This transcript has been edited for clarity.
Let's start with a patient whom we might all see in primary care. Bridget is a 63-year-old woman recently commenced on losartan 50 mg for hypertension and chronic kidney disease. Her home blood pressure average was 146/94 mm Hg despite several positive lifestyle changes.
Bridget also takes atorvastatin 20 mg daily for the primary prevention of cardiovascular disease. Baseline estimated glomerular filtration rate (eGFR) was 55 mL/min. Her urinary albumin-creatinine ratio was 6 mg/mmol, and potassium was 4.8 mmol/L. She attended for repeat urea and electrolytes around 3 weeks later.
Typically, her results are phoned back to you at 5:30 PM on a Friday evening when you're a duty doctor. Her eGFR has dropped to 50 mL/min, and potassium has risen to 6.0 mmol/L. Bridget is systemically well with no suggestion of acute kidney injury.
What do you do next? Do you start crying in the corner of your room? Or, more seriously, do you stop her losartan and recheck her urea and electrolytes on Monday? Do you reduce her losartan to 25 mg and recheck her urea and electrolytes on Monday? Do you maintain her losartan at 50 mg and recheck her urea and electrolytes within 14 days? Or would you check an ECG if you have access to a machine in your practice? Or would you consider hospital admission?
In this episode, we're going to talk about managing hyperkalemia in the community. One of the key questions to ask ourselves when we see cases like Bridget is whether we should admit Bridget to hospital for assessment and treatment. If we don't admit Bridget, when should the potassium be rechecked? Should we stop her losartan? And what other factors should we consider to prevent recurrence of hyperkalemia?
What are the main risk factors for hyperkalemia that we're likely to encounter in primary care? Key risk factors include kidney disease (either acute kidney injury or chronic kidney disease), heart failure (all subtypes of heart failure, including heart failure with reduced ejection fraction and heart failure with preserved ejection fraction), and diabetes (all subtypes of diabetes: type 1 diabetes, type 2 diabetes, type 3c or pancreatic diabetes). Also, adrenal insufficiency can cause hyperkalemia — both primary adrenal insufficiency or Addison disease and adrenal insufficiency secondary to long-term steroid use.
Finally, there are various iatrogenic or drug-related causes of hyperkalemia. Drugs that can predispose to hyperkalemia include angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs), angiotensin receptor neprilysin inhibitors, sacubitril/valsartan, and mineralocorticoid receptor antagonists (including steroidal drugs such as spironolactone and eplerenone, and nonsteroidal drugs such as finerenone). Potassium-sparing diuretics such as amiloride, of course, can increase potassium levels. So can good old trimethoprim, and remember — trimethoprim is also in cotrimoxazole. These drugs can also predispose to hyperkalemia. Nonselective beta-blockers such as propranolol and labetalol can also cause hyperkalemia, and, finally, so can heparin.
Now, you will have noticed that I started Bridget on losartan 50 mg rather than an ACE inhibitor. This has been a big change to my practice over recent years. One in 5 people, perhaps even 1 in 3 people, get a dry cough with an ACE inhibitor, which just generates more work for us in primary care and potentially impacts Bridget's trust and adherence with her therapies, current and future. For many years now, if a renin-angiotensin-aldosterone system (RAAS) inhibitor is required first line for hypertension, chronic kidney disease, or heart failure, I choose an ARB. Specifically, I choose losartan because of its simple posology: 50 mg titrated up to 100 mg for most individuals. Job done.
Another big change to my practice recently has been rechecking kidney function after initiation of a RAAS inhibitor. If eGFR is less than 60 mL/min when starting or increasing a RAAS inhibitor dose, we can recheck urea and electrolytes within 28 days rather than the traditional 7-14 days. This will have a significant impact on our available resources in primary care. However, if eGFR is over 60 mL/min, there's actually no need to routinely recheck urea and electrolytes. Again, this will have a significant impact on our available resources in primary care. This guidance is backed up by global guidelines from the International Society of Nephrology and Kidney Disease: Improving Global Outcomes (KDIGO), as well as expert consensus influenced by the prevalence of hyperkalemia across various GFR statuses. Hyperkalemia rarely occurs in those with normal kidney function started on a RAAS inhibitor.
How do we define hyperkalemia? If potassium is less than 5.5 mmol/L, no action is required. However, if potassium is greater than or equal to 5.5 mmol/L, further action is needed. The first question to ask ourselves is whether this is pseudohyperkalemia. This is false elevation of potassium secondary to a long sample transit time to the lab, usually over 6 hours in cold weather. Alternatively, ethylenediaminetetraacetic acid contamination of the blood tube can be a cause of pseudohyperkalemia. Always fill the urea and electrolytes tube first before other tubes. Finally, thrombocytosis, particularly a platelet count of over 600, can also cause pseudohyperkalemia. If thrombocytosis is an issue, send off urea and electrolytes in a lithium heparin blood tube for potassium levels to prevent coagulation.
If we do suspect pseudohyperkalemia, we can simply recheck urea and electrolytes within around 3 days. However, in the context of significant kidney impairment, it is usually safer to presume that hyperkalemia is real.
So, what do we do for Bridget? She has impaired kidney function, so we should presume her hyperkalemia is real. Remember, due to the drop in intraglomerular pressure associated with a RAAS inhibitor, we can expect a short-term drop in eGFR by up to 25% or up to a 50% rise in serum creatinine. This is physiologic and should not prompt cessation of the RAAS inhibitor therapy.
If Bridget was unwell or she had a greater than 25% drop in her eGFR or a greater than 50% rise in creatinine alongside a potassium of greater than or equal to 5.5 mmol/L, then we should definitely stop her losartan and consider hospital referral. However, as Bridget is well, and with less than a 25% drop in her eGFR, we can manage her in the community.
Current guidance and expert consensus advocates that if potassium is between 5.5 mmol/L and 6.1 mmol/L with a RAAS inhibitor in someone who is well, the RAAS inhibitor dose can be maintained, and urea and electrolytes can be rechecked within 14 days. On rechecking the urea and electrolytes, if that repeat potassium is less than or equal to 5.5 mmol/L, we can optimize the RAAS inhibitor dose and increase the losartan from 50 to 100 mg.
If that repeat potassium is 5.6 mmol/L to 5.9 mmol/L, we should maintain the RAAS inhibitor dose — maintain losartan at 50 mg. However, if the potassium comes back between 6 mmol/L and 6.4 mmol/L, we should suspend the RAAS inhibitor and discuss the initiation of potassium binders with our hospital colleagues. Finally, if that repeat potassium comes back at greater than or equal to 6.5 mmol/L, we should consider hospital referral.
I've coauthored a guide to interventions for chronic kidney disease in primary care, including a table on managing acute changes in kidney function related to RAAS inhibitors, which gives further detail. A link to this guide can be found in the transcript for this podcast. Or do drop me an email.
So, what did I do for Bridget? I maintained her losartan 50-mg dose and I rechecked her urea and electrolytes within 14 days. She had her repeat bloods done within 7 days, and those repeat urea and electrolytes revealed an eGFR of 55 mL/min (back to baseline) and a potassium of 4.9 mmol/L. I was reassured by those repeat urea and electrolytes, so I optimized the losartan dose (I increased it to 100 mg) and I rechecked her urea and electrolytes within 28 days, as her eGFR was below 60. Remember, if her eGFR was over 60, there would be no need to routinely recheck her urea and electrolytes.
Finally, I reiterated sick-day guidance to temporarily pause her relevant medications to prevent acute kidney injury, hyperkalemia, or, in the case of SGLT2 inhibitors, diabetic ketoacidosis. A useful mnemonic to remember is to temporarily pause the SAD MAN drugs during any acute dehydrating illness such as diarrhea and vomiting. Temporarily pause the SGLT2 inhibitor, ACE inhibitor, diuretic, metformin, ARB, and nonsteroidal. But importantly, we must remind patients to restart these drugs once they're eating and drinking normally and recovered from their illness.
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Cite this: Managing Hyperkalemia in the Community - Medscape - Feb 03, 2026.
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