Potassium homeostasis and clinical implications

doi:10.1016/S0002-9343(84)80002-9

The American Journal of Medicine

Volume 77, Issue 5, Supplement 1, 5 November 1984, Pages 3-10

https://doi.org/10.1016/S0002-9343(84)80002-9 Get rights and content

The clinical estimation of potassium balance generally depends onthe level of serum potassium. Since the extracellular fluid contains only 2 percent of the total body potassium, it must be recognized that potassium deficits are usually large before significant hypokalemia occurs, whereas smaller surfeits of potassium will cause hyperkalemia. The total body potassium is regulated by the kidney in which distal nephron secretion of potassium into the urine is enhanced by aldosterone, alkalosis, adaptation to a high potassium diet, and delivery of increased sodium and tubular fluid to the distal tubule. However, the distribution of potassium between the intracellular and extracellular fluids can markedly affect the serum potassium level without a change in total body potassium. Cellular uptake of potassium is regulated by insulin, acid-base status, aldosterone, and adrenergic activity. Hypokalemia, therefore, may be caused by redistribution of potassium into cells due to factors that increase cellular potassium uptake, in addition to total body depletion of potassium due to renal, gastrointestinal, or sweat losses. Similarly hyperkalemia may be caused by redistribution of potassium from the intracellular to the extracellular fluid due to factors that impair cellular uptake of potassium, in addition to retention of potassium due to decreased renal excretion. An understanding of the drugs that affect potassium homeostasis, either by altering the renal excretion of potassium or by modifying its distribution, is essential to the proper assessment of many clinical potassium abnormalities. Both hypokalemia and hyperkalemia may cause asymptomatic electrocardiographic changes, serious arrhythmias, muscle weakness, and death. Hypokalemia has also been associated with several other consequences, including postural hypotension, potentiation of digitalis toxicity, confusional states, glucose intolerance, polyuria, metabolic alkalosis, sodium retention, rhabdomyolysis, intestinal ileus, and decreased gastric motility and acid secretion.

References (29)

SilvaP et al.
Adaptation to potassium
Kidney Int
(1977)
GennariFJ et al.
Role of the kidney in potassium homeostasis: lessons from acid-base disturbances
Kidney Int
(1975)
FraleyDS et al.
Correction of hyperkalemia by bicarbonate despite constant blood pH
Kidney Int
(1977)
CarlssonE et al.
β-Adrenoceptor blockers, plasma-potassium, and exercise
Lancet
(1978)
WhangR et al.
Magnesium deficiency and refractoriness to potassium repletion
J Chron Dis
(1977)
TextorSC et al.
Hyperkalemia in azotemic patients during angiotensin-converting enzyme inhibition and aldosterone reduction with captopril
Am J Med
(1982)
RoweJW et al.
Effect of experimental potassium deficiency on glucose and insulin metabolism
Metabolism
(1980)
ValtinH
Renal dysfunction: mechanisms involved in fluid and solute imbalance
AdamWR et al.
Potassium tolerance in rats
Aust J Exp Biol Med Sci
(1972)
MalnicG et al.
Micropuncture study of renal potassium excretion in the rat
Am J Physiol
(1964)

AdamWR et al.

Renal potassium adaptation in the rat: role of glucocorticoids and aldosterone

Am J Physiol

(1984)

PrattJH

Role of angiotensin II in potassium-mediated stimulation of aldosterone secretion in the dog

J Clin Invest

(1982)

PetersonLN et al.

Effect of sodium intake on renal potassium excretion

Am J Physiol

(1977)

GoodDW et al.

Luminal influences on potassium secretion: sodium concentration and fluid flow rate

Am J Physiol

(1979)

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Few of the disturbances in fluid and electrolyte metabolism are as commonly encountered or as immediately life-threatening as disturbances in potassium balance. Many clinicians are already sensitized to the detrimental effects of potassium disorders, especially hyperkalemia, but sometimes the adverse effects of hypokalemia are nearly as harmful. This chapter discusses the clinical essentials of hypokalemia and hyperkalemia in the critically ill dog and cat and shows why both are important in patient care.
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A retrospective review was performed on 767 patients who underwent primary TJA at a single institution. Preoperative and postoperative potassium, sodium, creatinine, and glucose values were collected along with demographic data, comorbidities, and procedural characteristics. Multivariable logistic regression models were used to determine independent risk factors for abnormal postoperative laboratory values.
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Citation Excerpt :
If the patient is hypervolemic and able to produce urine, diuretics should be provided (8,9). Diuresis is a viable option while pursuing hemodialysis, though diuresis is unlikely to be beneficial in patients with chronic anuric renal failure (6–10). Urinary excretion is possible in patients with moderately compromised kidney function.
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Potassium (K+) plays a key role in determining the transmembrane potentials of “excitable membranes” present in nerve and muscle cells. K+ is the predominant intracellular cation, and clinical deterioration typically ensues when patients develop sufficiently marked elevation in extracellular fluid concentrations of K+ (hyperkalemia). Hyperkalemia is usually detected via serum clinical laboratory measurement. The most severe effect of hyperkalemia includes various cardiac dysrhythmias, which may result in cardiac arrest and death. Treatment includes measures to “stabilize” cardiac membranes, to shift K+ from extracellular to intracellular stores, and to promote K+ excretion. Calcium gluconate 10% dosed 10 mL intravenously should be provided for membrane stabilization, unless the patient is in cardiac arrest, in which case 10 mL calcium chloride is warranted. Beta-agonists and intravenous insulin should be given, and some experts recommend the use of synthetic short-acting insulins rather than regular insulin. Dextrose should also be administered, as indicated by initial and serial serum glucose measurements. Dialysis is the most efficient means to enable removal of excess K+. Loop and thiazide diuretics can also be useful. Sodium polystyrene sulfonate is not efficacious. New medications to promote gastrointestinal K+ excretion, which include patiromer and sodium zirconium cyclosilicate, hold promise.
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Hypokalemia, hyperkalemia, hyponatremia, hypernatremia, hypocalcemia, and hypercalcemia are commonly seen in emergency medicine. Severe abnormalities in any of these electrolytes can cause potentially life-threatening consequences to the patient. It is essential that the clinician understand and correct (if possible) the underlying cause of each disorder and recognize the importance of the rates of correction, especially with serum sodium disorders. The recommended doses in this article might have to be adjusted to the individual patient, and these modifications must be adjusted again to the pathophysiology of the primary underlying disorder.
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Hypokalemia is not an isolated disease but an associated finding in a vast number of different diseases; it poses a great challenge in correct diagnosis and proper management. Hypokalemia usually arises from a shift of potassium (K⁺) into cells and/or a net loss of K⁺. Besides a detailed history and physical examination, measurement of K⁺ excretion rate with freshly-voided and/or 24-hour urine and assessment of blood acid-base status can help discriminate between the various causes of hypokalemia. In patients with a low rate of K⁺ excretion, hypokalemia can be due to an acute shift of K⁺ into cells, intestinal/sweating K⁺ loss, or prior renal K⁺ excretion. In patients with a high rate of K⁺ excretion, there may be either increased flow rate or increased K⁺ secretion, seen with fast sodium (Na⁺) or slow chloride (Cl⁻) disorders, in the cortical collecting ducts (CCD). An increased flow rate in the CCD arises from increased osmole excretion (whether solutes or electrolytes). Patients with fast Na⁺ disorders have a high extracellular fluid (ECF) volume and thus high blood pressure associated with a state of high mineralocorticoid activity. Measurement of renin activity, aldosterone, and cortisol levels in plasma helps distinguish between the causes. Patients with slow Cl⁻ disorders usually have low to normal ECF volume and blood pressure and are usually associated with abnormal acid-base states. In patients with metabolic alkalosis, urine Na⁺ and Cl⁻ excretion rate reveal the basis for renal Na⁺ wasting and distinguish it from non-renal Na⁺ loss. In patients with hyperchloremic metabolic acidosis, an assessment of the ammonium excretion rate (NH₄⁺) separates those with renal tubular acidosis (low NH₄⁺ excretion) from those with other causes. The treatment of hypokalemia depends on the degree and timing of hypokalemia, clinical manifestations, underlying causes, and potential risks from associated conditions.

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¹: From the Charles A. Dana Research Institute andthe Harvard-Thorndike Laboratory, Department of Medicine, Harvard Medical School and Beth Israel Hospital, Boston, Massachusetts.

View full text

Potassium homeostasis and clinical implications

Kidney Int

Kidney Int

Kidney Int

Lancet

J Chron Dis

Am J Med

Metabolism

Renal dysfunction: mechanisms involved in fluid and solute imbalance

Potassium tolerance in rats

Aust J Exp Biol Med Sci

Micropuncture study of renal potassium excretion in the rat

Am J Physiol

Renal potassium adaptation in the rat: role of glucocorticoids and aldosterone

Am J Physiol

Role of angiotensin II in potassium-mediated stimulation of aldosterone secretion in the dog

J Clin Invest

Effect of sodium intake on renal potassium excretion

Am J Physiol

Luminal influences on potassium secretion: sodium concentration and fluid flow rate

Am J Physiol