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Syndrome of Inappropriate Antidiuretic Hormone Secretion Differential Diagnoses

  • Author: Christie P Thomas, MBBS, FRCP, FASN, FAHA; Chief Editor: Vecihi Batuman, MD, FACP, FASN  more...
 
Updated: Oct 28, 2015
 
 

Diagnostic Considerations

The differential diagnoses of SIADH include other hyponatremic conditions, which can be divided into those that cause impairment in urinary water excretion and those in which renal handling of water is normal. All patients with hyponatremia should have a plasma osmolality measured to confirm hypo-osmolality.

Conditions in which renal water handling is impaired include the following:

  • Effective circulating volume depletion - GI losses (eg, diarrhea, vomiting), renal losses (eg, diuretic therapy, adrenal insufficiency, primary renal salt wasting), skin losses, edematous disorders (congestive heart failure, cirrhosis with portal hypertension, severe nephrotic syndrome)
  • Renal failure - Acute kidney injury (AKI) or chronic kidney disease (CKD)
  • Other states of ADH excess - Cortisol deficiency, hypothyroidism, exogenous ADH (eg, deamino-D-arginine-vasopressin, vasopressin, oxytocin)
  • Decreased solute intake
  • Nephrogenic syndrome of inappropriate anti-diuresis (NSIAD)

Disorders with normal water excretion include the following:

  • Primary polydipsia
  • Reset osmostat
  • Cerebral salt wasting

Pseudohyponatremia

Extreme elevations in plasma lipids or proteins can increase the plasma volume and can reduce the measured plasma Na+ concentration. Na+ is contained in the aqueous phase of plasma; the proteins and lipids cause an increase in the nonaqueous phase of plasma, leading to an overall increase in plasma volume without an actual decrease or dilution of Na+ in the aqueous phase. This was more of an issue in the past in the United States, when the conventional method of measuring Na+ (ie, flame-emission spectrophotometry) measured the aqueous and nonaqueous phases of plasma. The correction factors are as follows:

  • Plasma triglycerides (g/L) x 0.002 = mEq/L decrease in Na +
  • Plasma protein level - 8 (g/L) x 0.025 = mEq/L decrease in Na +

The newer method (using ion-specific Na+ electrodes) measures the Na+ in the aqueous phase only, thus avoiding the error of pseudohyponatremia. Pseudohyponatremia should be suspected when the measured plasma osmolality is normal in the presence of hyponatremia. Pseudohyponatremia may continue to be a problem in parts of the world where flame photometry is still used to measure Na+.

Hyperglycemia

Elevated glucose levels decrease the measured serum Na+ levels by 1.6 mEq/L for every 100 mg/dL increase in glucose. This results from the osmotic effect of glucose drawing water into the intravascular space. Plasma osmolality is high in this situation. This is a form of transient hyponatremia that corrects itself as hyperglycemia is reversed.[13] A similar form of hyponatremia can occur with any osmotically active substance in plasma, such as mannitol or dextran.

Exercise-induced hyponatremia

Exercise-induced hyponatremia has been reported during prolonged exercise such as in marathon runners and triathletes, usually in warmer climates, which can lead to severe hyponatremia associated with neurological symptoms.[18] The syndrome appears to arise because of excessive water consumption during the physical exercise coupled with loss of sodium chloride in sweat and nonosmotic stimulation of AVP secretion (from stress, volume contraction, nausea, and NSAIDs). Some athletes with cerebral edema also develop noncardiogenic pulmonary edema.[11]

Cerebral salt wasting

The term cerebral salt wasting (CSW) was introduced in the 1950s to describe an entity seen with certain cerebral disorders that can impair the ability of the kidneys to conserve Na+, with resultant salt wasting and polyuria. CSW is defined as the renal loss of Na+ with intracranial disease, which leads to hyponatremia and a decrease in extracellular fluid volume.[19, 20] Vasopressin-resistant polyuria with hyponatremia, particularly in the setting of cerebral injury or cerebral disease or when accompanied by dehydration, should prompt consideration of CSW in the differential diagnosis. CSW must be distinguished from SIADH because management of these 2 conditions differs significantly.

The differences and similarities in findings for CSW and SIADH are itemized as follows:

  • Hyponatremia - Present in both CSW and SIADH
  • Urine Na - Increased in both CSW and SIADH
  • Volume - Reduced in CSW and normal or increased in SIADH
  • Salt wasting - Gross in CSW and self-limited in SIADH
  • Urine output - Polyuria in CSW and variable in SIADH
  • Hypouricemia - Occasionally in CSW and frequent in SIADH

Over the years, much debate has been focused on the existence of this entity. The evidence in favor of CSW rests on the following points: (1) the presence of a negative salt balance, (2) the development of volume contraction (by definition, patients with SIADH are euvolemic), and (3) the fact that patients with CSW respond to salt and volume replacement rather than to fluid restriction.

Various mechanisms have been postulated, including the roles of natriuretic peptides and neural regulatory mechanisms. Measurement of AVP or atrial natriuretic peptide levels is not helpful because they have been known to vary even in persons with SIADH.

CSW is treated with Na+ replacement, which is diametrically opposite to that for SIADH. Na+ administration in persons with CSW corrects the hyponatremia and the fluid loss; however, in patients with SIADH, the effect is temporary. The mineralocorticoid fludrocortisone has been used as part of the treatment of CSW.[20]

Adrenal insufficiency

Cortisol has a negative feedback effect on ADH and corticotropin-releasing hormone. The absence of cortisol thus removes this inhibitory effect, increasing the release of ADH.

Renal disease

With declining renal function, patients have a decreasing ability to excrete free water and the more advanced the reduction in GFR, the easier it is for patients to become hyponatremic with unrestricted fluid intake. In patients on long-term dialysis with no urine output, fluid intake no greater than insensible losses leads to a predictable fall in serum Na, which, however, is not sustained because of regular maintenance dialysis.

Reset osmostat

Persons with this entity have a normal response to changes in osmolality, but their threshold for ADH release is reduced. Therefore, they have a lower, but stable, plasma Na+ concentration. Some individuals probably carry a nonsynonymous polymorphism (P19S) in the transient receptor potential vanilloid 4 (TRPV4) channel, part of the osmoreceptor system, since this mutation has been shown to be associated with hyponatremia.[21]

The reset osmostat has been observed in pregnant women. Increased human chorionic gonadotropin levels have been implicated to play a role in this condition. The serum Na+ concentration falls by approximately 5 mEq/L in the first 2 months of pregnancy and remains stable until after delivery, when it returns to normal levels. Recognizing this entity is important because it does not require treatment.

Psychogenic polydipsia

This condition is characterized by an increase in water intake attributed to a defect in the thirst mechanism. In some patients, the osmotic threshold for thirst is reset below the reset for release of ADH. This disorder is mostly observed in patients with psychosis.

Water excretion is normal in these patients, and water restriction corrects the hyponatremia. In a patient on a normal diet and an average solute (protein and salts) intake, a substantial amount of water must be imbibed for hyponatremia to develop. Consider an individual who has 700 mOsm (primarily consisting of urea, Na+, potassium, and chloride) to excrete per day. Ordinarily, this person can vary his or her urine osmolality between 50 and 1400 mOsm/L and thus can excrete the osmotic load in a minimum of 500 mL and a maximum of 14 L. As long as his or her fluid intake is between these extremes, he or she adjusts urine osmolality to excrete the load. To become hyponatremic, such an individual must drink more than 14 L/d.

Decreased solute intake

This disorder is observed in persons who drink hyponatremic fluids without adequate food intake. The condition is described in individuals who drink beer (beer potomania) and thrive on little else and thus have substantially reduced protein and salt intake. The daily solute intake directly influences the osmotic load to be excreted. With poor nutritional intake, the osmotic load may be as little as 200 mOsm; in this situation, it can be excreted in a maximum of 4 L. Ingestion of a larger quantity of solute-free fluids without other avenues for water loss can result in the development of hyponatremia.

Diuretics and hyponatremia

Diuretics can cause mild-to-severe hyponatremia. Thiazide diuretics cause hyponatremia more often than loop diuretics. This is related to the different sites of action of these agents.

Loop diuretics act in the medullary thick ascending limb and prevent Na+ absorption in the medullary thick ascending limb. This interferes with the concentrating ability by diminishing medullary osmolality. The Na+ can be reabsorbed once it reaches the distal tubule and the collecting duct.

The thiazide diuretics prevent Na+ absorption in the distal tubule and do not interfere with the medullary concentrating ability or the effect of ADH. However, the distal tubule is the diluting segment of the nephron, and diminished Na+ absorption here increases urine osmolality and prevents the excretion of hypotonic urine. In patients who are susceptible to this effect, hyponatremia is usually observed within 2 weeks. After that, a new steady state is reached and further changes in serum Na+ only occur with an added stimulus such as vomiting and diarrhea.

Nephrogenic syndrome of inappropriate antidiuresis (NSIAD)

This is a rare X-linked recessive genetic disease secondary to gain of function mutations in the V2 receptor, resulting in a spontaneously active receptor and unregulated water reabsorption. The laboratory features are identical to those of SIADH, with euvolemic hyponatremia, plasma hypo-osmolality, and increased urinary osmolality. The disease is likely to present in early infancy, although so far only 2 patients have been described with this disorder.[22] If AVP levels are measured, they are predicted to be low.

Hypervolemic hyponatremia

Other conditions to consider in the differential diagnosis of hyponatremia are those that are associated with hypervolemia in which the baroreceptors perceive reduced effective circulating volume and stimulate AVP secretion. These conditions include congestive heart failure, cirrhosis, and nephrotic syndrome. These should be evident on clinical examination because of the presence of peripheral edema with elevated jugular venous pressure, pulmonary rales, ascites, or stigmata of advanced liver disease.

Differential Diagnoses

 
 
Contributor Information and Disclosures
Author

Christie P Thomas, MBBS, FRCP, FASN, FAHA Professor, Department of Internal Medicine, Division of Nephrology, Departments of Pediatrics and Obstetrics and Gynecology, Medical Director, Kidney and Kidney/Pancreas Transplant Program, University of Iowa Hospitals and Clinics

Christie P Thomas, MBBS, FRCP, FASN, FAHA is a member of the following medical societies: American College of Physicians, American Heart Association, American Society of Nephrology, Royal College of Physicians

Disclosure: Nothing to disclose.

Coauthor(s)

Mony Fraer, MD, FACP, FASN Associate Professor, Division of Nephrology, Department of Medicine, University of Iowa Hospitals and Clinics; Staff Physician, Iowa City Veterans Affairs Medical Center

Disclosure: Nothing to disclose.

Specialty Editor Board

Eleanor Lederer, MD, FASN Professor of Medicine, Chief, Nephrology Division, Director, Nephrology Training Program, Director, Metabolic Stone Clinic, Kidney Disease Program, University of Louisville School of Medicine; Consulting Staff, Louisville Veterans Affairs Hospital

Eleanor Lederer, MD, FASN is a member of the following medical societies: American Association for the Advancement of Science, International Society of Nephrology, American Society for Biochemistry and Molecular Biology, American Federation for Medical Research, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, Kentucky Medical Association, National Kidney Foundation, Phi Beta Kappa

Disclosure: Received grant/research funds from Dept of Veterans Affairs for research; Received salary from American Society of Nephrology for asn council position; Received salary from University of Louisville for employment; Received salary from University of Louisville Physicians for employment; Received contract payment from American Physician Institute for Advanced Professional Studies, LLC for independent contractor; Received contract payment from Healthcare Quality Strategies, Inc for independent cont.

Chief Editor

Vecihi Batuman, MD, FACP, FASN Huberwald Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Renal Section, Southeast Louisiana Veterans Health Care System

Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, International Society of Nephrology

Disclosure: Nothing to disclose.

Acknowledgements

Howard A Bessen, MD Professor of Medicine, Department of Emergency Medicine, UCLA School of Medicine; Program Director, Harbor-UCLA Medical Center

Howard A Bessen, MD is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Keenan Bora, MD Fellow, Medical Toxicology, Detroit Medical Center; Attending Physician, Medical Center Emergency Services, Detroit

Keenan Bora, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, and American Medical Association

Disclosure: Nothing to disclose.

Meher Chaudhry, MD Chief Resident, Department of Emergency Medicine, Detroit Receiving Hospital, University Health Center

Disclosure: Nothing to disclose.

Sonali Deshmukh, MBBS Consulting Staff, Omaha Nephrology, Nebraska

Sonali Deshmukh, MBBS is a member of the following medical societies: American Society of Nephrology

Disclosure: Nothing to disclose.

obert J Ferry Jr, MD Chief, Division of Pediatric Endocrinology and Metabolism, Le Bonheur Children's Hospital; Professor, Department of Pediatrics, University of Tennessee Health Science Center at Memphis; St. Jude Children's Research Hospital, Memphis, TN; Brigade Surgeon, 36th Sustainment Brigade, U.S. Army; Adjunct Professor, Pediatric Surgery Department, King Saud University, Riyadh, Saudi Arabia

Robert J Ferry Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Diabetes Association, American Medical Association, Endocrine Society, Lawson-Wilkins Pediatric Endocrine Society, Society for Pediatric Research, and Texas Pediatric Society

Disclosure: Nutropin Speakers Bureau Honoraria Speaking and teaching; Genotropin Speakers Bureau Honoraria Speaking and teaching; Eli Lilly & Co. Grant/research funds Investigator; MacroGenics, Inc. Grant/research funds Investigator; Ipsen, S.A. (formerly Tercica, Inc.) Grant/research funds Investigator; NovoNordisk SA Grant/research funds Investigator; Diamyd Investigator

Stephen Kemp, MD, PhD Professor, Department of Pediatrics, Section of Pediatric Endocrinology, University of Arkansas College of Medicine and Arkansas Children's Hospital

Stephen Kemp, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Association of Clinical Endocrinologists, American Pediatric Society, Endocrine Society, Phi Beta Kappa, Southern Medical Association, and Southern Society for Pediatric Research

Disclosure: Nothing to disclose.

Eleanor Lederer, MD Professor of Medicine, Chief, Nephrology Division, Director, Nephrology Training Program, Director, Metabolic Stone Clinic, Kidney Disease Program, University of Louisville School of Medicine; Consulting Staff, Louisville Veterans Affairs Hospital

Eleanor Lederer, MD is a member of the following medical societies: American Association for the Advancement of Science, American Federation for Medical Research, American Society for Biochemistry and Molecular Biology, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, International Society of Nephrology, Kentucky Medical Association, National Kidney Foundation, and Phi Beta Kappa

Disclosure: Dept of Veterans Affairs Grant/research funds Research

Lynne Lipton Levitsky, MD Chief, Pediatric Endocrine Unit, Massachusetts General Hospital; Associate Professor of Pediatrics, Harvard Medical School

Lynne Lipton Levitsky, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Diabetes Association, American Pediatric Society, Endocrine Society, Lawson-Wilkins Pediatric Endocrine Society, and Society for Pediatric Research

Disclosure: Pfizer Grant/research funds P.I.; Tercica Grant/research funds Other; Eli Lily Grant/research funds PI; NovoNordisk Grant/research funds PI

Chike Magnus Nzerue, MD Associate Dean for Clinical Affairs, Vice-Chairman of Internal Medicine, Meharry Medical College

Chike Magnus Nzerue, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Society of Nephrology, and National Kidney Foundation

Disclosure: Nothing to disclose.

Jose F Pascual-y-Baralt, MD Chief, Division of Pediatric Nephrology, San Antonio Military Pediatric Center; Clinical Professor, Department of Pediatrics, University of Texas Health Science Campus

Jose F Pascual-y-Baralt, MD is a member of the following medical societies: American Academy of Pediatrics, American Society of Nephrology, American Society of Pediatric Nephrology, Association of Military Surgeons of the US, and International Society of Nephrology

Disclosure: Nothing to disclose.

Alexandr Rafailov, MD Staff Physician, Department of Emergency Medicine, State University of New York Downstate/Kings County Hospital

Disclosure: Nothing to disclose.

Arlan L Rosenbloom, MD Adjunct Distinguished Service Professor Emeritus of Pediatrics, University of Florida; Fellow of the American Academy of Pediatrics; Fellow of the American College of Epidemiology

Arlan L Rosenbloom, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Epidemiology, American Pediatric Society, Endocrine Society, Florida Pediatric Society, Lawson-Wilkins Pediatric Endocrine Society, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Erik D Schraga, MD Consulting Staff, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates; Consulting Staff, Permanente Medical Group, Kaiser Permanente, Santa Clara Medical Center

Disclosure: Nothing to disclose.

Richard H Sinert, DO Associate Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, Research Director, State University of New York College of Medicine; Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center

Richard H Sinert, DO is a member of the following medical societies: American College of Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Pharmacy Editor, Medscape

Disclosure: Nothing to disclose.

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