Suppresses renin release, leading to decreased aldosterone synthesis, decreased potassium secretion in collecting duct. Decreases aldosterone synthesis; most common in patients on dialysis who drink water with high fluoride levels.
Hypertonicity caused by hyperglycemia from glucose infusions can drive potassium out of the intracellular space, leading to hyperkalemia. Hyperkalemia may occur with continuous infusions or with boluses of hypertonic glucose. May be present with hypertonicity caused by other agents such as mannitol Osmitrol as well. Can cause hyperkalemia in patients with decreased renal function; inhibits adrenal aldosterone synthesis. All these agents act by decreasing sodium-potassium ATPase activity, leading to elevated extracellular potassium.
Decreased prostaglandin production leads to decreased afferent arteriolar flow, suppressing renin and aldosterone secretion. Herbs containing high potassium levels e. Can cause hyperkalemia in patients with impaired renal function caused by increased potassium load; can be administered orally or intravenously. Ingestion of potassium can lead to hyperkalemia, particularly if renal function is impaired; dietary sources include bananas, melon, and orange juice.
Increases nicotinic acetylcholine receptors in damaged skeletal muscle e. Suppresses renin release, leading to decreased aldosterone synthesis and decreased potassium secretion in collecting duct. It is unknown whether oral dietary amino acid supplements cause hyperkalemia.
Information from references 4 through Two mechanisms normally regulate potassium levels in response to variation of potassium intake. First, ingested potassium rapidly enters the portal circulation, stimulating the pancreas to release insulin. Elevated insulin levels induce rapid transport of potassium from the extracellular space into cells via cellular sodium-potassium adenosine triphosphatase.
Second, increased potassium in the circulation causes the renal juxtaglomerular cells to release renin. This stimulates hepatic activation of angiotensin I that is then converted in the lungs to angiotensin II. Angiotensin II stimulates the adrenal zona glomerulosa to secrete aldosterone. Elevated serum aldosterone causes the renal cortical collecting ducts to excrete potassium and retain sodium, further lowering serum potassium.
The first step in the evaluation of a patient with elevated serum potassium is to exclude spurious potassium elevation Table 3 2 , 3. If the elevation is shown to be real, the next step is to consider: 1 the effects of medications, including increased potassium intake Table 2 4 — 10 ; 2 the impaired distribution of potassium between the intracellular and extracellular space; or 3 the impaired renal excretion of potassium. All three factors often are present e.
Drawing blood samples from a vein or line into which potassium is being infused. Familial pseudohyperkalemia. Hereditary spherocytosis. Pseudohyperkalemia occurs when laboratory reports of potassium do not reflect actual values. The most common cause is lysis of red cells in a phlebotomy specimen. Other causes are listed in Table 3 2 , 3. Potassium released from platelets can lead to spuriously high levels of potassium in a blood sample allowed to clot to collect serum.
Pseudohyperkalemia can be excluded by repeating the sample collection as atraumatically as possible and obtaining serum and plasma potassium levels. In patients with pseudohyperkalemia, the plasma potassium will be normal in the face of an elevated serum potassium. Effective excretion of potassium is dependent on aldosterone and sufficient distal delivery of sodium and water within the nephron.
Hyperkalemia may occur when one of these mechanisms is impaired because of renal failure, renal hypoperfusion e. Hypoaldosteronism may be the cause of hyperkalemia in patients who do not have advanced renal failure or hypoperfusion. Hyporeninemic hypoaldosteronism, a syndrome associated with type IV renal tubular acidosis, may be part of the mechanism behind hyperkalemia in patients with mild renal failure, particularly diabetic nephropathy.
Hyporeninemic hypoaldosteronism can cause patients who have diabetic nephropathy to develop acute elevations of potassium because of medications or stress e.
The factors that decrease potassium excretion also increase the risk of medication-induced hyperkalemia. Because of the relative decline in renal function with age, family physicians should use caution when prescribing medications that alter potassium metabolism in older patients. Judicious monitoring of potassium levels is important in at-risk patients receiving these medicines.
Neurohumoral inhibition with angiotensin-converting enzyme ACE inhibitors or angiotensin receptor blockers benefits patients with chronic heart failure; adding spironolactone Aldactone reduces morbidity and mortality in patients with severe heart failure. Non-steroidal anti-inflammatory drugs NSAIDs decrease renin secretion, leading to decreased potassium secretion.
The addition of NSAIDs in these patients can impair renal function to the degree of inducing life-threatening hyperkalemia. The possibility of adrenal insufficiency should be considered in all patients with hyperkalemia.
Clinical suspicion is increased by the presence of hyponatremia and muscular weakness. Plasma cortisol is measured 45 to 60 minutes later, and values less than 20 mcg per dL nmol per L suggest adrenal insufficiency. Congenital abnormalities of aldosterone synthesis also can lead to potassium elevation and excessive sodium loss.
Severe forms of these disorders lead to electrolyte imbalances in neonates that can be fatal if not corrected promptly. If these patients survive infancy, the disorder tends to be less severe as they get older.
Patients suspected to have one of these unusual genetic abnormalities should be referred to a pediatric endocrinologist to establish appropriate initial treatment; patients may then be managed by their family physician with occasional consultation.
The initial diagnostic approach begins with the clinical history, review of medications, and physical examination. Symptoms and signs include muscular weakness or flaccid paralysis, ileus, and characteristic electrocardiograph ECG changes Figure 1 Laboratory tests should be directed towards causes suggested by the history and physical examination, with attention to serum electrolytes, creatinine, and blood urea nitrogen.
A spot urine test for potassium, creatinine, and osmoles should be obtained to calculate the fractional excretion of potassium and the transtubular potassium gradient Table 4 22 , The transtubular potassium gradient is an assessment of renal potassium handling, with a normal value of eight to nine, rising at times to 11 after an increase in potassium intake.
Values lower than five in the face of hyperkalemia suggest an inappropriate renal response to high potassium 22 ; a very low value suggests hypoaldosteronism. Reprinted with permission from Slovis C, Jenkins R. ABC of clinical electrocardiography: conditions not primarily affecting the heart. BMJ ; FEK less than 10 percent indicates renal etiology FEK greater than 10 percent indicates extrarenal cause. Gradient less than 6 to 8 indicates renal cause Gradient greater than 6 to 8 indicates extrarenal cause.
Information from references 22 and Hyporeninemic hypoaldosteronism should be considered in patients with diabetes and hyperkalemia, who generally have a low serum aldosterone. A trial of oral fludrocortisone Florinef is generally the most practical way to empirically establish this diagnosis; if the patient has hyporeninemic hypoaldosteronism, potassium levels will return to normal in a day or two after initiation of fludrocortisone.
Factors necessitating emergent treatment of hyperkalemia include changes on ECG, a rapid rise of serum potassium, decreased renal function, and the presence of significant acidosis 23 Figure 2.
Urgent treatment should not be delayed while a work-up for the etiology is undertaken, although urine potassium, creatinine, and osmolarity studies should be obtained before serum potassium levels are significantly altered.
Among the topics discussed under these headings is the important revelation that a variety of mechanisms account for the hyperkalemia in acidosis.
So that for example, the mechanisms for the hyperkalemia associated with diabetic ketoacidosis differ from the mechanisms of the hyperkalemia associated with lactic acidosis. This review article, which is one of eleven contained in the May issue of Seminars in Nephrology all devoted to different aspects of potassium homeostasis, provides much detail of an aspect of acid-base pathophysiology that often receives minimal explanation in medical texts.
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October For example, a recent review article on hyperkalemia failed to mention diuresis at all Elliott For a patient with life-threatening hyperkalemia, it is often reasonable to make a single attempt at kaliuresis prior to proceeding to dialysis or simultaneously to pursuing dialysis e.
Of course in some situations such as chronic anuric renal failure, kaliuresis is unlikely to succeed, so it may be more sensible to proceed immediately to dialysis. A loop diuretic e. For patients with life-threatening hyperkalemia and renal insufficiency, it may be reasonable to use multiple diuretics, as these will operate in a synergistic fashion by blocking potassium reabsorption at different sites in the nephron figure above.
The combination of a loop diuretic and thiazide is commonly used in diuretic-resistant patients, with increased efficacy and potassium loss Jentzer There is no evidence regarding the number or dose of diuretic which should be used. For life-threatening hyperkalemia there is generally time for a single attempt at kaliuresis. Therefore, typically this attempt is fairly aggressive. For a patient with renal dysfunction who is expected to respond poorly, high doses of multiple agents may be considered e.
The risk of over-diuresis and electrolyte depletion may be minimized with close monitoring of electrolytes and repletion as needed. Urine output and volume status must be carefully monitored, with ongoing volume administration to return urinary losses and maintain a euvolemic state.
In the absence of evidence, selection of the number and dosage of diuretics must be based on clinical judgement. For example, at Genius General we once admitted a pleasant elderly man with chronic renal failure complicated by hyperkalemia causing bradycardia and shock.
He wished never to undergo dialysis and was not amenable to this therapy even temporarily. Given probable death if he failed to respond promptly to diuretics, he was treated with maximal kaliuresis mg i. He responded well, and ultimately required potassium and fluid repletion. In retrospect, he likely would have responded to a less aggressive diuretic regimen. However, in the face of life-threatening hyperkalemia, it may be safer to err on the side of over-treatment followed by meticulous replacement of electrolytes and fluid as needed.
Given that every liter of isotonic bicarbonate contains mEq of bicarbonate, this deficit correlates to roughly 1. Therefore, for this patient 1. These are all very rough calculations, but may provide a general concept about how much bicarbonate is required.
Further discussion of isotonic bicarbonate may be found on a prior post regarding pH-guided resuscitation. Theoretically, acetazolamide may be expected to be more kaliuretic than a thiazide diuretic. However, acetazolamide overall may be a less powerful agent, and less effective at eliciting diuresis in a patient with renal dysfunction.
A common practice of nephrologists and intensivists at Genius General Hospital has been to combine intravenous furosemide and chlorothiazide, and this seems to be effective. Image credits:. Author Recent Posts. The relation of serum potassium concentration with cardiovascular events and mortality in community-living individuals. Clin J Am Soc Nephrol ; 12 : — Elevated baseline potassium level within reference range is associated with worse clinical outcomes in hospitalised patients.
Sci Rep ; 7 : Toto RD. Serum potassium and cardiovascular outcomes: the highs and the lows. Fisch C. Relation of electrolyte disturbances to cardiac arrhythmias. Circulation ; 47 : — Electrophysiology of hypokalemia and hyperkalemia.
Circ Arrhythm Electrophysiol ; 10 : e El-Sherif N , Turitto G. Electrolyte disorders and arrhythmogenesis. Cardiol J ; 18 : — Circ Res ; 44 : — The clinical significance of hyperkalaemia-associated repolarization abnormalities in end-stage renal disease. Nephrol Dial Transplant ; 28 : 99 — Calcium salt during hyperkalemia. Kidney Int ; 90 : — Sodium is the secret re-agent of bicarbonate therapy during hyperkalemia. Evidence for a causal relationship between hyperkalaemia and axonal dysfunction in end-stage kidney disease.
Clin Neurophysiol ; : — Randomized, controlled trial of the effect of dietary potassium restriction on nerve function in CKD. Nagami GT. Effect of bath and luminal potassium concentration on ammonia production and secretion by mouse proximal tubules perfused in vitro. J Clin Invest ; 86 : 32 — Effects of chronic hyperkalemia on renal production and proximal tubule transport of ammonium in rats.
Karet FE. Mechanisms in hyperkalemic renal tubular acidosis. J Am Soc Nephrol ; 20 : — Mechanism of hyperkalemia-induced metabolic acidosis. J Am Soc Nephrol ; 29 : — Serum potassium and short-term clinical outcomes among hemodialysis patients: impact of the long interdialytic interval. Am J Kidney Dis ; 70 : 21 — Factors associated with underuse of mineralocorticoid receptor antagonists in heart failure with reduced ejection fraction: an analysis of 11 patients from the Swedish Heart Failure Registry: MRA underuse in HFrEF.
Eur J Heart Fail ; 20 : The treatment gap in patients with chronic systolic heart failure: a systematic review of evidence-based prescribing in practice.
Heart Fail Rev ; 21 : — Serum potassium as a predictor of adverse clinical outcomes in patients with chronic kidney disease: new risk equations using the UK clinical practice research datalink. BMC Nephrol ; 19 : Patiromer in patients with kidney disease and hyperkalemia receiving RAAS inhibitors. Veltassa Patiromer Lokelma 10 g powder for oral suspension. Oxford University Press is a department of the University of Oxford.
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Volume Article Contents Abstract. Hyperkalemia: pathophysiology, risk factors and consequences. Oxford Academic. Matthew A Bailey. Correspondence to: Matthew A. Bailey; E-mail: Matthew. Bailey ed. Select Format Select format. Permissions Icon Permissions.
Abstract There have been significant recent advances in our understanding of the mechanisms that maintain potassium homoeostasis and the clinical consequences of hyperkalemia. Open in new tab Download slide. Table 1 Drug causes of hyperkalemia. Open in new tab. CNIs, calcineurin inhibitors. Google Scholar Crossref. Search ADS. Google Scholar PubMed. Issue Section:. Download all slides. Comments 0. Add comment Close comment form modal. I agree to the terms and conditions. You must accept the terms and conditions.
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