio

et al. 2014

European Journal of Endocrinology

Self Cite

627

671

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“…It does so by inducing a solute (urea) diuresis that, by increasing urine flow rate, decreases the concentration of sodium and potassium in the urine and hence increases excretion of electrolyte-free water (22). Although a recent study by Soupart and colleagues in 13 patients with SIADH found that urea was as effective in raising serum sodium levels and was as well tolerated as the vasopressin antagonist tolvaptan (23), in my experience and in informal surveys of practicing nephrologists in North America, urea is not widely used in North America, primarily because of limited availability. There is no US Pharmacopeia-approved formulation, and it is not available at most pharmacies.…”

Section: Ureamentioning

confidence: 99%

An Elderly Patient with Chronic Hyponatremia

Berl

2013

Clinical Journal of the American Society of Nephrology

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SummaryHyponatremia is the most common electrolyte disorder. With the aging of the population and the greater propensity of the elderly to develop hyponatremia, this electrolyte disorder is of increasing importance to the practicing nephrologist. In this Attending Rounds, an illustrative patient with hyponatremia is presented. The reasons for the increased incidence and prevalence of hyponatremia in the elderly are discussed, with emphasis on the effects of aging on urinary dilution, the frequently multifactorial nature of hyponatremia in this population, and the absence of a definite cause for inappropriate and persistent vasopressin release in many such patients. The rationale for treating the hyponatremia, even when apparently asymptomatic, is discussed, with attention to cognitive function, gait, and bone structure disturbances that increase the risk for fractures. The various available treatment approaches, including water restriction, demeclocycline, loop diuretics with NaCl supplementation, urea, and vasopressin antagonists are summarized, with emphasis on the efficacy and limitations of each of these therapies.Clin J Am Soc Nephrol 8: 469-475, 2013469-475, . doi: 10.2215 Case Description L.G. is a 73-year-old woman referred for management of chronic hyponatremia. She was known to have had hyponatremia for several years, with serum sodium levels in the range of 121-127 mEq/L. She has had four pulmonary bacterial infections during the last 7 years and was found to have radiologic evidence of bronchiectasis. She has also had several episodes of transient cerebral ischemia leading to numbness and weakness. In the last year she has had increased gait instability and sustained a fall that resulted in a pelvic fracture. She had no history of cardiac or liver disease. She has long-standing rheumatoid arthritis. Medications included omeprazole, 20 mg daily; conjugated estrogens (Premarin), 0.3 mg daily; folic acid, 0.4 mg three times daily; aspirin, 81 mg daily; and monthly vitamin B 12 injections. On physical examination she appeared to be a fragile elderly woman in no acute distress. BP was 148/78 mmHg, pulse rate was 98 beats/min, and she weighed 65 kg. She appeared to be euvolemic by examination. There were deformities of the proximal interphalangeal joints. Her neurologic examination revealed that she was fully oriented, with no focal findings, but she had an obvious gait disturbance that necessitated a walker for ambulation. Laboratory results were as follows: serum sodium, 124 mEq/L; chloride, 95 mEq/L; potassium, 4.1 mEq/L; bicarbonate, 22 mEq/L; creatinine, 0.7 mg/dl; glucose, 66 mg/dl; and uric acid, 3.8 mg/dl. Urinary sodium concentration was 75 mEq/L with a urine osmolality of 382 mOsm/kg. Result of a cosyntropin stimulation test was normal, with a baseline cortisol level of 9.2 mg/dl and a stimulated level of 18.7 mg/dl. Thyroid-stimulating hormone was normal at 3.29 mIU/L. Magnetic resonance imaging of the brain and pituitary revealed no significant abnormalities. DiscussionGiven the absence of liv...

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“…Urea powder may be obtained from the pharmacy. This modality is very cost effective and has been used to correct hyponatremia in SIADH slowly, by 2-3 mmol/liter/day, a rate comparable to the effect of water restriction [Decaux, 2001;Soupart and Decaux, 2009]. An easy procedure is to dissolve 15-30 g of urea in a glass of orange juice and to administer two or three glasses a day after meals.…”

Section: Treatment Of Siadh Using General and Indirect Meansmentioning

confidence: 99%

Clinical management of SIADH

Groß¹

2012

Therapeutic Advances in Endocrinology

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Hyponatremia is the most frequent electrolyte disorder and the syndrome of inappropriate antidiuretic hormone secretion (SIADH) accounts for approximately one-third of all cases. In the diagnosis of SIADH it is important to ascertain the euvolemic state of extracellular fluid volume, both clinically and by laboratory measurements. SIADH should be treated to cure symptoms. While this is undisputed in the presence of grave or advanced symptoms, the clinical role and the indications for treatment in the presence of mild to moderate symptoms are currently unclear. Therapeutic modalities include nonspecific measures and means (fluid restriction, hypertonic saline, urea, demeclocycline), with fluid restriction and hypertonic saline commonly used. Recently vasopressin receptor antagonists, called vaptans, have been introduced as specific and direct therapy of SIADH. Although clinical experience with vaptans is limited at this time, they appear advantageous to patients because there is no need for fluid restriction and the correction of hyponatremia can be achieved comfortably and within a short time. Vaptans also appear to be beneficial for physicians and staff because of their efficiency and reliability. The side effects are thirst, polydipsia and frequency of urination. In any therapy of chronic SIADH it is important to limit the daily increase of serum sodium to less than 8-10 mmol/liter because higher correction rates have been associated with osmotic demyelination. In the case of vaptan treatment, the first 24 h are critical for prevention of an overly rapid correction of hyponatremia and the serum sodium should be measured after 0, 6, 24 and 48 h of treatment. Discontinuation of any vaptan therapy for longer than 5 or 6 days should be monitored to prevent hyponatremic relapse. It may be necessary to taper the vaptan dose or restrict fluid intake or both.

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Efficacy and Tolerance of Urea Compared with Vaptans for Long-Term Treatment of Patients with SIADH

Cited by 130 publications

References 48 publications

Clinical practice guideline on diagnosis and treatment of hyponatraemia

Clinical practice guideline on diagnosis and treatment of hyponatraemia

An Elderly Patient with Chronic Hyponatremia

Clinical management of SIADH

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