Syndrome Of Hyponatremia Research Articles

Efficacy of Low-Dosage Tolvaptan for Treatment of Profound Hyponatremia in Syndrome of Inappropriate Antidiuresis: An Open-Label Randomized Controlled Trial

Efficacy of Low-Dosage Tolvaptan for Treatment of Profound Hyponatremia in Syndrome of Inappropriate Antidiuresis: An Open-Label Randomized Controlled Trial

Cerebral Salt-wasting Syndrome in a Critically Ill Patient: An Easily Neglected Syndrome in Intensive Care Unit (ICU)

BackgroundCerebral salt-wasting syndrome (CSWS), which usually secondary to cerebral diseases, is characterized by hyponatremia and hypovolemia. In clinical practice, it is quite difficult to distinguish CSWS from other hyponatremia syndrome, especially in Intensive Care Unit (ICU) where the conditions of patients are more complicated. Nonetheless, it is crucial because treatments might be fundamentally different. Case presentationWe discuss a case of patient who presented with refractory hyponatremia and hypovolemia after traumatic brain injury, finally was diagnosed with CSWS, and successfully treated with corticotropin. ConclusionsThis case report provides a unique opportunity to observe the trigger of subdural effusion-induced CSWS, and also it provides the classical therapy for CSWS in a critically ill patient. In view of the difficulty to tell CSWS from other similar diseases in ICU, ICU doctors should be aware of such condition.

Comparison Between Tolvaptan and Three Percent Sodium Chloride in Hyponatremia of Syndrome of Inappropriate Secretion of Anti-Diuretic Hormone Patients

Comparison Between Tolvaptan and Three Percent Sodium Chloride in Hyponatremia of Syndrome of Inappropriate Secretion of Anti-Diuretic Hormone Patients

A case of nephrogenic syndrome of inappropriate antidiuresis caused by a mutation of the vasopressin type 2 receptor

Nephrogenic syndrome of inappropriate antidiuresis (NSIAD) is a rare X-linked disorder of water balance, which was first described in two unrelated male infants with severe symptomatic hyponatremia. NSIAD is caused by activating mutations of the arginine vasopressin receptor 2 (AVPR2) gene, resulting in impaired reabsorption of free water, which leads to increased osmolarity of urine, plasma hypo-osmolarity, and persistent hyponatremia. We report, for the first time in the domestic literature, a case of isolated euvolemic hyposmolality hyponatremia in a child with oligodipsia. Because hypocorticism and renal pathology were excluded, and there was no antidiuretic hormone hypersecretion, NSIAD was suggested. A molecular genetic study revealed a new mutation L312S, not described earlier, in the seventh transmembrane domain of the AVPR2 gene. Pathogenicity of the mutation was proved by a functional study. We provide the clinical and laboratory characteristics of SIAD and the main principles of treatment. This disease should be considered in the differential diagnosis of hyponatremia syndrome.

Beer Potomania: A Challenging Case of Hyponatremia

Beer potomania is a syndrome of hyponatremia associated with excessive beer drinking. Little or no salt content of beer results in marked reduction in the solute load to the kidney. This leads to impaired water clearance and dilutional hyponatremia. A 66-year-old man with history of alcoholism and alcoholic cardiomyopathy presented to the emergency room with tremors of his upper and lower extremities. He had a significant history of alcohol consumption, usually drinking 4 - 5 cans of beer per night for the past 34 years. In addition, he had consumed a fifth of a vodka bottle the day before presentation. He had a pattern of often skipping meals though was compliant with both his diuretics medications: furosemide 40 mg once daily and spironolactone 25 mg daily. On physical exam, he was euvolemic. Neurological exam revealed resting tremors of both his hands. Labs were remarkable for plasma sodium of 122, brain natriuretic peptide of 474, serum osmolality of 268, urine osmolality of 223, and urine sodium of 20. Patient was assessed to have moderate euvolemic hypotonic hyponatremia. The combination of euvolemic hyponatremia with history of excessive beer drinking made beer potomania very likely. His urine osmolality and urine sodium, however, were higher than expected in beer potomania. These could be explained by the two diuretics that the patient was taking. Patient was managed with fluid restriction, appropriate nutritional and sodium intake and withholding of his diuretics. Plasma sodium slowly corrected to 130 over the course of 3 days. This case illustrates the condition beer potomania, an infrequent cause of hyponatremia. Findings in hyponatremia do not always point in one direction, especially with the concomitant use of diuretics. Recognition of beer potomania is critical as it is associated with serious neurologic sequelae that should be part of counseling against alcohol abuse. J Endocrinol Metab. 2016;6(4):123-126 doi: http://dx.doi.org/10.14740/jem350e

Diagnosing and Treating the Syndrome of Inappropriate Antidiuretic Hormone Secretion

BackgroundThe syndrome of inappropriate antidiuretic hormone secretion is the most common cause of hyponatremia in clinical practice, but current management of hyponatremia and outcomes in patients with syndrome of inappropriate antidiuretic hormone secretion are not well understood. The objective of the Hyponatremia Registry was to assess the current state of management of hyponatremia due to syndrome of inappropriate antidiuretic hormone secretion in diverse hospital settings, specifically which diagnostic and treatment modalities are currently used and how rapidly and reliably they result in an increase in serum sodium concentration ([Na+]). A secondary objective was to determine whether treatment choices and outcomes differ across the United States and the European Union. MethodsThe Hyponatremia Registry recorded selected diagnostic measures and use, efficacy, and outcomes of therapy for euvolemic hyponatremia diagnosed clinically as syndrome of inappropriate antidiuretic hormone secretion in 1524 adult patients with [Na+] ≤130 mEq/L (1034 from 146 US sites and 490 from 79 EU sites). A subgroup of patients with more rigorously defined syndrome of inappropriate antidiuretic hormone secretion via measurement of relevant laboratory parameters was also analyzed. ResultsThe most common monotherapy treatments for hyponatremia in syndrome of inappropriate antidiuretic hormone secretion were fluid restriction (48%), isotonic (27%) or hypertonic (6%) saline, and tolvaptan (13%); 11% received no active agent. The mean rate of [Na+] change (mEq/L/d) was greater for all active therapies than no active treatment. Hypertonic saline and tolvaptan produced the greatest mean rate of [Na+] change (interquartile range, both 3.0 [6.0] mEq/L/d) compared with lower interquartile range rates of [Na+] change for isotonic saline (1.5 [3.0] mEq/L/d) and fluid restriction (1.0 [2.3] mEq/L/d). The general pattern of responses was similar in both the US and EU cohorts. At discharge, [Na+] was <135 mEq/L in 75% of patients and ≤130 mEq/L in 43% of patients. Overly rapid correction occurred in 10.2% of patients. ConclusionsCurrent treatment of hyponatremia in syndrome of inappropriate antidiuretic hormone secretion often uses therapies with limited efficacy; the most commonly chosen monotherapy treatments, fluid restriction and isotonic saline, failed to increase the serum [Na+] by ≥5 mEq/L in 55% and 64% of monotherapy treatment episodes, respectively. Appropriate laboratory tests to diagnose syndrome of inappropriate antidiuretic hormone secretion were obtained in <50% of patients; success rates in correcting hyponatremia were significantly higher when such tests were obtained. Few outcome differences were found between the United States and the European Union. A notable exception was hospital length of stay; use of tolvaptan was associated with significantly shorter length of stay in the European Union but not in the United States. Despite the availability of effective therapies, most patients with syndrome of inappropriate antidiuretic hormone secretion were discharged from the hospital still hyponatremic.

GreenLight HPS™ 120‐W laser vaporization vs transurethral resection of the prostate (&lt;60 mL): a 2‐year randomized double‐blind prospective urodynamic investigation

What's known on the subject? and What does the study add? Photovaporization of the prostate (PVP) is now challenging TURP as the standard treatment for lower LUTS caused by BPH. The learning curve for PVP is short and the main advantages of this method over TURP are a shorter period of hospitalization, a shorter period of postoperative vesical catheterization, lower levels of retrograde ejaculation, rare development of dilutional hyponatraemia syndrome, the lack of a need for postoperative vesical irrigation as a result of extremely low indices of postoperative haematuria, and the lack of a need to suspend anticoagulant medication for the surgery. Traditionally, comparisons of the effectiveness of TURP vs PVP have involved parameters such as peak flow urinary rate and post-void residual urine volume measurements, and have employed questionnaires such as the IPSS and the International Index of Erectile Function instruments. However, studies evaluating detailed urodynamic parameters remain scarce and non-comparative The present study compared postoperative, medium-term urodynamic parameters among patients receiving TURP and high-power PVP. We consider the present study to be distinctive because it involved a double-blind, detailed functional analysis of the vesical emptying stage over the course of 2 years, and did not simply comprise an evaluation of clinical parameters and uroflowmetrics. We saw a reduction of infravesical obstruction, as shown by the significant reduction of ≥20 cm H(2)O in the mean micturition pressure for the groups studied, as well as a significant reduction in bladder outlet obstruction index. Thus, the present data show that high-power PVP can achieve and maintain the same results as TURP over a period of 24 months regarding an aspect that is particularly important for maintaining vesical health (i.e. detrusor pressure during the evacuation of the bladder). Such urodynamic data describing the functional outcome of PVP are currently missing from the literature. To assess the impact of GreenLight HPS™ 120-W (American Medical System Incorporation, Minnetonka, MN, USA) laser photovaporization of the prostate (PVP) compared to transurethral resection of the prostate (TURP) on urodynamic results, voiding function and sexual function. In total, 20 men with intermediate/severe lower urinary tract symptoms as a result of benign prostatic hyperplasia (BPH) were randomly selected and equally divided into two groups: TURP and PVP. Urodynamic evaluation was performed and International Prostate Symptom Score (IPSS), International Index of Erectile Function-5 and International Consultation on Incontinence Questionnaire - Short Form questionnaires were completed. The results were assessed at 2 years. Mean IPSS scores were reduced in both groups, although they did not differ between the TURP and PVP groups. There was no significant change in International Index of Erectile Function-5 scores. Half of the patients in the PVP group developed urge urinary incontinence with spontaneous resolution. The urodynamic parameters analyzed showed an improvement for both groups, although the values in the TURP group values were not significantly different from those in the PVP group. Bladder storage symptoms may represent a major concern, although they are of limited duration in patients undergoing PVP. High-power PVP can achieve and maintain the same results as TURP over a period of 24 months.

Hyponatraemic syndrome in a patient with tuberculosis always the adrenals?

Hyponatraemic syndrome in a patient with tuberculosis always the adrenals?

Successful Long-Term Treatment of Hyponatremia in Syndrome of Inappropriate Antidiuretic Hormone Secretion with Satavaptan (SR121463B), an Orally Active Nonpeptide Vasopressin V2-Receptor Antagonist

The effects of satavaptan (SR121463B), a novel long-acting orally active vasopressin V(2)-receptor antagonist, were investigated in patients with the syndrome of inappropriate antidiuretic hormone secretion (SIADH). In the first part of this randomized, double-blind study, 34 patients first were treated with satavaptan (versus placebo) for up to 5 d and then during 23 d of open-label dosage-adjustment period. In the second part of the study, long-term efficacy and safety of satavaptan was assessed in an open-label trial during at least 12 mo. Mean (+/-SD) serum sodium (SNa) levels before treatment were 127 +/- 2 mmol/L (placebo, n = 8), 125 +/- 6 mmol/L (25 mg, n = 14), and 127 +/- 5 mmol/L (50 mg, n = 12). Responders (patients SNa levels normalized or increased by at least 5 mmol/L from baseline during the double-blind period) were 79% in the 25-mg group (SNa 136 +/- 3 mmol/L; P = 0.006), 83% in the 50-mg group (SNa 140 +/- 6 mmol/L; P = 0.005), and 13% in the placebo group (SNa 130 +/- 5 mmol/L). No drug-related serious adverse events were recorded. During the long-term treatment, 15 of 18 enrolled patients achieved 6 mo and 10 achieved 12 mo of treatment. The SNa response was maintained during this time with a good tolerance. The new oral vasopressin V(2)-receptor antagonist satavaptan adequately corrects mild or moderate hyponatremia in patients with SIADH and has a good safety profile.

Syndrome of inappropriate antidiuresis

The syndrome of inappropriate antidiuresis is the most common cause of euvolemic hyponatremia and complicates a wide spectrum of diseases and neurosurgical conditions. The syndrome is characterized by clinical euvolemia, dilute plasma osmolality and inappropriately concentrated urine, with normal renal, adrenal and thyroid function. Hyponatremia in syndrome of inappropriate antidiuresis represents an excess of plasma water, rather than sodium deficiency. The severity of hyponatremia is limited by renal escape from antidiuresis. Treatment varies according to symptoms, severity and speed of onset of hyponatremia. Acute, severe, symptomatic hyponatremia may require rapid treatment with hypertonic saline, with care to avoid central pontine myelinosis. Chronic hyponatremia is managed with fluid restriction and demeclocycline for unresponsive cases. Vasopressin antagonists represent a new option for chronic hyponatremia of syndrome of inappropriate antidiuresis.

Reduction of hyponatremia in a schizophrenic with polydipsia–hyponatremia syndrome by surgical intervention

In a chronic schizophrenic with polydipsia–hyponatremia syndrome, we observed physiological data consecutively before and after a successful LAPIDES vesicostomy for his bladder retention. Although his polydipsia was unchanged, frequency of hyponatremia was significantly reduced after the operation. We found that bladder retention might be one of the factors relevant to the prediction of hyponatremia from diurnal weight gain. © 1997 Elsevier Science Ireland Ltd.

Validation study of a central venous pressure-based protocol for the management of neurosurgical patients with hyponatremia and natriuresis.

We had previously suggested a protocol for the management of neurosurgical patients with hyponatremia and natriuresis that was based on their volume status as determined by actual blood volume measurements. All patients in that study were found to be hypovolemic or normovolemic and responded, within 72 hours, to salt and fluid replacement. In the present study, the validity of that protocol was tested using central venous pressure as the sole measure of volume status of patients with hyponatremia and natriuresis. Twenty-five consecutive patients (26 cases) who fulfilled the inclusion criteria typically used to diagnose the syndrome of inappropriate secretion of antidiuretic hormone were included in the study. Central venous pressure was used to classify patients as hypovolemic (< 5 cm of water), normovolemic (6-10 cm of water), or hypervolemic (> 11 cm of water). Hypovolemic patients were given fluids (50 ml/kg/d) and salt (12 g/d). Normovolemic patients were given normal fluid with 12 g of salt per day. In addition, patients with anemia (hematocrit, < 27%) were administered whole blood. The end point was a serum sodium of more than or equal to 130 mEq/L measured in two consecutive samples 12 hours apart or 72 hours after entry into the study. If the serum sodium was less than 130 mEq/L at the end of 72 hours, the clinical condition of the patient determined further management. Nineteen of 25 patients (26 cases) were hypovolemic, the rest were normovolemic. No patient was hypervolemic. Nineteen of 25 patients (26 cases) attained normal serum sodium values within 72 hours, and an additional 3 responded within the next 36 hours (108 h after entry into the study). One patient who was discharged on request had normalized her serum sodium a week later. Among the three nonresponders, who were severely hypovolemic, as revealed by blood volume measurement, and responded to increased fluid and salt administration. One was normovolemic and responded to increased salt administration. There were no complications related to the therapy. Hyponatremia with natriuresis in the neurosurgical setting responds to salt and fluid replacement guided by the patients' volume status as determined by the central venous pressure. This study also offers further indirect evidence to suggest that the syndrome of hyponatremia with natriuresis is most often caused by "cerebral salt wasting" rather than by the syndrome of inappropriate secretion of antidiuretic hormone.

Absence of postoperative hyponatremia syndrome in young, healthy females

Young and previously healthy females have been reported to develop severe postoperative hyponatremia with a fatal outcome. The clinical presentation is dramatic, with seizures, respiratory arrest, and permanent, often catastrophic, brain damage. The true incidence is unknown. We report a survey of 290,815 surgical procedures on females at the Mayo Clinic from 1976 to 1992. Postoperatively 1,498 females had cardiopulmonary arrest, 255 had a metabolic encephalopathy, 32 had new-onset seizures, and 6 had central pontine myelinolysis. We failed to identify any association of respiratory arrest with postoperative hyponatremia. Our findings indicate that the postoperative hyponatremia syndrome in young, healthy females with respiratory arrest is extremely uncommon.

A study of serum antidiuretic hormone and atrial natriuretic peptide levels in a series of patients with intracranial disease and hyponatremia

Patients with intracranial disease are at risk of developing clinical deterioration due to a hyponatremic syndrome associated with an inappropriate degree of natriuresis, the "syndrome of inappropriate secretion of anti-diuretic hormone (ADH)" or SIADH. To investigate the hypothesis that atrial natriuretic peptide (ANP) is related to the natriuresis in SIADH, serum samples were obtained from 8 neurosurgical patients with intracranial disease seen consecutively who fulfilled the traditional clinical and laboratory criteria for SIADH. In one patient with a hemorrhagic cerebral infarction an elevation of serum ADH (5.7 pg/ml; normal = 1 to 5 pg/ml) in association with a normal level of serum ANP (49.8 pg/ml; normal = 10 to 60 pg/ml) was seen. Six patients (2 with intracerebral hemorrhage and 1 with hemorrhagic cerebral infarction, 1 with aneurysmal subarachnoid hemorrhage, 1 with glioblastoma multiforme, and 1 with Creutz-feldt-Jakob disease) had elevated serum ANP levels (197.0, 112.0, 92.0, 432.0, 97.5, and 138.0 pg/ml, respectively) associated with either normal or low ADH levels (1.3, 2.5, 1.2, 0.7, 2.3, and 0.5 pg/ml, respectively). Another patient with an intracerebral hemorrhage had a normal serum ANP level (37.0 pg/ml) and undetectable ADH level (less than 0.5 pg/ml). In the 7 patients in whom either ADH or ANP alone was elevated, a reciprocal relationship was observed between serum ADH and ANP levels, which could be expressed in logarithmic form (correlation coefficient, r = 0.727). In the 6 patients in whom serum ANP level alone was elevated, a near linear relationship was observed between serum ANP levels and urine sodium excretion (r = 0.851).(ABSTRACT TRUNCATED AT 250 WORDS)

Hyponatremia Due to Cerebral Salt-Wasting Syndrome. Combined Cerebral and Distal Tubular Lesion

A 76-year-old white man was evaluated for a syndrome of hyponatremia, hypotension, and high urinary sodium excretion. There was evidence of inappropriate secretion of antidiuretic hormone and renal salt in the presence of a normal glomerular filtration rate. He had a distal tubular acidification defect and unresponsiveness to standard doses of mineralocorticoids. The renin aldosterone axis was normal, as were thyroid and adrenal function. The patient could not dilute the urine, nor excrete a standard water load. Renal concentrating ability was normal, but there was no additional response to exogenous vasopressin. With modest salt restitution, the patient continued to lose large quantities of sodium in the urine, resulting in severe postural hypotension. Renal biopsy showed normal glomeruli with distinct degeneration of the distal tubules. There was no evidence of an acute inflammatory interstitial nephritis. The patient did not respond to therapeutic doses of mineralocorticoid (fludrocortisone), but treatment with water restriction, increased salt intake, and large doses of mineralocorticoids resulted in a normal serum sodium level and blood pressure. This case falls in the category of cerebral salt wasting syndrome. The cause was a combination of idiopathic secretion of antidiuretic hormone and distal tubular degeneration resulting in pseudohypoaldosteronism.

Hyponatremia due to cerebral salt-wasting syndrome: Combined cerebral and distal tubular lesion

A 76-year-old white man was evaluated for a syndrome of hyponatremia, hypotension, and high urinary sodium excretion. There was evidence of inappropriate secretion of antidiuretic hormone and renal salt wasting in the presence of a normal glomerular filtration rate. He had a distal tubular acidification defect and unresponsiveness to standard doses of mineralocorticoids. The renin aldosterone axis was normal, as were thyroid and adrenal function. The patient could not dilute the urine, nor excrete a standard water load. Renal concentrating ability was normal, but there was no additional response to exogenous vasopressin. With modest salt restitution, the patient continued to lose large quantities of sodium in the urine, resulting in severe postural hypotension. Renal biopsy showed normal glomeruli with distinct degeneration of the distal tubules. There was no evidence of an acute inflammatory interstitial nephritis. The patient did not respond to therapeutic doses of mineralocorticoid (fludrocortisone), but treatment with water restriction, increased salt intake, and large doses of mineralocorticoids resulted In a normal serum sodium level and blood pressure. This case falls in the category of “cerebral salt wasting” syndrome. The cause was a combination of idiopathic secretion of antidiuretic hormone and distal tubular degeneration resulting in pseudohypoaldosteronism.

Hyponatremia due to sulfonylurea compounds.

In a 68-yr-old female with diabetes mellitus and idiopathic cerebral atrophy, therapeutic doses of chlorpropamide or tolbutamide induced a hyponatremic syndrome identical with that of inappropriate secretion of ADH (serum Na 117 mEq/1). Metabolic studies revealed that the hyponatremia was due in part to negative sodium balance. There was no evidence of acute fluid retention since body weight, free water clearance and isotopic extracellular fluid volume were identical during control and drug periods. Diuresis was also absent, indicating inappropriate ADH activity during sulfonylurea-induced hyponatremia. Physicians using sulfonylurea drugs in the management of diabetes mellitus must be alert to the possible complication of hyponatremia.

Unstable osmolar homeostasis with and without renal sodium wastage

In two hyponatremic patients with bronchogenie carcinoma metastatic to the mediastinum, dilutional factors were clearly demonstrated. One patient had a cerebral metastasis, and at times showed profound renal sodium wastage, responding to either fluid restriction, ACTH, or Florinef. The second patient, despite overhydration and diminution of urinary aldosterone excretion, could not be induced to diurese substantial amounts of sodium, although his renal conservation was not optimally efficient. Analysis of previously reported cases seems to correlate the presence of cerebral disease with pronounced salt wasting in patients with dilutional hyponatremia. Experimental and clinical evidence also indicates a state of variable renal refractoriness to sustained administration of Pitressin and to ACTH and mineralocorticoid therapy during Pitressin administration—a state which appears to occur in the dilutional hyponatremia syndrome. The complex interplay of central and peripheral factors involved in the secretion and renal effects of antidiuretic hormone (ADH) and aldosterone probably accounts for the diverse observations previously reported.

Abnormal electrolyte and water metabolism in acute intermittent porphyria: The transient inappropriate secretion of antidiuretic hormone

Two patients with symptomatic acute intermittent porphyria transiently exhibited a syndrome of hyponatremia, water retention and urinary loss of electrolytes. It is suggested that this was due to inappropriate secretion of antidiuretic hormone, rendering them incapable of excreting water loads normally which, in turn, induced the observed derangements in sodium metabolism, and may have contributed to urinary loss of calcium and magnesium as well. In one patient, hypomagnesemia and hypocalcemia developed, with concomitant tetany. Excessive loss of magnesium and calcium, coupled with inadequate intake, presumably was responsible for the low serum values.

The syndrome of hyponatremia and renal sodium loss probably resulting from inappropriate secretion of antidiuretic hormone.

Case Reports1 December 1959THE SYNDROME OF HYPONATREMIA AND RENAL SODIUM LOSS PROBABLY RESULTING FROM INAPPROPRIATE SECRETION OF ANTIDIURETIC HORMONEH. J. ROBERTS, M.D.H. J. ROBERTS, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-51-6-1420 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThis paper reports a patient with a bronchogenic carcinoma who developed profound hyponatremia and hypochloremia in association with considerable loss of both sodium and chloride in the urine. Clinically he was found to have normal renal and adrenal function and at autopsy the kidneys and the adrenals showed no significant pathologic change.Two earlier instances of this particular syndrome were included in the report by Schwartz et al. in 1957.1It was the opinion of these investigators that this unusual electrolyte derangement could best be explained by a sustained and inappropriate secretion of antidiuretic hormone, and that this disorder was...Bibliography1. SchwartzBennettCurelopBartter WBWSFC: A syndrome of renal sodium loss and hyponatremia probably resulting from inappropriate secretion of antidiuretic hormone, Am. J. Med. 23: 529, 1957. CrossrefMedlineGoogle Scholar2. PorterFrantz MRVK: Tumors associated with hypoglycemia—pancreatic and extrapancreatic, Am. J. Med. 21: 944, 1956. CrossrefMedlineGoogle Scholar3. 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BrickGlazer IBL: Marked eosinophilia with cancer: a poor prognostic sign, Ann. Int. Med. 35: 213, 1951. LinkGoogle Scholar9. WeltSeldinNelsonGermanPeters LGDWWPWJJP: Role of central nervous system in metabolism of electrolytes and water, Arch. Int. Med. 90: 355, 1952. CrossrefGoogle Scholar10. Cort JH: Cerebral salt wasting, Lancet 1: 752, 1954. CrossrefGoogle Scholar11. Wise BL: Relation of brain stem to renal electrolyte excretion, Proc. Soc. Exper. Biol. and Med. 91: 557, 1956. CrossrefMedlineGoogle Scholar12. EpsteinLevitin FHH: "Cerebral salt-wasting": an example of sustained inappropriate release of antidiuretic hormone, abstract, J. Clin. Investigation 38: 1001, 1959. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: West Palm Beach, Florida*Received for publication August 18, 1958.Requests for reprints should be addressed to H. J. Roberts, M.D., 1525 North Flagler Drive, West Palm Beach, Florida. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byLung Cancer MarkersPituitary insufficiency, inappropriate antidiuretic hormone (ADH) secretion, and carcinoma of the bronchusParaneoplastic syndromes Resulting from elaboration of ectopic hormones, antigens and bizarre toxinsAuswirkungen der renalen Insuffizienz auf die Zusammensetzung der Cerebrospinalflüssigkeit, den Stoffwechsel des ZNS und zentralnervöse FunktionenDie zentralnervöse klinische Symptomatologie der akuten und chronischen NiereninsuffizienzStörungen der HarnkonzentrierungHormonal Syndromes Associated with NeoplasiaCase 30-1967The syndrome of inappropriate secretion of antidiuretic hormoneAn investigation into the cause of hyponatremia in the syndrome of inappropriate secretion of antidiuretic hormoneInappropriate Renal Sodium Loss Reverted by Vena Cava ObstructionHENRY O. HEINEMANN, M.D., JOHN H. LARAGH, M.D., F.A.C.P.Hyponatremia from inappropriate antidiuretic hormone elaboration in carcinoma of the lungPARANEOPLASTIC DISORDERS“Inappropriate” secretion of antidiuretic hormone without corresponding hyponatraemia in cerebral pathologyHypoadrenocorticotropism with Hyponatremia, Resembling Antidiuretic Hormone ExcessJOSEPH L. GRANT, M.D., F.A.C.P., ALASTAIR MACDONALD, STEPHEN R. BROVENDER, M.D., NICHOLAS YANKOPOULOS, M.D.Physiology of the kidneyDisorders of renal functionBronchogenic Carcinoma with Inappropriate Antidiuretic Activity in Plasma and TumorA review of unusual systemic manifestations associated with carcinomaCarcinoma of the Lung with Inappropriate AntidiuresisHyponatremia and the inappropriate secretion of antidiuretic hormoneHyponatremia and bronchogenic carcinoma associated with renal excretion of large amounts of antidiuretic materialElectrolyte disturbances associated with cancerHYPONATREMIA IN ACUTE INTERMITTENT PORPHYRIA PROBABLY RESULTING FROM INAPPROPRIATE SECRETION OF ANTIDIURETIC HORMONE*Use of a low-sodium formula as an improved Karell diet, with emphasis upon the outpatient management of heart failure and lymphedemaAldosterone in Cerebral Salt WastingThe Clinical and Physiologic Significance of the Serum Sodium ConcentrationUnstable osmolar homeostasis with and without renal sodium wastageIdiopathic, episodic inappropriate secretion of antidiuretic hormoneAbnormal electrolyte and water metabolism in acute intermittent porphyriaHypo- and HypernatremiaLOUIS G. WELT, M.D., F.A.C.P.Cerebral HyponatremiaSodium BalanceHyponatremia and Renal Wasting of Sodium in Patients with Malfunction of the Central Nervous System 1 December 1959Volume 51, Issue 6Page: 1420-1426KeywordsAntidiuretic hormoneAutopsyBlood plasmaBradycardiaChloridesHyponatremiaKidneysPathogenesisSodiumUrine ePublished: 1 December 2008 Issue Published: 1 December 1959 PDF downloadLoading ...