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Acid-base and electrolyte abnormalities with

diarrhea
Acid-base and electrolyte abnormalities with diarrhea
Authors:
Michael Emmett, MD

Biff F Palmer, MD
Section Editor:
Richard H Sterns, MD

Deputy Editor:
John P Forman, MD, MSc

Literature review current through: Dec 2022. | This topic last updated: Jul 11, 2022.

INTRODUCTION — Diarrhea can cause a variety of fluid volume, acid-base,

and electrolyte abnormalities. The alterations in serum chemistries that can occur, their
etiologic mechanisms, and the issues related to diagnosis and treatment are reviewed in
this topic.

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FLUID AND ELECTROLYTE CONTENTYour OFactivity: 25 p.v.

NORMAL STOOL — The composition of normal and diarrheal stool must
be known in order to understand the consequences of diarrhea:

●Normal stool has an alkaline pH.

●Sodium and potassium salts are the primary stool solutes. The sodium plus potassium
concentration in stool usually ranges between 130 and 150 mEq/L. Other cations, such as
calcium and magnesium, are present at much lower concentrations.

●The main inorganic stool anions are bicarbonate (approximately 30 mEq/L), chloride
(approximately 10 to 20 mEq/L), and a small amount of phosphate and sulfate.

●Various organic acid anions (eg, propionate and butyrate, approximately 80 to 90 mEq/L)
account for most of the anions in normal stool [1-4].

Organic acid anions represent "decomposed bicarbonate" and can also be considered
"potential bicarbonate." When bicarbonate salts enter the colon and encounter strong
organic acids, such as lactic and butyric acid, which have been produced by bacterial
fermentation of non-absorbed food, mainly carbohydrates, the bicarbonate is titrated by
the dissociated hydrogen ions to form carbon dioxide and water (ie, decomposition of
bicarbonate). What remain are sodium and potassium salts of the organic acid anions.
These organic acid anions also represent "potential bicarbonate" because, if they are
absorbed, they will be converted back to bicarbonate by the body. Thus, losing these
organic anions in the stool as sodium or potassium salts has the same acid-base effect as
losing sodium or potassium bicarbonate.

●Stool water osmolality is similar to the osmolality of serum (approximately 300 mOsm/kg).
Although the stomach is capable of maintaining an osmotic gradient, more distal segments
of the bowel are permeable to water, and therefore, the luminal contents are in osmotic
equilibrium with the serum by the time the fluid has passed the ligament of Treitz [1-4].

It must be emphasized that, normally, only approximately 100 mL of water is excreted in the
stool each day. Thus, despite the high stool electrolyte concentrations, only approximately 4
mEq of sodium and 9 mEq of potassium are lost in normal stool each day, and the total daily
loss of bicarbonate plus organic acid anion salts is only approximately 11 mEq/day [1,2,4].

FLUID, ELECTROLYTE, AND NON-

ELECTROLYTE CONTENT OF DIARRHEA — When
diarrhea develops, stool osmolality remains similar to serum (approximately 300 mOsm/L).

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Depending upon the etiology of the diarrhea, osmotically active solutes in diarrheal stool
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may be electrolytes, magnesium salts, phosphate salts, substances derived from
carbohydrates such as mannitol, sorbitol, or lactulose, the bacterial fermentation products
of these substances (ie, lactic, butyric, acetic acid, and others), large synthetic molecules
such as polyethylene glycol (PEG), and combinations of these substances. Some forms of
diarrhea may be primarily due to fat malabsorption (ie, steatorrhea); stool volumes in such
patients are generally small but may increase markedly if the steatorrhea is also associated
with carbohydrate malabsorption.

The origin of osmotically active molecules in stool may be endogenous, exogenous, or both.
Examples of diarrhea due to loss of endogenous osmotic molecules include:

●Cholera toxin or enteropathic Escherichia coli causes secretory diarrhea by increasing

intestinal secretion of sodium, potassium, chloride, and bicarbonate, and by variably
impairing their reabsorption. These ions are then eliminated with enough water to create
stool with an osmolality of approximately 300 mOsm/L. The diarrhea generated by
Clostridioides difficile infection (CDI) can also have a major secretory etiology.

●Certain tumors secrete hormones such as vasoactive intestinal peptide (VIP) that can cause
marked gastrointestinal electrolyte secretion and massive, watery, electrolyte-rich diarrhea.

●A mutation in a gastrointestinal chloride-bicarbonate exchanger causes the loss of

endogenous chloride salts and a chloride-rich diarrhea (congenital chloridorrhea).

Examples of diarrhea due to loss of exogenous osmotic molecules include:

●Ingestion of poorly absorbed carbohydrates, such as lactose (in lactase-deficient patients),

lactulose, sorbitol, or mannitol, generates diarrhea that is relatively electrolyte poor.

●Ingestion of high doses of magnesium or phosphate salts overwhelm gastrointestinal

absorptive processes, thereby causing diarrhea in which the major osmotically active agent
is the ingested salt.

ACID-BASE, ELECTROLYTE, AND VOLUME

ABNORMALITIES ASSOCIATED WITH
DIARRHEA — Common derangements that can result from diarrhea include the
following:

●Hypovolemia, which can reduce glomerular filtration rate, and, when severe, generate
shock (see 'Hypovolemia' below)

●Metabolic acidosis (see 'Metabolic acidosis' below)

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●Hypokalemia (see 'Hypokalemia' below)

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Less commonly, the following abnormalities may be seen:

●Hypernatremia (see 'Hypernatremia' below)

●Metabolic alkalosis (see 'Metabolic alkalosis' below)

Hypovolemia — Because stool water is relatively isotonic and typically electrolyte-

rich, large-volume diarrhea can generate marked volume depletion. Volume depletion will
stimulate ADH secretion, and if excessive quantities of water are ingested, hyponatremia
may develop. (See "Causes of hypotonic hyponatremia in adults".)

The treatment of severe hypovolemia is discussed in detail elsewhere. (See "Treatment of

severe hypovolemia or hypovolemic shock in adults".)

Metabolic acidosis — The most common acid-base disorder that develops in

patients with diarrhea is metabolic acidosis. Although some bicarbonate is present in stool,
it is usually the loss of salts of organic acid anions (eg, propionate, lactate, acetate, and
butyrate) that is the most important cause of metabolic acidosis in patients with diarrhea.
The loss of large quantities of sodium or potassium salts of organic acid anions (which
represent potential bicarbonate) is physiologically equivalent (from an acid-base
perspective) to losing equal quantities of sodium or potassium bicarbonate. Because
potential bicarbonate usually exceeds actual bicarbonate in diarrheal stool, the stool pH can
be acidic. Thus, stool pH is generally of little importance in the determination of how
diarrhea will impact systemic acid-base balance. A better index is the mathematical
difference between the sum of the stool sodium plus potassium concentration and the stool
chloride concentration; this difference approximates the concentration of stool bicarbonate
plus organic acid anion salts (potential bicarbonate).

Diarrhea caused by cholera is more commonly associated with high stool concentrations of
true bicarbonate. These patients generally have markedly reduced oral intake and therefore
limited delivery of carbohydrate and other substrates to the colon. Thus bacterial
fermentation products that would react with bicarbonate are limited.

In addition to the loss of potential and actual bicarbonate salts, several other factors often
contribute to the metabolic acidosis that develops in patients with diarrhea:

●Hypovolemia will reduce the glomerular filtration rate and accelerate renal salt
reabsorption. The resulting decrease in sodium delivery to the distal tubule impairs renal
acid excretion. (See "Overview and pathophysiology of renal tubular acidosis and the effect
on potassium balance" and 'Evaluating the renal response to metabolic acidosis in patients
with diarrhea' below.)
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●Severe hypovolemia reduces tissue perfusion and can generate an element of lactic
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acidosis. (See "Causes of lactic acidosis".)

●If the diarrhea is associated with prolonged anorexia and fasting, ketoacidosis may
develop. (See "Fasting ketosis and alcoholic ketoacidosis".)

Serum anion gap in patients with metabolic acidosis due

to diarrhea — Patients with large-volume diarrhea who lose a large amount of
bicarbonate and potential bicarbonate (eg, propionate, butyrate, lactate, citrate salts) will
generally develop a normal anion gap (ie, hyperchloremic) acidosis. (See "Approach to the
adult with metabolic acidosis".)

However, severe diarrhea with volume depletion can also cause a high anion gap acidosis as
a result of the following [5,6]:

●Lactic acidosis, which can result from decreased tissue perfusion when severe
hypovolemia develops.

●Hyperphosphatemia, which can result from the combination of a reduced glomerular

filtration rate and acidemia-induced release of intracellular phosphate into the extracellular
fluid.

●Reduced kidney function can increase the concentration of other "unmeasured" acid
anions.

●Increased serum albumin concentration, which can result from hemoconcentration;

negative charges on albumin constitute a large part of the anion gap, and therefore, high
albumin concentrations elevate the anion gap.

Thus, in patients with diarrhea, the fall in the serum bicarbonate concentration may be
partially balanced by a rise in chloride concentration and partially by a rise of the anion gap
[6]. (See "The delta anion gap/delta HCO3 ratio in patients with a high anion gap metabolic
acidosis".)

Evaluating the renal response to metabolic acidosis in

patients with diarrhea — The normal renal response to metabolic acidosis is to
increase acid excretion. Initially, urine pH falls and titratable acid excretion increases. If the
acidosis persists, then renal ammonia synthesis and excretion also increase. In general, if
the metabolic acidosis persists for more than several days, the ammonia excretory response
to metabolic acidosis exceeds the increase in titratable acid. (See "Urine anion and osmolal
gaps in metabolic acidosis", section on 'Brief overview of renal acid excretion'.)

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If kidney function and kidney perfusion are normal, then the kidney can largely compensate
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for major losses of bicarbonate and potential bicarbonate that occur in patients with
diarrhea. However, if the diarrhea generates hypovolemia, this will simultaneously reduce
glomerular filtration and markedly enhance proximal renal tubule sodium and chloride
reabsorption. The resulting decrease in distal tubule sodium chloride delivery reduces renal
acid secretion and excretion. (See "Overview and pathophysiology of renal tubular acidosis
and the effect on potassium balance".)

The renal response to metabolic acidosis in patients with diarrhea can be evaluated by
measuring the changes in creatinine concentration, the urine pH, and the urine sodium
concentration. Calculation of the urine anion or osmolal gap may also be helpful in
assessing the renal response to diarrhea-induced metabolic acidosis. (See 'Urine pH and
urine ammonium and sodium concentrations' below.)

Urine pH and urine ammonium and sodium

concentrations — Acute metabolic acidosis should increase distal tubule hydrogen ion
secretion and initially reduce urine pH below 5.5. However, if the acidosis persists and
becomes chronic, a major increase in urine ammonium excretion will develop. This large
increase in urine ammonium will increase the urine pH. The development of potassium
depletion and hypokalemia will further increase renal ammonia generation and excretion.
High urine ammonia (NH3) concentrations bind hydrogen ions (H+) to form ammonium
(NH4+) and thereby raise the urine pH:

 NH3 + H+  ↔  NH4+

Thus, a relatively high urine pH in a patient with chronic metabolic acidosis does not
necessarily indicate the existence of a renal acidification defect. (See "Urine anion and
osmolal gaps in metabolic acidosis", section on 'Urine anion gap'.)

If the urine pH is relatively high (greater than 5.5) in a patient with diarrhea and metabolic
acidosis, measurement or estimation of urine ammonium excretion can be used to
determine if the renal response is appropriate. If urine ammonium measurements are not
available, a helpful surrogate marker for urine ammonium is the calculated urine osmolal
gap [7]. This calculation indirectly estimates the urine ammonium concentration. A high
urine ammonium concentration is consistent with a normal renal response to metabolic
acidosis, despite a high urine pH. (See "Urine anion and osmolal gaps in metabolic
acidosis".)

If the renal response to metabolic acidosis is inadequate, then the urine sodium
concentration should be measured. If it is less than 25 mEq/L, inadequate distal sodium
chloride delivery due to hypovolemia may be the cause of inadequate renal distal tubule

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acid secretion and excretion. The evaluation of renal acidification should be repeated after
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volume status has been restored.

Hypokalemia — The potassium concentration in stool water is normally relatively

high. Although the potassium concentration falls as stool volume increases, large-volume
diarrhea commonly results in hypokalemia due to stool potassium loss. Hypokalemia can
occur with all forms of diarrhea but is especially common with diarrhea due to cholera,
certain pancreatic islet cell tumors (VIPomas), villous adenomas, congenital chloride-
wasting diarrhea, and laxative abuse [2,3,8]. Some patients with intestinal pseudo-
obstruction secrete large amounts of potassium into the colonic fluid and develop marked
hypokalemia [9]. (See "Causes of hypokalemia in adults", section on 'Increased
gastrointestinal losses'.)

Two common causes of hyperchloremic (ie, normal anion gap) metabolic acidosis and
hypokalemia are diarrhea and proximal or distal tubule RTA. The hypokalemia of diarrhea is
mainly caused by stool potassium loss (and reduced intake), while the hypokalemia of
proximal or distal tubule RTA is due to renal potassium loss. The hypokalemia that develops
in patients with congenital chloride-wasting diarrhea is an exception to this paradigm; it is
largely due to renal potassium losses. In most cases, measurement of urinary potassium
excretion may help to distinguish between gastrointestinal and renal losses of potassium
(see "Overview and pathophysiology of renal tubular acidosis and the effect on potassium
balance" and "Evaluation of the adult patient with hypokalemia"):

●The hypokalemia that develops in patients with hyperchloremic metabolic acidosis due to
proximal or distal tubule RTA is largely due to renal potassium loss, and the urine potassium
concentrations are generally greater than 25 mEq/L.

●By contrast, when hypokalemia is due to gastrointestinal loss, the kidney conserves
potassium, and the urine potassium concentration is typically less than 25 mEq/L. When
severe hypovolemia results in secondary hyperaldosteronism, the urine potassium
concentration may increase above 25 mEq/L. However, under those conditions, the urine
volume will be low, and therefore, daily urinary potassium excretion will be quite low
despite the relatively high potassium concentration. The daily potassium excretion rate can
be measured with a 24-hour urine collection or estimated using the urine potassium-to-
creatinine ratio [10].

Hypernatremia — Diarrhea is sometimes due to the presence of non-electrolyte,

osmotically active substances in the stool, such as carbohydrates or organic anion salts
generated by bacterial metabolism of carbohydrates. This can occur in patients with
malabsorption, or after ingestion of nonabsorbable carbohydrates such as mannitol,
sorbitol, or lactulose. In addition, ingestion of other non-carbohydrate, non-electrolyte

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substances such as polyethylene glycol (PEG) can also generate diarrhea. These osmotically
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active substances obligate enough water to maintain the osmolality of the gastrointestinal
lumen and stool at approximately 300 mOsm/L (ie, similar to serum).

Since the osmolality of stool water in these conditions is largely due to non-electrolytes, the
diarrhea represents the loss of electrolyte-free water. Large-volume diarrhea due to these
mechanisms, with large electrolyte-free water loss, can generate hypernatremia [1-3,11,12].
However, the development of hypernatremia is uncommon in such patients if they have
access to water and are able to respond normally to thirst. Hypernatremia may develop in
those who do not experience or respond to thirst normally, such as patients with impaired
mental status or infants who experience thirst but require others to provide fluid intake.
(See "Etiology and evaluation of hypernatremia in adults".)

Metabolic alkalosis — Although uncommon, some patients with diarrhea

develop metabolic alkalosis rather than metabolic acidosis. This occurs in a rare disease
called congenital chloride wasting diarrhea (congenital chloridorrhea) (see 'Congenital
chloride wasting diarrhea' below). It can also develop in patients who chronically abuse
laxatives. (See 'Laxative abuse' below.)

Congenital chloride wasting diarrhea — Metabolic alkalosis and

hypokalemia occur in patients with congenital chloride wasting diarrhea (congenital
chloridorrhea). This disorder is due to a mutation in the "down-regulated in adenoma," or
the DRA, gene that encodes an intestinal Cl-/HCO3- exchanger (SLC26A3) that normally
absorbs chloride from the intestinal lumen and secretes bicarbonate.

The mutation markedly reduces the activity of this chloride-bicarbonate exchanger and
results in very high stool chloride concentrations (>100 mEq/L). The stool chloride
concentration generally exceeds the sum of the stool sodium and potassium
concentrations. The difference between stool chloride and the sum of sodium and
potassium is largely ammonium (NH4) and organic cations. The excretion of chloride salts of
NH4 and organic cations in the stool generates a systemic alkali load and results in
metabolic alkalosis [13,14]. These patients also become hypokalemic and potassium
depleted because they lose potassium (with bicarbonate) in the urine. The mechanism of
urinary potassium loss in this disorder is similar to that responsible for the loss of urine
potassium that occurs with vomiting and other gastric fluid losses. (See "Causes of
hypokalemia in adults", section on 'Upper gastrointestinal losses'.)

The etiology and treatment of this disorder are discussed in greater detail elsewhere. (See
"Approach to chronic diarrhea in neonates and young infants (<6 months)", section on
'Evaluation for suspected congenital diarrheas and enteropathies'.)

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Laxative abuse — Chronic laxative abuse can produce chronic hypovolemia and25 p.v.
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hypokalemia. Such patients may develop metabolic acidosis, metabolic alkalosis, or have no
systemic acid-base disorder [15-17].

When metabolic alkalosis develops, it is probably generated by the combination of severe

hypokalemia, potassium depletion, and hypovolemia. Hypokalemia generates and
maintains metabolic alkalosis via a number of mechanisms (see "Potassium balance in acid-
base disorders"):

●Hypokalemia causes a shift of potassium from the intracellular fluid (ICF) to the
extracellular fluid (ECF) and simultaneous movement of hydrogen ions from the ECF into the
ICF. This produces a relative intracellular acidosis (including acidification of the cells of the
proximal and distal tubules) and increases the extracellular bicarbonate concentration.

●Intracellular acidosis in proximal tubule cells increases ammonia generation and secretion
into the renal tubule.

●Intracellular acidosis in distal tubule cells stimulates hydrogen ion secretion, which
increases renal excretion of both titratable acid and ammonium. Hydrogen ion secretion
causes bicarbonate reabsorption and bicarbonate generation (figure 1).

●Hypokalemia also increases distal tubule acidification by stimulating hydrogen-potassium

exchange via the distal tubule H-K-ATPase exchanger, which reabsorbs and thereby
conserves potassium when it secretes hydrogen ions (figure 1) [18].

●Although several reports hypothesize that severe hypokalemia may produce an acquired
form of intestinal chloridorrhea, this remains unproven [14]. (See 'Congenital chloride
wasting diarrhea' above.)

Another important consideration is that a patient who surreptitiously ingests laxatives may
also be surreptitiously taking diuretics, which can generate metabolic alkalosis.

Thus, occult, or surreptitious, laxative abuse should be considered when patients present
with unexplained hypokalemia. Their acid-base status may be normal, or they may have a
metabolic acidosis (usually hyperchloremic) or a metabolic alkalosis. (See "Evaluation of the
adult patient with hypokalemia".)

If the laxative contains magnesium salts, then hypermagnesemia may develop. Magnesium-
induced diarrhea can occasionally develop in patients who ingest magnesium-rich antacids
or food supplements [11,17]. (See "Factitious diarrhea: Clinical manifestations, diagnosis,
and management".)

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If surreptitious laxative-related diarrhea is suspected, stool and/or urine can be analyzed for
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laxatives. However, the assays for senna and bisacodyl, two common ingredients in readily
available laxatives, are unreliable [19]. Although a room search for laxatives (and diuretics)
can be diagnostic, it is a procedure which raises significant legal and ethical issues. (See
"Factitious diarrhea: Clinical manifestations, diagnosis, and management", section on
'Evaluation'.)

TREATMENT — The treatment of diarrhea and the common, associated acid-

base and electrolyte abnormalities are discussed in other topics:

●Treatment of diarrhea (see "Approach to the adult with acute diarrhea in resource-limited
countries" and "Approach to the adult with acute diarrhea in resource-rich settings" and
"Oral rehydration therapy")

●Treatment of hypovolemia (see "Treatment of hypovolemia (dehydration) in children" and

"Maintenance and replacement fluid therapy in adults" and "Treatment of severe
hypovolemia or hypovolemic shock in adults")

●Treatment of metabolic acidosis (see "Approach to the child with metabolic acidosis" and
"Approach to the adult with metabolic acidosis")

●Treatment of hypokalemia (see "Clinical manifestations and treatment of hypokalemia in

adults")

SOCIETY GUIDELINE LINKS — Links to society and government-

sponsored guidelines from selected countries and regions around the world are provided
separately. (See "Society guideline links: Fluid and electrolyte disorders in adults".)

SUMMARY
●Knowledge of the composition of normal stool water and of diarrheal stool water is
necessary to understand the impact of diarrhea on body fluids, electrolytes, and acid-base
status. (See 'Fluid and electrolyte content of normal stool' above and 'Fluid, electrolyte, and
non-electrolyte content of diarrhea' above.)

●Common derangements that can result from diarrhea include the following (see 'Acid-
base, electrolyte, and volume abnormalities associated with diarrhea' above):

•Hypovolemia, which, if combined with excessive water ingestion, can result in

hyponatremia (see 'Hypovolemia' above)

•Metabolic acidosis, usually with a normal anion gap (see 'Metabolic acidosis' above)

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•Hypokalemia (see 'Hypokalemia' above)

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●Less commonly, the following abnormalities may be seen in patients with diarrhea (see
'Acid-base, electrolyte, and volume abnormalities associated with diarrhea' above):

•Hypernatremia, which can occur in patients with electrolyte-poor diarrhea who do not
experience or respond to thirst normally (see 'Hypernatremia' above)

•Metabolic alkalosis, which can be seen in patients with congenital chloride wasting
diarrhea and in some patients who chronically abuse laxatives (see 'Metabolic alkalosis'
above)

●The treatment of diarrhea and the common, associated acid-base and electrolyte
abnormalities are discussed elsewhere. (See "Approach to the adult with acute diarrhea in
resource-limited countries" and "Approach to the adult with acute diarrhea in resource-rich
settings" and "Oral rehydration therapy" and "Treatment of hypovolemia (dehydration) in
children" and "Maintenance and replacement fluid therapy in adults" and "Treatment of
severe hypovolemia or hypovolemic shock in adults" and "Approach to the child with
metabolic acidosis" and "Approach to the adult with metabolic acidosis" and "Clinical
manifestations and treatment of hypokalemia in adults".)
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Sci 1987; 32:1033.
2. Gennari FJ, Weise WJ. Acid-base disturbances in gastrointestinal disease. Clin J Am Soc
Nephrol 2008; 3:1861.
3. Steffer KJ, Santa Ana CA, Cole JA, Fordtran JS. The practical value of comprehensive stool
analysis in detecting the cause of idiopathic chronic diarrhea. Gastroenterol Clin North
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hyperproteinemia, lactic acidemia, and hyperphosphatemia to an increased serum
anion gap. N Engl J Med 1986; 315:1591.
7. Uribarri J, Oh MS. The Urine Anion Gap: Common Misconceptions. J Am Soc Nephrol
2021; 32:1025.
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secretion by the human intestine. Gastroenterology 1994; 107:548.
9. van Dinter TG Jr, Fuerst FC, Richardson CT, et al. Stimulated active potassium secretion
in a patient with colonic pseudo-obstruction: a new mechanism of secretory diarrhea.
Gastroenterology 2005; 129:1268.
10. Palmer BF, Clegg DJ. The Use of Selected Urine Chemistries in the Diagnosis of Kidney
Disorders. Clin J Am Soc Nephrol 2019; 14:306.
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11. Donowitz M, Kokke FT, Saidi R. Evaluation of patients with chronic diarrhea. N Engl J
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Med 1995; 332:725.
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congenital chloride diarrhoea. Aliment Pharmacol Ther 2010; 31:477.
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Med 1991; 324:1012.
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triphosphatases by aldosterone and potassium. J Clin Invest 1993; 91:2385.
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Topic 2320 Version 20.0

References

1 : Acid-base disturbances in gastrointestinal disease.

2 : Acid-base disturbances in gastrointestinal disease.

3 : The practical value of comprehensive stool analysis in detecting the cause of idiopathic
chronic diarrhea.

4 : Speculations on the pathogenesis of diarrhea.

5 : Electrolyte disturbances in elderly patients with severe diarrhea due to cholera.

6 : The acidosis of cholera. Contributions of hyperproteinemia, lactic acidemia, and

hyperphosphatemia to an increased serum anion gap.

7 : The Urine Anion Gap: Common Misconceptions.

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Your activity: 25 p.v.

8 : Pathophysiology of potassium absorption and secretion by the human intestine.

9 : Stimulated active potassium secretion in a patient with colonic pseudo-obstruction: a new

mechanism of secretory diarrhea.

10 : The Use of Selected Urine Chemistries in the Diagnosis of Kidney Disorders.

11 : Evaluation of patients with chronic diarrhea.

12 : Hypernatremia due to repeated doses of charcoal-sorbitol.

13 : Review article: the clinical management of congenital chloride diarrhoea.

14 : CONGENITAL CHLORIDORRHOEA OR SO-CALLED CONGENITAL ALKALOSIS WITH

DIARRHOEA.

15 : Bulimarexia and related serious eating disorders with medical complications.

16 : Laxative abuse syndrome.

17 : Diagnosis of magnesium-induced diarrhea.

18 : Regulation of collecting tubule adenosine triphosphatases by aldosterone and potassium.

19 : Factitious diarrhea induced by stimulant laxatives: accuracy of diagnosis by a clinical

reference laboratory using thin layer chromatography.

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