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Non-Dietary Causes of Hyperkalemia
Jean Stover
| The Issues in Renal Nutrition
in Nephrology Nursing department is designed to focus on nutritional
issues for nephrology patients. Address correspondence to: Deborah Brommage,
Department Editor, Nephrology Nursing Journal; East Holly Avenue/Box
56; Pitman NJ 08071-0056; (856) 256-2320. The opinions and assertions
contained herein are the private views of the contributors and do not
necessarily reflect the views of the American Nephrology Nurses'
Association. |
Herbal
products and dietary supplements are complementary and alternative
medicine (CAM) therapies that have grown faster than any other CAM
treatments. Little information is available about the use of these
products in the stage 5 chronic kidney disease (CKD) population.
Information on the use, safety, efficacy, adverse effects, and
recommended dosages in the nondialysis population are summarized in
this article.
Hyperkalemia
is the term for “an excessive amount of potassium in the blood.”
(Thomas, 1997, p. 934). Most of the potassium in the body is
intracellular (98%), thus serum levels measure only the 2% which is
extracellular. The movement of potassium into or out of cells can
impact on the measurement of a serum potassium level without changing
total body potassium. A very small “shift” of potassium can greatly
affect the serum level (Palmer, Toto, & Alpern, 1997).
Potassium
is a mineral that has many functions. One function is to regulate the
activity of muscles, including the heart and skeletal muscles. Severe
hyperkalemia can cause cardiac arrhythmias and even cardiac arrest.
Skeletal muscle weakness, paralysis, and respiratory arrest can also
occur (Allon, 1998). Patients with chronic kidney disease (CKD) are at
greater risk for hyperkalemia than individuals who have normal kidney
function. As CKD progresses, the kidneys are increasingly unable to
filter excess potassium for excretion in the urine. Although ingestion
of food and beverages rich in potassium can play a significant role for
this patient population, there are other factors that may contribute to
hyperkalemia. Frequently the cause is a combination of factors.
When
high potassium levels are apparent, pseudohyperkalemia must first be
ruled out. This term refers to a falsely high reading that can occur
due to in vitro release of potassium from blood cells. This can be seen
with hemolysis during phlebotomy or when processing blood samples, and
with severe thrombocytosis (a very high platelet count) or leukocytosis
(a very high white blood cell count) (Allon, 1998). The following
discussion includes causes of true hyperkalemia.
Medications
During
the early stages of CKD, potassium excretion is usually sufficient to
maintain a normal serum level. Medications, however, such as
angiontensin-converting enzyme (ACE) inhibitors and angiotensin II
receptor blockers (ARBs), prescribed for blood pressure control and to
slow the progression of CKD, may promote high serum potassium levels.
Angiotensin II stimulates the production of the hormone, aldosterone,
in the adrenal cortex. Since aldosterone regulates the excretion of
sodium and potassium, interference in its synthesis or function can
cause the retention of potassium and result in hyperkalemia. (Allon,
1998). In this situation, to continue the beneficial aspects of these
medications, dietary potassium restriction and/or diuretic therapy may
be necessary (Mangrum & Bakris, 2004).
Other
medications that can contribute to hyperkalemia in the early stages of
CKD or after renal transplantation include potassium-sparing diuretics
such as spironolactone and nonselective beta-blockers such as
propanalol and nadolol. Prostaglandin inhibitors such as nonsteroidal
anti-inflammatory drugs (NSAIDs) and heparin (which may be given to
hospitalized patients to prevent venous thrombosis) can also inhibit
aldosterone production and lead to hyperkalemia. Tacrolimus and
cyclosporine, immunosuppressive drugs given after renal
transplantation, can also cause hyperkalemia by interfering in the
renin-angiontensin-aldosterone process (Allon, 1998; Palmer et al.,
1997).
Cellular Shifts
During
all stages of CKD, metabolic acidosis, a disturbance in the acid-base
balance of the blood, may occur (evident by a low serum bicarbonate
level). When there is renal impairment, acidosis is caused by either
excess bicarbonate excretion or the inability to excrete phosphoric and
sulfuric acids (Thomas, 1997). Both of these conditions can cause
potassium to move from intracellular to extracellular fluids, and thus
result in hyperkalemia (Palmer et al., 1997). The administration of
sodium bicarbonate or another “buffering” agent can correct acidosis
and improve serum potassium levels. Individuals undergoing hemodialysis
often benefit from dialysate with a higher bicarbonate content as well.
Another
cause of hyperkalemia due to cellular shifts is often seen in patients
with diabetes due to insulin deficiency. When severe hyperglycemia
occurs, the osmolality of the blood is increased, which causes
potassium to move out of the cells (Palmer et al., 1997).
Tissue Injury
Hyperkalemia
can be caused by muscle breakdown due to a traumatic crush injury
(Palmer et al., 1997) or rhabdomyolosis with drugs such as lovastatin
or cocaine. Potassium is released from the injured cells and
hyperkalemia results. It may be more severe if there is resultant renal
damage or existing impairment of kidney function. Tumor lysis syndrome,
occurring either spontaneously or when chemotherapy is given for acute
leukemia or high grade lymphoma may also cause hyperkalemia due to
release of intracellular potassium (Allon, 1998).
Some
patients with CKD periodically develop gastrointestinal bleeding.
Elevated potassium levels may result when the bleeding occurs, as
potassium is released from blood cells (Salem & Batlle, 2001). The
breakdown of tissue due to wounds (such as foot ulcers), burns,
infection or major surgical procedures is another potential source of
elevated serum potassium (Beto & Bansal, 1992). For this reason,
patients with CKD undergoing dialysis usually do not have planned
surgical procedures during their longest interdialytic period.
Dialysis Issues
When
an individual undergoing dialysis has a high serum potassium level, it
is important to be sure his or her treatment has been adequate.
Patients on hemodialysis who miss treatments or often cut them short,
may have inadequate potassium removal. If the dialysis access is not
functioning properly to permit adequate blood flow through the
dialyzer, the same problem may occur (Beto & Bansal, 1992).
Individuals on peritoneal dialysis may become hyperkalemic if they skip
prescribed exchanges.
The content of the dialysate used for hemodialysis must also be
considered, as a new patient with good urine output or poor dietary
intake may initially require a higher potassium concentration. As urine
output diminishes, urinary potassium excretion decreases, and the serum
levels may rise. This may occur especially if the patient’s appetite
improves with regular dialysis therapy. Patients on peritoneal dialysis
who require oral potassium supplements may begin to eat better, or
suddenly become more compliant with these medications, and become
hyperkalemic. Also, if patients on peritoneal dialysis switch to
hemodialysis, these medications may need to be discontinued due to less
consistent potassium removal.
Other Causes
Other
causes of hyperkalemia include decreased gut excretion of potassium
with chronic constipation and the presence of diseases such as
Addisons’s disease and sickle cell anemia (Beto & Bansal, 1992).
Summary
This
discussion is not all inclusive of nondietary causes of hyperkalemia,
but is meant to alert healthcare providers to possible factors other
than excessive dietary potassium intake.
References
Allon,
M. (1998). Disorders of potassium metabolism. In A. Greenberg (Ed.),
Primer on kidney disease (2nd ed.) (pp. 103-105). San Diego:
Academic Press.
Beto, J., & Bansal, V. (1992).
Hyperkalemia: Evaluating dietary and nondietary etiology. Journal of
Renal Nutrition, 2(1), 28-29.
Mangrum, A.J., & Bakris, G.L. (2004).
Angiotensin-converting enzyme inhibitors and angiotensin receptor
blockers in chronic renal disease: Safety issues. Seminars in
Nephrology, 24(2),168-75.
Palmer, B.E., Toto, R.D., & Alpern,
R.J. (1997). Sodium and potassium disturbances in renal patients. In D.
Levine (Ed.), Caring for the renal patient (pp.45-49).
Philadelphia: W.B. Saunders Company.
Salem, M.M., & Batlle, D.C. (2001).
Hyperkalemia and hypokalemia. Best practice of medicine. Retrieved
February 21, 2006, from
http://merck.micromedex.com/index.asp?page=bpm_brief&article_id=CPM01NP258
Thomas, C.L. (Ed.). (1997). Taber’s cyclopedic medical dictionary. Philadelphia: F.A. Davis Company.
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