Study on the Etiology of the Syndrome of Inappropriate Antidiuretic Hormone (SIADH) Among the Hospital Admitted Patient (original) (raw)
Related papers
Clinical kidney journal, 2013
Despite being the most common electrolyte disturbance encountered in clinical practice, the diagnosis and treatment of hyponatremia (defined as a serum sodium concentration <135 mmol/L) remains far from optimal. This is extremely troubling because not only is hyponatremia associated with increased morbidity, length of hospital stay and hospital resource use, but it has also been shown to be associated with increased mortality. The reasons for this poor management may partly lie in the heterogeneous nature of the disorder; hyponatremia presents with a variety of possible etiologies, differing symptomology and fluid volume status, thereby making its diagnosis potentially complex. In addition, a general lack of awareness of the clinical impact of the disorder, a fear of adverse outcomes through overcorrection of sodium levels, and a lack of effective targeted treatments until recent years, may all have contributed to a reticence to actively treat cases of hyponatremia. There is ther...
Diagnosing and Treating the Syndrome of Inappropriate Antidiuretic Hormone Secretion
The American journal of medicine, 2015
The syndrome of inappropriate antidiuretic hormone secretion (SIADH) is the most common cause of hyponatremia in clinical practice, but current management of hyponatremia and outcomes in patients with SIADH are not well understood. The objective of the Hyponatremia Registry was to assess the current state of management of hyponatremia due to SIADH in diverse hospital settings, specifically: which diagnostic and treatment modalities are currently employed and how rapidly and reliably they result in an increase in serum [Na(+)]. A secondary objective was to determine whether treatment choices and outcomes differ across the United States (US) and the European Union (EU). The HN Registry recorded selected diagnostic measures and utilization, efficacy, and outcomes of therapy for euvolemic HN diagnosed clinically as SIADH in 1,524 adult patients with serum sodium concentration ([Na(+)]) ≤130 mEq/L (1,034 from 146 US and 490 from 79 EU sites). A subgroup of patients with more rigorously d...
Clinical Laboratory Evaluation of the Syndrome of Inappropriate Secretion of Antidiuretic Hormone
Clinical Journal of the American Society of Nephrology, 2008
Hyponatremia secondary to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is a frequent cause of hypotonicity. Although the differential diagnosis with other causes of hypotonicity such as salt depletion is sometimes challenging, some simple and readily available biologic parameters can be helpful in the diagnosis of SIADH. In SIADH, urea is typically low; this is less specific for elderly patients, for whom lower clearance of urea accounts for higher values. Low levels of uric acid are more often seen in SIADH (70%) compared with salt-depleted patients (40%). Typically, patients with SIADH will show a lower anion gap with nearly normal total CO 2 and serum potassium, this despite dilution. In patients with hyponatremia secondary to hypocorticism, total CO 2 is usually lower than in nonendocrine SIADH despite low urea and uric acid levels. Urine biology can also be helpful in diagnosis of SIADH because patients with SIADH have high urine sodium (Na; >30 mEq/L), and most of them will have a high fractional excretion of Na (>0.5% in 70% of cases), reflecting salt intake. Conversely, low urine Na in patients with SIADH and poor alimentation is not rare. Finally, measurement of urine osmolality is useful for the diagnosis of polydipsia and reset osmostat and could further help in the choice of therapeutic strategy because patients with low urine osmolality will benefit from water restriction or urea, whereas those with high urine osmolality (>600 mOsm/kg) would be good candidates for V 2 antagonist.
American Journal of Kidney Diseases, 2000
The high fractional excretion (FE) of uric acid observed in hyponatremia associated with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is commonly attributed to the volume-expanded state, although volume expansion in normonatremic volunteers is unable to increase urate clearance to a degree similar to that in SIADH. The goal of the present study is to analyze whether hyponatremia by itself could influence the FE of uric acid, as well as the effects of intravascular volume and glomerular filtration rate on FE of uric acid in SIADH. This study examines the effects of a 2-L infusion of isotonic saline over 24 hours on FE of uric acid in 9 normonatremic volunteers and 17 hyponatremic patients with SIADH. We also studied the FE of uric acid in 6 patients with SIADH with only mild water retention and the urate and creatinine clearances in 18 hyponatremic patients with SIADH before and after normalization of serum sodium levels by water restriction. When infusing 2 L of isotonic saline over 24 hours in healthy subjects, there was a decrease in plasma protein concentration of 8%, suggesting a similar degree of volume expansion than in patients with SIADH. The FE of uric acid did not increase to the same extent (9% ؎ 1.5% versus 17% ؎ 1.5%; P < 0.01). Conversely, in 6 hyponatremic patients with mild water retention (1 L), the FE of uric acid was still high despite indirect signs of only a small increase in plasma volume. The mainstay of these observations is that chronicity of hyponatremia by itself could affect urate excretion. We also observed that in the patients with SIADH, high FE of uric acid inversely correlated with glomerular filtration rate (r ؍ -0.66; P < 0.01) only during the hyponatremic state. These data suggest that hyponatremia by itself, combined with mild volume expansion and glomerular filtration rate, has a role in the high FE of uric acid in the SIADH.
Risks of inappropriate secretion of antidiuretic hormone in multiple system atrophy
Movement disorders : official journal of the Movement Disorder Society, 2011
Multiple system atrophy (MSA) affects the hypothalamus, similar to other neurological diseases. 1 Hypothalamic cells synthesize antidiuretic hormone (ADH), which increases water reuptake in the kidney. Hypothalamic disturbances can lead to the syndrome of inappropriate antidiuretic hormone secretion (SIADH) and resultant hyponatremia. ADH levels usually increase in SIADH. However, normal ADH levels are occasionally seen, but they are inappropriate in the presence of abnormally decreased osmolarity (<280 mOsm/kg), a condition thought to suppress physiological ADH secretion. 2 To date, 6 patients with MSA had SIADH (Table 1). 3 We describe the first MSA patient with extreme hyponatremia (99 mEq/L) and the highest reported ADH concentration. We also measured ADH in 14 severely disabled patients with MSA, but not symptomatic SIADH.
Cureus
Hyponatremia is one of the common electrolyte imbalances among hospitalized patients with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) being a common etiology for hyponatremia. There are multiple pathophysiologic considerations in the differential diagnosis of the etiologic factor for SIADH, including infections such as pneumonia and meningitis, as well as coronavirus disease 2019 (COVID-19) infection. However, SIADH, as the sole initial presentation of the infection of COVID-19, is rarely reported. In this report, we present a case of SIADH as the initial and only presentation of a COVID-19 infection, highlighting the clinical course and treatment strategy while providing the putative pathophysiologic insights into this unusual and potentially serious complication of COVID-19 infection.
Inappropriate antidiuretic hormone secretion of unknown origin
Kidney international, 1980
Case presentation This 52-year-old woman was first admitted to the New England Medical Center Hospital (NEMCH) for evaluation of hyponatremia. She was in good health until 6 weeks prior to admission when she began to experience fatigue, confusion, vomiting, and transient diarrhea. There was no history of fever, chills, weight loss, or anorexia, nor of cardiovascular, genitourinary, or central nervous system symptoms. Two weeks before admission, she consulted her own physician. Physical examination was not remarkable but laboratory studies disclosed: serum sodium 112 mEq, potassium 3.3 mEq, chloride 84 mEq, and bicarbonate 22 mEq per liter. Other laboratory values included: BUN 7 mg%, serum creatinine 0.9 mg%, serum uric acid 1.5 mg%, calcium 9.3 mg%, phosphorus 3.4 mg%, total protein 6.5 g%, albumin 4.4 g%, bilirubin 0.9 mg%, and alkaline phosphatase 31 IU; the SOOT, SGPT, and LDH were normal. Extensive evaluation by the referring physician disclosed normal chest x-ray, upper gastrointestinal series, oral cholecystogram, barium enema, intravenous pyelogram, skull series, brain scan, and liver-spleen scan. A bone scan revealed slight uptake in the mid-right cervical