CAUSAS DE HIPERCALEMIA

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CAUSAS DE HIPERCALEMIA

Mensagem  Renato de Oliveira em Dom Jan 27, 2013 5:48 pm

Causes and evaluation of hyperkalemia in
adults



INCREASED POTASSIUM RELEASE FROM CELLS


Pseudohyperkalemia — Pseudohyperkalemia refers to those
conditions in which the elevation in the measured serum potassium concentration
is usually due to potassium movement out of the cells during or after the blood
specimen has been drawn. The possible presence of pseudohyperkalemia should be
suspected when there is no apparent cause for the hyperkalemia in an
asymptomatic patient who has no electrocardiographic manifestations of
hyperkalemia.



Technique of blood drawing — Pseudohypokalemia can be seen in
a variety of settings. The most common causes are related to the technique of
blood drawing and can involve one or both of the following mechanisms:




  • Mechanical trauma during venipuncture can
    result in the release of potassium from red cells and a characteristic
    reddish tint of the serum due to the concomitant release of hemoglobin.

    Red serum can also represent severe intravascular hemolysis rather than a
    hemolyzed specimen. When intravascular hemolysis is present, the measured
    serum potassium may represent the true circulating value.

  • Potassium moves out of muscle cells with
    exercise. As a result, repeated fist clenching during blood drawing can
    acutely raise the serum potassium concentration by more than 1 to 2 meq/L
    in that forearm.



In these settings, venipuncture without a tourniquet, repeated fist
clenching, or trauma will demonstrate the true serum potassium concentration.
If a tourniquet is required, the tourniquet should be released after the needle
has entered the vein, followed by waiting for one to two minutes before
drawing the blood sample.



Less common causes of an increase in serum potassium related to
collection and storage include cooling of the sample and specimen deterioration
because of prolonged length of storage.



Other causes — There are several other settings in which
pseudohyperkalemia can occur:




  • Potassium moves out of platelets after
    clotting has occurred. Thus, the serum potassium concentration normally
    exceeds the true value in plasma by 0.1 to 0.5 meq/L. Although this
    difference in normal individuals is not clinically important, the increase
    in the measured serum potassium concentration can be much greater in
    normokalemic patients with thrombocytosis, rising by approximately 0.15
    meq/L per 100,000/microL elevation in the platelet count. In one study,
    hyperkalemia in a serum sample occurred in 34 percent of patients with a
    platelet count above 500,000/microL compared with 9 percent of patients
    with a platelet count less than 250,000/microL. The concentration of
    potassium in plasma (obtained by centrifugation of heparinized, unclotted
    blood) was normal.

    A similar phenomenon has been reported in acute myeloid leukemia. However,
    hypokalemia is more common in this disorder, due to movement
    of potassium into rapidly proliferating cells after the blood has been
    drawn (pseudohypokalemia) or to renal potassium wasting (true
    hypokalemia).

  • High white blood cell counts
    (>120,000/microL) caused by chronic lymphocytic leukemia can lead to
    falsely elevated potassium concentrations due to cell fragility. Unlike
    thrombocytosis, this form of pseudohyperkalemia occurs in both serum
    and plasma samples and may be more prominent when blood is sampled in
    heparinized tubes. Centrifugation of a heparinized tube causes in vitro
    cell destruction and release of potassium as these cells are freely
    suspended in plasma.

    Accurate assessment of the potassium concentration in this setting can be
    achieved by allowing clotting to separate serum (plasma without the
    clotting factors) from cells before centrifugation. The fibrin
    clot entraps and protects fragile leukemic cells, minimizing cell lysis.

    Pseudohyperkalemia in patients with very high white blood cell counts due
    to leukemia or lymphoma has also been reported after mechanical disruption
    of white blood cells during transport of blood samples via pneumatic tube
    systems.

  • Potassium can move out of red cells after the
    specimen is collected in patients with hereditary (familial) forms of
    pseudohyperkalemia, which are caused by an increase in the passive
    potassium permeability of erythrocytes. Pseudohyperkalemia may be the only
    manifestation of the disorder, or it may be accompanied by abnormal red
    cell morphology (eg, stomatocytosis), varying degrees of hemolysis, and/or
    perinatal edema in specific kindreds.
    This genetically heterogeneous condition is
    discussed in detail elsewhere.



Metabolic
acidosis
— In patients with metabolic acidosis other than organic
acidosis due to lactic acidosis or ketoacidosis, buffering of excess hydrogen
ions in the cells leads to potassium movement into the extracellular fluid, a
transcellular shift that is obligated in part by the need to maintain
electroneutrality
.


Although this shift will tend to raise the plasma potassium
concentration, some patients have concurrent potassium losses due to gastrointestinal
disease (eg, diarrhea) or increased urinary losses (eg, renal tubular
acidosis). In these settings, the measured serum potassium concentration may be
normal or reduced despite the presence of metabolic acidosis. However, the
plasma potassium will be higher than it would have been if the same degree of
potassium loss had occurred in the absence of metabolic acidosis.



Smaller effect in lactic acidosis or ketoacidosis — In
contrast to the above finding, hyperkalemia due to an acidosis-induced shift of
potassium from the cells into the extracellular fluid does not occur
in the organic acidoses lactic acidosis and ketoacidosis. A possible
contributory factor in both disorders is the ability of the organic anion and
the hydrogen ion to enter into the cell via a sodium-organic anion
cotransporter. The transport mechanisms involved and how they minimize
potassium movement out of the cells are discussed in detail elsewhere.



As described below, the development of hyperkalemia in patients with
diabetic ketoacidosis is primarily due to insulin deficiency and
hyperosmolality, not acidemia.



Smaller effect in respiratory acidosis — Hyperkalemia due to
respiratory acidosis is not a common clinical problem. The effect of
respiratory acidosis on the plasma potassium concentration has been primarily
evaluated in acute rather than chronic respiratory acidosis. In a review of the
available human data, respiratory acidosis produced no significant
effect on the plasma potassium, although the degree of acidemia in the reviewed
studies was usually mild (fall in plasma pH about 0.1); in addition, the
increase in plasma potassium for a given reduction in pH was smaller when the
fall in pH was induced by respiratory as compared with metabolic acidosis. The
effect of respiratory acidosis on the plasma potassium is greater with more
severe acidosis and with a longer duration of acidosis.The mechanisms
responsible for the lesser increase in plasma potassium in respiratory acidosis
compared with metabolic acidosis are not well defined.



Studies in animal models of acute respiratory acidosis have shown
variable increases in plasma potassium with the severity and duration of the
acidosis.
The
following illustrates the range of findings:




  • In a study in dogs, severe acute respiratory
    acidosis (a decrease in mean plasma pH from 7.4 to 7) had no effect on the
    plasma potassium at ten minutes but, at two and six hours, the plasma
    potassium had increased from 4 to 6 meq/L (approximately 0.5 meq/L per 0.1
    reduction in plasma pH). The increase in plasma potassium was due to
    potassium movement out of cells and was approximately twice as large when
    the ureters were ligated, suggesting a role for urinary excretion of some
    of the excess potassium.

  • As might be expected, other studies in dogs
    with less severe acute respiratory acidosis found no or only small
    elevations in the plasma potassium concentration.



Insulin
deficiency, hyperglycemia, and hyperosmolality
— Insulin
promotes potassium entry into cells. Thus, the ingestion of glucose
(which stimulates endogenous insulin secretion) minimizes the rise in the serum
potassium concentration induced by concurrent potassium intake
, while
glucose ingestion alone in patients without diabetes modestly lowers the serum
potassium
.


The findings are different in uncontrolled diabetes mellitus. In this
setting, the combination of insulin deficiency (either impaired secretion or
insulin resistance) and hyperosmolality induced by hyperglycemia frequently
leads to hyperkalemia even though there may be marked potassium depletion due
to urinary losses caused by the osmotic diuresis
.


The increase in plasma osmolality results in osmotic water movement from
the cells into the extracellular fluid. This is accompanied by potassium
movement out of the cells by two proposed mechanisms:




  • The loss of cell water raises the cell
    potassium concentration, thereby creating a favorable gradient for passive
    potassium exit through potassium channels in the cell membrane.

  • The friction forces between solvent (water)
    and solute can result in potassium being carried along with water through
    the water pores in the cell membrane. This phenomenon of solvent drag is
    independent of the electrochemical gradient for potassium diffusion.



Causes other than diabetes mellitus — Disorders other than
diabetes mellitus have been associated with hyperkalemia due to insulin
deficiency and/or hyperosmolality.
As examples:



  • Insulin levels fall in response to therapy
    with somatostatin or the somatostatin agonist, octreotide, and can lead to
    elevations in serum potassium. The magnitude of this effect varies with
    the clinical setting. In one study, for example, the mean increase in
    serum potassium was 0.5 to 0.6 meq/L in normal individuals and patients
    with type 2 diabetes; in contrast, there was no change in serum potassium
    in patients with type 1 diabetes since they make little or no insulin. The
    effect of somatostatin or octreotide is much greater in patients with
    end-stage renal disease requiring dialysis in whom the serum potassium can
    rise above 7 meq/L.

  • Fasting is associated with an appropriate
    reduction in insulin levels that can lead to an increase in plasma
    potassium. This may be a particular problem in dialysis patients.

    The risk of hyperkalemia during preoperative fasting can be minimized by
    the administration of insulin and glucose in patients with diabetes, or
    glucose alone in patients without diabetes
    .
  • In addition to hyperglycemia induced by insulin
    deficiency, hyperkalemia induced by hyperosmolality has also been
    described with hypernatremia, sucrose contained in intravenous immune
    globulin, radiocontrast media, and the administration of hypertonic
    mannitol.
    Most
    of the reported patients had renal failure.



Increased
tissue catabolism
— Any cause of
increased tissue breakdown leads to the release of intracellular potassium into
the extracellular fluid. Hyperkalemia can occur in this setting, particularly
if renal failure is also present. Clinical examples include trauma (including
non-crush trauma), the administration of cytotoxic or radiation therapy to
patients with lymphoma or leukemia (the tumor lysis syndrome), and severe
accidental hypothermia.



Beta
blockers
— Increased beta-2-adrenergic activity drives potassium into
the cells and lowers the serum potassium.



Beta blockers interfere with the beta-2-adrenergic facilitation of
potassium uptake by the cells, particularly after a potassium load
. An
increase in serum potassium is primarily seen with nonselective beta blockers
(such as propranolol and labetalol). In contrast, beta-1-selective blockers
such as atenolol have little effect on serum potassium since beta-2 receptor
activity remains intact.



The rise in serum potassium with nonselective beta blocker therapy is
usually less than 0.5 meq/L. True hyperkalemia is rare unless there is a large
potassium load, marked exercise (as described in the next section), or an
additional defect in potassium handling that prevents excretion of the excess
extracellular potassium, such as hypoaldosteronism or renal failure. In one
report, for example, three renal transplant recipients developed severe
hyperkalemia after the administration of labetalol for postoperative
hypertension.



Exercise — Potassium is normally released from muscle cells during
exercise. The increase in plasma potassium is rarely important clinically, with
the one major exception that fist clenching during blood drawing can interfere
with accurate assessment of the serum potassium concentration. Repeated fist
clenching during blood drawing can acutely raise the serum potassium concentration
by more than 1 meq/L in that forearm, thereby representing a form of
pseudohyperkalemia.



The increase in plasma potassium during exercise may be mediated by two
factors:




  • A delay between potassium exit from the cells
    during depolarization and subsequent reuptake into the cells via the
    Na-K-ATPase pump.

  • With marked exercise, an increased number of
    open potassium channels in the cell membrane. These channels are inhibited
    by ATP, an effect that is removed by the exercise-induced decline in ATP
    levels.



The release of potassium during exercise may have a physiologically
important role. The local increase in potassium concentration has a
vasodilator effect, thereby increasing blood flow and energy delivery to the
exercising muscle.



The degree of elevation in the plasma potassium concentration in the systemic
circulation
is less pronounced and varies directly with the degree of
exercise: 0.3 to 0.4 meq/L with slow walking; 0.7 to 1.2 meq/L with moderate
exertion (including prolonged aerobic exercise with marathon running); and as
much as 2 meq/L following exercise to exhaustion, which may be associated with
both ECG changes and lactic acidosis.



The peak increase in plasma potassium during exercise is less pronounced
with prior physical conditioning (perhaps due to increased Na-K-ATPase
activity) and more pronounced in patients treated with nonselective
beta blockers or those with end-stage renal disease even though there is often
a lesser degree of attained exercise.



The rise in plasma potassium concentration induced by exercise is
reversed after several minutes of rest and is typically associated with a mild
rebound hypokalemia (averaging 0.4 to 0.5 meq/L below the baseline level). It
has been suggested that the changes in plasma potassium might be arrhythmogenic
in susceptible patients, such as those with angina pectoris.



Hyperkalemic
periodic paralysis
— Hyperkalemic
periodic paralysis is an autosomal dominant disorder in which episodes of
weakness or paralysis are usually precipitated by cold exposure, rest after
exercise, fasting, or the ingestion of small amounts of potassium. The most
common abnormality in hyperkalemic periodic paralysis is a point mutation in
the gene for the alpha subunit of the skeletal muscle cell sodium channel.



Other — Other rare causes of hyperkalemia due to translocation
of potassium from the cells into the extracellular fluid include:




  • Digitalis overdose, due to dose-dependent
    inhibition of the Na-K-ATPase pump. Hyperkalemia can also occur after
    poisoning with structurally related digitalis glycosides, as may occur
    after ingestion of the plants, common oleander or yellow oleander, or
    extracts of the cane toad, Bufo marinus (bufadienolides).

  • Red cell transfusion due to leakage of
    potassium out of the red cells during storage.
    Hyperkalemia primarily
    occurs in infants and with massive transfusions.

  • Administration of succinylcholine to patients
    with burns, extensive trauma, prolonged immobilization, chronic infection,
    or neuromuscular disease. Acetylcholine receptors are normally concentrated
    within the neuromuscular junction, and the efflux of intracellular
    potassium caused by depolarization of these receptors is confined to this
    space. Hyperkalemia occurs when succinylcholine is given under conditions
    that cause upregulation and widespread distribution of acetylcholine
    receptors throughout the entire muscle membrane.

  • Administration of arginine hydrochloride,
    which is metabolized in part to hydrochloric acid and has been used to
    treat refractory metabolic alkalosis. The entry of cationic arginine into
    the cells presumably obligates potassium exit to maintain
    electroneutrality. The drug, aminocaproic acid, can cause hyperkalemia by
    the same mechanism since it is structurally similar to arginine.

  • Use of drugs that activate ATP-dependent
    potassium channels in cell membranes, such as calcineurin inhibitors (eg,
    cyclosporine and tacrolimus), diazoxide, minoxidil, and several volatile
    anesthetics (eg, isoflurane). As described elsewhere, other mechanisms are
    also involved in calcineurin inhibitor-induced hyperkalemia, including
    hyporeninemic hypoaldosteronism and inhibition of the luminal potassium
    channel through which potassium is secreted (
    figure 1).


REDUCED
URINARY POTASSIUM EXCRETION
— Urinary
potassium excretion is primarily mediated by potassium secretion in the
principal cells in the two segments that follow the distal tubule: the
connecting segment and cortical collecting tubule
. Three
major factors are required for adequate potassium secretion at these sites: adequate aldosterone
secretion
, adequate responsiveness to aldosterone, and adequate
distal sodium and water delivery
. The widely used term, hypoaldosteronism,
applies to both reduced aldosterone secretion and reduced response to aldosterone.



The four major causes of hyperkalemia due to reduced urinary potassium
secretion are:




  • Reduced aldosterone secretion
  • Reduced response to aldosterone (aldosterone
    resistance)

  • Reduced distal sodium
    and water delivery as occurs in effective arterial blood volume depletion

  • Acute and chronic
    kidney disease in which one or more of the above factors are present



Other mechanisms for reduced urinary potassium secretion have rarely
been described.



In addition to directly causing hyperkalemia, impaired urinary potassium
excretion can also contribute to hyperkalemia induced by potassium release from
the cells (
table 1).

TABLE 01:


Major causes of hyperkalemia
Increased potassium release from cells
Pseudohyperkalemia
Metabolic acidosis
Insulin deficiency, hyperglycemia, and hyperosmolality
Increased tissue catabolism
Beta blockers
Exercise
Hyperkalemic periodic paralysis
Other
Overdose of digitalis or related digitalis glycosides
Red cell transfusion
Succinylcholine
Arginine hydrochloride
Activators of ATP-dependent potassium channels (eg, calcineurin inhibitors, diazoxide, minoxidil, and some volatile anesthetics)
Reduced urinary potassium excretion
Reduced aldosterone secretion
Reduced response to aldosterone
Reduced distal sodium and water delivery
Effective arterial blood volume depletion
Acute and chronic kidney disease
Other
Selective impairment in potassium secretion
Gordon's syndrome
Ureterojejunostomy

Reduced aldosterone secretion — Any cause of decreased
aldosterone release, such as that induced by hyporeninemic hypoaldosteronism or
certain drugs, can diminish the efficiency of potassium secretion and lead to
hyperkalemia and metabolic acidosis (called type 4 renal tubular acidosis)
. Drugs
commonly implicated include angiotensin inhibitors, nonsteroidal
anti-inflammatory drugs, calcineurin inhibitors, and heparin.



Hyperkalemia is a common problem in patients treated with the
calcineurin inhibitors, cyclosporine and tacrolimus. These drugs can induce
hyporeninemic hypoaldosteronism and can also interfere with the effect of
aldosterone on the potassium-secreting cells in the connecting segment and
cortical collecting tubule.



The rise in plasma potassium concentration induced by reductions in
aldosterone secretion or aldosterone response directly stimulates potassium
secretion, partially overcoming the relative absence of aldosterone. The net
effect is that the rise in the plasma potassium concentration is generally
small in patients with normal renal function but can be clinically important in
the presence of underlying renal insufficiency and/or other causes of
hyperkalemia (
table 1).


Reduced response to aldosterone — There are a number of causes
of hyperkalemia that are due to a reduced response to aldosterone, also called
aldosterone or mineralocorticoid resistance. The most common are the
administration of potassium-sparing diuretics and acute and chronic kidney
disease in which other factors may also contribute.



Potassium-sparing
diuretics
— Two classes of medications impair renal potassium secretion
despite normal or high levels of aldosterone: aldosterone antagonists that
compete with aldosterone for receptor sites (spironolactone and eplerenone),
and drugs that directly block the sodium channels in the apical (luminal)
membrane of the principal cells in the collecting tubule (amiloride and
triamterene)
.


Voltage-dependent
renal tubular acidosis
— In some
patients with distal renal tubular acidosis (RTA), the primary defect is
impaired sodium reabsorption in the principal cells in the two segments that
follow the distal tubule (the connecting segment and the cortical collecting
tubule). The movement of sodium from the lumen into the principal cells makes
the lumen electronegative, thereby promoting the secretion of both hydrogen
ions and potassium
. In
contrast, an impairment in sodium reabsorption will reduce both hydrogen and
potassium secretion, which will promote the development of metabolic acidosis
and hyperkalemia. This disorder, which has been called voltage-dependent RTA,
has been associated with urinary tract obstruction, lupus nephritis, sickle
cell disease, and renal amyloidosis.



A somewhat similar defect is induced by hypoaldosteronism since
aldosterone normally increases the number of open sodium channels in the
luminal membrane. In contrast to hypoaldosteronism, voltage-dependent RTA is
associated with normal or even high aldosterone levels and an inability to
normally acidify the urine, as the urine pH is above 5.5.



Pseudohypoaldosteronism
type 1
— Pseudohypoaldosteronism type 1 is a rare hereditary
disorder that is characterized by aldosterone resistance. The autosomal
recessive form affects the collecting tubule sodium channel (ENaC)
, and
the autosomal dominant form in most patients affects the mineralocorticoid
receptor.



Reduced distal sodium and water delivery — Even in the
presence of normal or increased plasma aldosterone levels, potassium secretion
and therefore urinary potassium excretion can be impaired if there is a
substantial reduction in sodium and water delivery to the potassium secretory
sites in the distal nephron (connecting segment and cortical collecting
tubule). As an example, potassium secretion by perfused rabbit cortical
collecting ducts is dramatically inhibited at a luminal sodium concentration of
8 mmol/L and essentially stops at a luminal sodium concentration of 0 mmol/L.
Dietary sodium intake also influences potassium excretion; the potassium
secretory capacity is enhanced by excess sodium intake and reduced by sodium
restriction.



The most common cause of reduced distal sodium and water delivery is
effective arterial blood volume depletion, which may be accompanied by other
factors that promote the development of hyperkalemia. Measurement of urinary
sodium concentration, combined with a therapeutic response to saline hydration,
can help confirm this pathophysiology.



Effective arterial blood volume depletion — The effective
arterial blood volume (also called effective circulating volume) refers to the
arterial blood volume that is effectively perfusing the tissues. Effective
arterial blood volume depletion includes any cause of true volume depletion
(eg, gastrointestinal or renal losses) as well as heart failure and cirrhosis
in which decreased tissue perfusion is due to a reduced cardiac output and
vasodilation, respectively.



Any cause of effective arterial blood volume depletion can lead
sequentially to decreased delivery of sodium and water to the sites of potassium
secretion in the distal nephron (connecting segment and cortical collecting
tubule), impaired potassium secretion into the tubular lumen, and hyperkalemia
.
However, the effect of impaired potassium secretion can be minimized or
overcome, possibly resulting in hypokalemia, if there are concurrent potassium
losses, as in patients with vomiting or diarrhea, or those treated with
diuretic therapy.



In addition to decreased distal delivery of sodium and water, other
potentially important contributing factors to hyperkalemia in patients with
heart failure and cirrhosis include angiotensin inhibitor therapy in heart
failure (but not cirrhosis) and aldosterone antagonists in both heart failure
and cirrhosis.



Acute and chronic kidney disease — Hyperkalemia is a common
complication of acute and chronic kidney disease. In patients with acute kidney
injury, hyperkalemia is most prevalent in oliguric patients who also have
increased potassium release from cells due, for example, to rhabdomyolysis or
tumor lysis syndrome.



In patients with chronic kidney disease, the ability to excrete
potassium at near-normal levels without the development of hyperkalemia
generally persists as long as both the secretion of and responsiveness to
aldosterone are intact and distal delivery of sodium and water are maintained.
Hyperkalemia is most commonly seen in patients who are oliguric or have an
additional problem such as a high-potassium diet, increased tissue breakdown,
reduced aldosterone secretion or responsiveness, or fasting in dialysis
patients which may both lower insulin levels and cause resistance to
beta-adrenergic stimulation of potassium uptake. In dialysis patients who
fasted prior to surgery, the administration of insulin and glucose or, to a
lesser degree, glucose alone in nondiabetic patients can minimize the elevation
in the serum potassium concentration.



Impaired cell uptake of potassium also contributes to the development of
hyperkalemia in advanced renal failure
.
Diminished Na-K-ATPase activity may be particularly important in this setting.
How this occurs is not clear, but retained uremic toxins may decrease the
transcription of mRNA for the alpha1 isoform of the Na-K-ATPase pump in
skeletal muscle.



Multiple factors — The presence of multiple factors that
impair potassium secretion can lead to more severe and possibly
life-threatening hyperkalemia. One setting in which this can occur is in
patients with moderate to severe heart failure. These patients often have
reduced distal sodium and water delivery due to the associated renal
hypoperfusion, relatively decreased aldosterone release (from treatment with
angiotensin-converting enzyme [ACE] inhibitors and/or angiotensin II receptor
blockers [ARBs]), and reduced aldosterone effect (from treatment with
spironolactone or eplerenone).



Other mechanisms of impaired potassium secretion — In addition
to the common mechanisms of hyperkalemia due to reduced urinary potassium
excretion described above, there are other, less common causes of hyperkalemia
in which urinary potassium excretion is impaired due to mechanisms not directly
related to reduced secretion of or response to aldosterone or to reduced distal
sodium and water delivery.



Selective impairment in potassium secretion — Some patients
with hyperkalemia have impaired urinary potassium excretion despite normal
aldosterone release and normal distal sodium and water delivery. This seemingly
selective impairment in potassium secretion, which does not respond to exogenous
mineralocorticoid, has been described with lupus nephritis, acute transplant
rejection, and sickle cell disease. These patients do not have sodium wasting
and have a normal antinatriuretic response to mineralocorticoids, indicating a
selective potassium defect, not aldosterone resistance. In at least
some cases, the potassium secretory defect may be due to interstitial
nephritis.



A selective impairment in potassium secretion can also occur in patients
treated with cyclosporine or tacrolimus. One or more mechanisms involved in
tubular potassium secretion may be impaired.



Pseudohypoaldosteronism
type 2 (Gordon's syndrome)
— An inherited
syndrome of hyperkalemia, volume expansion, hypertension, and otherwise normal
renal function has been called pseudohypoaldosteronism type 2, Gordon's
syndrome, or familial hyperkalemic hypertension. The reduction in aldosterone
secretion represents an appropriate response to volume expansion.



Ureterojejunostomy — A
rise in the serum potassium concentration can occur in patients with a urinary
diversion procedure in which the ureters are inserted into the jejunum (called
a ureterojejunostomy). Hyperkalemia in this setting is presumably due to
absorption of urinary potassium by the jejunum.

Referência
- UpToDate - Causes and evaluation of hyperkalemia in adults

Renato de Oliveira

Mensagens : 12
Data de inscrição : 01/12/2012

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