Evaluation of adults with hyponatremia

Author
Richard H Sterns, MD
Section Editor
Michael Emmett, MD
Deputy Editor
John P Forman, MD, MSc
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jul 2015. &#124 This topic last updated: May 13, 2014.
INTRODUCTION Hyponatremia is commonly defined as a serum sodium concentration below 135 meq/L but can vary to a
small degree in different clinical laboratories [1]. In virtually all patients, hyponatremia results from the intake (either oral or
intravenous) and subsequent retention of water [2]. A water load will, in normal individuals, be rapidly excreted as the dilutional
fall in serum osmolality suppresses the release of antidiuretic hormone (ADH), also called vasopressin, (figure 1), thereby
allowing excretion of the excess water in a dilute urine.
In contrast to the response in normal individuals, patients who develop hyponatremia typically have an impairment in renal water
excretion, most often due to an inability to suppress ADH secretion. An uncommon exception occurs in patients with primary
polydipsia who can become hyponatremic because they drink such large quantities of fluid that they overwhelm the excretory
capacity of the kidney even though ADH release is appropriately suppressed.
The diagnostic approach to the patient with hyponatremia will be reviewed here. Most patients with hyponatremia have a single
cause but, in selected patients, multiple factors contribute to the fall in plasma sodium. Symptomatic infection with human
immunodeficiency virus (HIV) is an example of this phenomenon, as volume depletion, the syndrome of inappropriate ADH
secretion, and adrenal insufficiency all may be present. (See "Electrolyte disturbances with HIV infection".)
The causes and treatment of hyponatremia are discussed separately. (See "Causes of hyponatremia in adults" and "Overview of
the treatment of hyponatremia in adults" and "Treatment of hyponatremia: Syndrome of inappropriate antidiuretic hormone
secretion (SIADH) and reset osmostat".)
EVALUATION The diagnostic approach to the patient with hyponatremia consists of a directed history and physical
examination, appropriate laboratory tests, and, in selected patients, assessing the response to volume expansion with isotonic
saline.
History and physical examination The history and physical examination in hyponatremic patients should be directed toward
identification of findings that are typical of the particular causes of hyponatremia (table 1) [2-4].
These include:
A history of fluid loss (eg, vomiting, diarrhea, diuretic therapy) and, on examination, signs of extracellular volume depletion,
such as decreased skin turgor, a low jugular venous pressure (which is not diagnostic), or orthostatic or persistent hypotension.
(See "Etiology, clinical manifestations, and diagnosis of volume depletion in adults".)
A history of low protein intake and/or high fluid intake. (See "Causes of hyponatremia in adults", section on 'Low dietary solute
intake'.)
A history consistent with one of the causes of SIADH, such as small cell carcinoma or central nervous system disease. (See
"Pathophysiology and etiology of the syndrome of inappropriate antidiuretic hormone secretion (SIADH)".)
Use of medications associated with hyponatremia.
Signs of peripheral edema and/or ascites, which can be due to heart failure, cirrhosis, or renal failure. (See "Clinical
manifestations and diagnosis of edema in adults" and "Evaluation of the patient with suspected heart failure" and "Cirrhosis in
adults: Etiologies, clinical manifestations, and diagnosis".)
Symptoms and signs suggestive of adrenal insufficiency or hypothyroidism. (See "Diagnosis of adrenal insufficiency in adults"
and "Diagnosis of and screening for hypothyroidism in nonpregnant adults".)
Although the history and physical examination often provide important clues to the cause of hyponatremia, identification of subtle
degrees of volume depletion or edema may be difficult [4,5]. As a result, laboratory testing is almost always required to establish
the diagnosis, particularly measurement of the urine sodium concentration [5].

Laboratory tests Three laboratory tests provide important initial information in the differential diagnosis of hyponatremia [2]:
Serum osmolality
Urine osmolality
Urine sodium, potassium, and chloride concentrations
Serum osmolality The serum osmolality (Sosm), which normally ranges from 275 to 290 mosmol/kg, is reduced in most
hyponatremic patients, because it is primarily determined by the serum sodium concentration and accompanying anions. (See
"Causes of hyponatremia in adults", section on 'Hyponatremia with a low serum osmolality'.)
The Sosm is part of the routine evaluation in patients with hyponatremia because some have an Sosm that is high or normal.
These disorders are discussed elsewhere. (See "Causes of hyponatremia in adults", section on 'Hyponatremia with a high or
normal serum osmolality'.)
The three most common causes of hyponatremia with a high or normal Sosm are marked hyperglycemia, severe azotemia, and
alcohol intoxication:
Hyperglycemia In patients with marked hyperglycemia, which is almost always a manifestation of uncontrolled diabetes, the
increase in serum glucose raises the Sosm, which pulls water out of the cells and lowers the serum sodium concentration. (See
"Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Clinical features, evaluation, and diagnosis", section on
'Serum sodium'.)
Azotemia In patients with advanced renal failure, the hyponatremia is due to an inability to excrete water resulting from the
impairment in renal function. Although this will tend to lower the Sosm, this effect is counterbalanced to a variable degree by the
associated elevation in blood urea nitrogen (BUN), resulting in an Sosm that may be normal or elevated. However, there is a
difference between the measured serum osmolality and the effective serum osmolality in patients with renal failure. In contrast to
sodium and glucose, urea is an ineffective osmole since it can freely cross cell membranes and therefore does not obligate
water movement out of the cells. Thus, patients with hyponatremia and renal failure have a low effective serum osmolality
(Sosm) that becomes apparent if the measured Sosm is corrected for the effect of urea:
Corrected Sosm = Measured Sosm - (BUN 2.8)
Dividing the BUN by 2.8 converts mg/dL into mmol/L, which is required when measuring osmolality. In countries in which blood
urea is measured in units of mmol/L, the formula is:
Corrected Sosm = Measured Sosm - blood urea concentration
Alcohol intoxication True hyponatremia is common in patients with alcoholism. The reduction in the Sosm associated with
hyponatremia can be offset in some patients by high circulating levels of ethanol. Ethanol, like urea, is an ineffective osmole
since it can freely cross cell membranes and therefore does not obligate water movement out of cells. Thus, patients with
hyponatremia and alcoholism may have a low serum sodium concentration, a low calculated Sosm, but a measured Sosm that
is not low [6]. The reason for the gap between the calculated and measured Sosm becomes apparent when the blood alcohol
level is measured. (See "Serum osmolal gap", section on 'Ethanol intoxication'.)
Less common causes of hyponatremia with a high or normal Sosm include infusion or absorption of solutions containing sugars
that act as effective osmoles, systemic absorption of irrigant solutions containing glycine, sorbitol, or mannitol, and
pseudohyponatremia due to hyperlipidemia or hyperproteinemia:
Intravenous infusions of sugars Administration of either hypertonic mannitol or maltose or sucrose in conjunction with
intravenous immune globulin will cause hyponatremia in patients with renal failure. In such patients, these sugars are retained
and, because they are effective osmoles, pull water out of cells and thereby lower the serum sodium concentration. (See
"Complications of mannitol therapy".)
Irrigant absorption The absorption of nonconductive glycine, sorbitol, or mannitol irrigation solutions during transurethral
resection of the prostate or bladder (called the transurethral resection syndrome) or during hysteroscopy or laparoscopic surgery
can lower the serum sodium by increasing the extracellular fluid volume with these sodium free solutions. These disorders are
discussed in detail separately. (See "Hyponatremia following transurethral resection or hysteroscopy", section on 'Pathogenesis
of neurologic symptoms' and "Hysteroscopy: Managing fluid and gas distending media".)

Pseudohyponatremia Hyperlipidemia or hyperproteinemia lower the serum sodium concentration (and therefore the
calculated Sosm) without changing the measured Sosm [7]. This laboratory artifact is called pseudohyponatremia. (See "Causes
of hyponatremia in adults", section on 'Pseudohyponatremia' and 'Ion-selective electrodes' below.)
Ion-selective electrodes In normal individuals, each liter of plasma is approximately 93 percent water, with fats and proteins
accounting for the remaining 7 percent. Thus, a normal serum sodium concentration of 142 meq/L (measured per liter of
plasma) actually represents a concentration in the physiologically important plasma water of 154 meq/L (142 0.93 = 154). In
patients with marked hyperlipidemia or hyperproteinemia, the proportion of the plasma that is water falls to a lower value. As a
result, the sodium concentration per liter of plasma will fall, which is an artifact since the physiologically important sodium
concentration per liter of plasma water is normal.
In such patients, ion-selective electrodes will reveal a normal serum sodium concentration if an instrument employing direct
potentiometry is used [3,8,9]. However, many laboratory analyzers that measure sodium with ion-selective electrodes utilize
indirect potentiometry in which the plasma sample is diluted before measurement; these analyzers will report a low sodium
concentration [9].
To understand why this occurs, consider an instrument that dilutes the plasma specimen 1:100 [8]. Suppose that the plasma
water constitutes 80 percent of the plasma in a patient with hyperlipidemia. In this setting, each L of plasma contains 120 meq of
sodium even though the plasma water sodium concentration is normal. If this is now diluted to a total volume of 100 L, there will
be only 120 meq of sodium present and, correcting for dilution, the measured sodium concentration will appear reduced at
120 meq/L.
Other instruments directly measure the sodium concentration without dilution. Falsely low levels may still be obtained in patients
with hyperlipidemia; why this occurs is not well understood [10].
As an alternative to using ion-selective electrodes, the water content of plasma in patients with hyperlipidemia or
hyperproteinemia can be estimated from the following formula [8]:
Plasma water content, percent = 99.1 - (0.1 x L) - (0.07 x P)
where L and P refer to the total lipid and protein concentrations in g/L, respectively. This value is then adjusted to the normal
value for plasma water content of 93 percent.
Urine osmolality In patients with hyponatremia and a low plasma osmolality, the urine osmolality can be used to distinguish
between impaired water excretion (which is present in almost all cases) and primary polydipsia, in which water excretion is
normal but intake is so high that it exceeds excretory capacity.
The normal response to hyponatremia (which is maintained in primary polydipsia) is to markedly suppress ADH secretion,
resulting in the excretion of a maximally dilute urine with an osmolality below 100 mosmol/kg and a specific gravity 1.003.
Values above this level indicate an inability to normally excrete free water, most commonly because of persistent secretion of
ADH. Most hyponatremic patients have a relatively marked impairment in urinary dilution that is sufficient to maintain the urine
osmolality at 300 mosmol/kg or higher. The primary causes of persistent ADH release are effective circulating volume depletion
(true hypovolemia, heart failure, and cirrhosis) and the syndrome of inappropriate ADH secretion (SIADH). (See "Causes of
hyponatremia in adults".)
There are three settings other than primary polydipsia in which the urine osmolality may be below 100 mosmol/kg:
Malnutrition, described primarily in beer drinkers (called beer drinkers potomania), in which dietary solute intake (sodium,
potassium, protein) and therefore solute excretion is so low that the rate of water excretion is markedly diminished even though
urinary dilution is intact. (See "Causes of hyponatremia in adults", section on 'Low dietary solute intake'.)
Reset osmostat, in which a water load appropriately suppresses ADH release but at a lower serum osmolality than in normal
individuals. The major clinical clue to the presence of this disorder, which presents with clinical features similar to the SIADH, is
a moderately reduced plasma sodium concentration (usually between 125 and 135 meq/L) that is stable on multiple
measurements. (See "Treatment of hyponatremia: Syndrome of inappropriate antidiuretic hormone secretion (SIADH) and reset
osmostat", section on 'Reset osmostat'.)
The urine osmolality will also be below 100 mosmol/kg if it is measured after the reason for ADH release has been corrected
(eg, following volume expansion with isotonic saline in a patient with hypovolemia or reversal of SIADH by cessation of an
offending drug or glucocorticoid replacement in adrenal insufficiency). In such patients, the low urine osmolality heralds the
spontaneous and rapid correction of hyponatremia. (See "Overview of the treatment of hyponatremia in adults", section on 'Treat
the underlying disease'.)

Urine sodium and chloride concentration In patients with hyponatremia, hypoosmolality, and an inappropriately concentrated
urine, the urine sodium and, in certain settings, the urine chloride concentrations can be used to distinguish between
hyponatremia caused by effective circulating volume depletion (true hypovolemia, heart failure, and cirrhosis) and that caused
by euvolemic hyponatremia (most often due to SIADH) [2]:
The urine sodium concentration is usually below 25 meq/L in hypovolemia, unless there is renal salt wasting, due most often to
diuretic therapy and infrequently to adrenal insufficiency or cerebral salt wasting [5]. (See "Cerebral salt wasting".)
The urine sodium concentration is usually above 40 meq/L in patients with the SIADH who are normovolemic and whose rate
of sodium excretion is determined by sodium intake, as it is in normal individuals [5,11,12].
In hypovolemic hyponatremic patients who have metabolic alkalosis caused by vomiting, the urine sodium concentration may
be greater than 25 meq/L, but the urine chloride concentration will be low (less than 25 meq/L).
The diagnostic value of the urine sodium concentration was illustrated in a study of 58 hyponatremic patients without edema [5].
The mean urine sodium concentration was 18 meq/L in patients who were judged to be hypovolemic (as determined by a
significant rise in serum sodium following isotonic saline) compared to 72 meq/L in those with SIADH (as determined by no
increase in serum sodium following isotonic saline). In contrast to the utility of the urine sodium concentration, clinical
assessment of volume status correctly identified only 48 percent of patients.
In addition to the initial value, serial monitoring of the urine sodium concentration may be helpful in selected cases in which the
correct diagnosis may not be apparent. Suppose, for example, that the urine sodium concentration falls from 50 to
10 meq/L following the administration of 1 to 2 L of isotonic saline. Surreptitious diuretic ingestion should be suspected in this
setting. The urine sodium concentration was elevated on the first measurement because of the action of the diuretic. Once this
wore off, the true state of volume depletion was unmasked even though the hypovolemia had been partially corrected. (See
"Diuretic-induced hyponatremia".)
In another example, suppose that the initial urine sodium concentration is 35 meq/L, an intermediate value that could be seen
with either true hypovolemia (ie, not heart failure or cirrhosis) or SIADH. Serial monitoring of the urine osmolality and urine
sodium concentration in response to the administration of isotonic saline (or salt tablets) can help to clarify the diagnosis:
If the patient is hypovolemic, isotonic saline should suppress the hypovolemic stimulus to ADH release, promoting the excretion
of a dilute urine (urine osmolality usually less than 100 mosmol/kg) and rapid correction of the hyponatremia
If the patient has SIADH, ADH release occurs independently of the volume status, and the urine osmolality will remain elevated
following isotonic saline therapy
In both disorders, the urine sodium concentration will increase with saline therapy, although the increase in hypovolemic patients
will not be seen until the hypovolemia is mostly corrected.
Urine to serum electrolyte ratio The sum of the urine sodium plus potassium concentrations divided by the serum sodium
concentration has been called the urine to serum (or urine to plasma) electrolyte ratio [13]. A ratio less than 0.5 (meaning that
the tonicity of the urine is likely less than half that of the serum) indicates that urinary losses of electrolyte-free water are high
and that fluid restriction may therefore be effective. In contrast, a urine to serum electrolyte ratio greater than 1 indicates that the
urine is hypertonic compared to the serum and that other therapeutic measures in addition to fluid restriction will be necessary to
correct the hyponatremia.
Fractional excretion of sodium In patients with acute kidney injury, the fractional excretion of sodium (FENa) provides a more
accurate assessment of volume status than the urine sodium concentration because it corrects for the effect that variations in
urine volume have on the urine sodium. A FENa below 1 percent suggests effective volume depletion, while a value about 2
percent suggests acute tubular necrosis. (See "Fractional excretion of sodium, urea, and other molecules in acute kidney injury
(acute renal failure)".)
This observation has led some clinicians to use the FENa in any situation in which measurement of the urine sodium
concentration might be helpful. Calculators for the FENa are available using either standard units (calculator 1) or SI units
(calculator 2).
However, such an approach can lead to an erroneous diagnosis. A urine sodium concentration less than 25 meq/L suggests
effective volume depletion independent of the glomerular filtration rate. In contrast, a FENa below 1 percent as an indicator of
effective volume depletion applies only to patients with advanced renal failure; it does not apply to patients with normal or mild
to moderate renal dysfunction who have a much higher glomerular filtration rate and a much greater filtered sodium load.

As an example, patients with a normal glomerular filtration rate of 180 L/day (125 mL/min) have a filtered sodium load of
approximately 27,000 meq/day at a normal serum sodium concentration. The FENa that is diagnostic of effective volume
depletion may be as low as 0.1 percent, which represents the excretion of 27 meq of sodium per day. In contrast, patients with
SIADH are euvolemic and urinary sodium excretion is roughly equal to dietary sodium intake. Since sodium intake is usually less
than 270 meq/day, the FENa is typically less than 1 percent. These issues are discussed in detail elsewhere. (See "Fractional
excretion of sodium, urea, and other molecules in acute kidney injury (acute renal failure)".)
Serum uric acid and urea concentrations The initial water retention and volume expansion in the SIADH is frequently
associated with hypouricemia (serum uric acid concentration less than 4 mg/dL or 238 micromol/L) due to increased uric acid
excretion in the urine [11,14-16].
It is presumed that the early volume expansion diminishes proximal sodium reabsorption, leading to a secondary decline in the
net reabsorption of uric acid and increased uric acid excretion. However, stimulation of the vasopressor V1a receptor (which
primarily causes vasoconstriction) may also contribute to the uric acid wasting via an uncertain mechanism. If hyponatremia is
induced in normal volunteers with desmopressin (dDAVP), an agent that stimulates the V2 receptor (which primarily mediates
the antidiuretic response) but not the V1a receptor, the serum uric acid concentration does not fall as much (29 versus 53
percent) as it does in patients with a similar degree of hyponatremia caused by the SIADH (in which the native hormone
stimulates both the V1a and V2 receptors) [17]. (See "Hypouricemia: Causes and clinical significance".)
Hypervolemia (and perhaps V1a receptor stimulation) also increases urinary urea clearance. Thus, in hyponatremia due to
SIADH, the blood urea nitrogen (BUN) is usually less than 5 mg/dL (1.8 mmol/L) [15,18]. However, in older patients with SIADH,
the BUN is seldom this low because of the decreased fractional excretion of urea that occurs with aging [19]. Thus, the absence
of a low BUN cannot be used to exclude SIADH in older patients.
Similar reductions in uric acid and urea levels can occur in patients with thiazide diuretic-induced hyponatremia in whom water
overload, rather than volume depletion, is the primary cause of the hyponatremia [20]. (See "Diuretic-induced hyponatremia",
section on 'Impaired water excretion'.)
Acid-base and potassium balance Evaluation of acid-base and potassium balance may be helpful in selected hyponatremic
patients in whom the diagnosis is not apparent. As examples, metabolic alkalosis and hypokalemia suggest diuretic use or
vomiting, metabolic acidosis and hypokalemia suggest diarrhea or laxative abuse, and metabolic acidosis and hyperkalemia
suggest primary adrenal insufficiency in patients without renal failure [2]. (See "Hyponatremia and hyperkalemia in adrenal
insufficiency".)
On the other hand, the serum bicarbonate and potassium concentrations are typically normal in the SIADH [11]. Although water
retention tends to lower these values by dilution (as it does the plasma sodium and chloride concentrations), normal levels are
restored by the factors that regulate acid-base and potassium balance. The release of potassium from cells in an attempt to
minimize cell swelling induced by hypoosmolality is an additional factor that will raise the serum potassium concentration to
normal [11] and increased acid excretion due to mild hyperaldosteronism induced by hyponatremia can raise the plasma
bicarbonate concentration [11,21]. (See "Manifestations of hyponatremia and hypernatremia".)
Patients with hypopituitarism develop hyponatremia with many features of the SIADH (including normal serum potassium and
low BUN and serum uric acid) because they lack cortisol but not aldosterone. However, they tend to have slightly lower plasma
bicarbonate concentrations than do other patients with the SIADH, most likely because of lower plasma aldosterone levels [21].
Findings in SIADH Given the importance of diagnosing the SIADH in patients with hyponatremia, it is worthwhile to
summarize the general findings in this disorder and the laboratory tests that should be performed [22]:
A low serum osmolality
An inappropriately elevated urine osmolality (above 100 mosmol/kg and usually above 300 mosmol/kg)
A urine sodium concentration usually above 40 meq/L
Low blood urea nitrogen and serum uric acid concentration
A relatively normal serum creatinine concentration
Normal acid-base and potassium balance
Normal adrenal and thyroid function

(See "Pathophysiology and etiology of the syndrome of inappropriate antidiuretic hormone secretion (SIADH)".)
As noted above, patients with SIADH will have a low urine sodium concentration if they are also volume depleted or if their
sodium intake is extremely low. In such patients, the diagnosis of SIADH is made by observing the response to a saline load: the
urine sodium rises as the hypovolemia is corrected but the urine osmolality remains high. (See 'Urine sodium and chloride
concentration' above.)
Measurement of plasma ADH levels has no role in the routine diagnosis of SIADH.
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Basics topics (see "Patient information: Hyponatremia (The Basics)")
SUMMARY AND RECOMMENDATIONS The diagnosis of hyponatremia is based upon a combination of findings on history,
physical examination, appropriate laboratory tests, and, in selected patients, assessing the response to volume expansion with
isotonic saline.
The history and physical examination in hyponatremic patients should be directed toward identification of findings that are
typical of the particular causes of hyponatremia and assessment of volume status (table 1). These include a history of fluid loss
with associated clinical findings, an edematous state such as heart failure or cirrhosis, or a cause of the syndrome of
inappropriate antidiuretic hormone (ADH) secretion. (See 'History and physical examination' above.)
In the initial evaluation, we recommend obtaining six laboratory tests: chemistry panel, serum osmolality, urine osmolality, and
urine sodium, potassium, and chloride concentrations.
Chemistry panel A laboratory panel that includes serum electrolytes, urea nitrogen, creatinine, and glucose concentrations
may identify hyponatremia due to hyperglycemia or renal failure. In addition, low or high serum potassium or bicarbonate
concentrations may be useful. As an example, hypokalemia and metabolic acidosis favor diarrhea or laxative abuse as the
cause of hyponatremia, while hypokalemia and metabolic alkalosis suggest vomiting or diuretic therapy. (See 'Acid-base and
potassium balance' above.)
Serum osmolality Most cases of hyponatremia are associated with a reduced serum osmolality (Sosm) since sodium salts are
the main determinant of Sosm. However, the Sosm can be normal or elevated in selected causes of hyponatremia (table 1). The
most important causes are marked hyperglycemia in patients with uncontrolled diabetic mellitus and advanced renal failure. In
patients with renal failure, the increase in Sosm above that expected from the serum sodium concentration is due to the
retention of urea, which is an ineffective osmole since it equilibrates across the cells. These patients have a low effective serum
osmolality if the osmotic contribution of urea is subtracted from the measured value. (See 'Serum osmolality' above.)
Urine osmolality A urine osmolality (Uosm) of more than 100 mosmol/kg (and usually substantially higher) is consistent with
an inability to normally excrete free water, which is generally due to continued secretion of ADH (table 1). A Uosm less than
100 mosmol/kg indicates appropriate suppression of ADH may be due to primary polydipsia or certain other causes. (See 'Urine
osmolality' above.)
Urine sodium and chloride concentrations The urine sodium concentration is used to help distinguish between effective
volume depletion and other causes of hyponatremia in which normovolemia is present. The urine sodium should be less
than 25 meq/L with hypovolemia unless there is salt wasting due, for example, to diuretic therapy. By comparison, the urine
sodium is generally above 40 meq/L in the SIADH. In patients with intermediate values, serial monitoring of the urine sodium
concentration in response to isotonic saline should be performed. The urine chloride rather than the urine sodium is used to
identify volume depletion in patients with metabolic alkalosis due to gastric fluid losses. (See 'Urine sodium and chloride
concentration' above.)

Urine to serum electrolyte ratio The sum of urine sodium plus potassium divided by the serum sodium concentration is helpful
in predicting the response of the serum sodium concentration to therapeutic fluid restriction. (See 'Urine to serum electrolyte
ratio' above.)
In patients in whom the diagnosis is not apparent after the above initial evaluation, measurement of the serum uric acid and
urea concentrations, the fractional excretion of sodium, and adrenal and thyroid function tests may be helpful. (See 'Serum uric
acid and urea concentrations' above.)
The diagnosis of SIADH is usually made from the history, physical examination (no edema or signs of hypovolemia), and
laboratory tests. (See 'Findings in SIADH' above.)