Jessica Coleman, MD
As a practicing nephrologist, I often see chronic kidney disease (CKD) patients with hyperkalemia—defined as a serum potassium level >5.0 mEq/L. That is not surprising given that the prevalence of hyperkalemia among patients with CKD is considerably higher than in the general population—40% to 50% versus 2% to 3%.1 These patients tend to be elderly, possibly because they are more likely than younger patients to suffer from a comorbidity—diabetes, cardiovascular disease, or advanced stages of heart failure, for example—that interferes with renal potassium excretion. For these patients, hyperkalemia can be a chronic problem.
Another group at increased risk of chronic hyperkalemia is CKD patients who are taking a renin angiotensin aldosterone system (RAAS) inhibitor to manage the progression of their renal disease. Among the most commonly prescribed RAAS inhibitors, which can cause hyperkalemia as a side effect, are angiotensin receptor blockers, mineralocorticoid receptor antagonists, and angiotensin-converting enzyme inhibitors. Aldosterone blocking agents, such as spironolactone, beta blockers, and nonsteroidal anti-inflammatory drugs are among other drugs frequently prescribed to CKD patients that can cause hyperkalemia.
Because hyperkalemia can cause potentially fatal cardiac arrhythmias and even sudden death, it is imperative that hyperkalemic CKD patients be managed consistently and over the long term. The goal of chronic management is to prevent recurrence by correcting the underlying potassium imbalance. For decades, however, the nephrology community was limited in the options we had to treat these patients.
We could recommend a low potassium diet to reduce high potassium intake, but patients have difficulty adhering to such a diet because potassium is found in many popular and healthy foods. Moreover, CKD patients often suffer from concomitant conditions and may already be on a restricted low-sodium or low-carbohydrate diet. Another option was to prescribe Kayexalate, a sodium polystyrene sulfonate (SPS), but this treatment can be difficult for some patients to tolerate and has a label warning of potential gastrointestinal (GI) injuries. Additionally, published data on the safety and efficacy of SPS for the chronic management of hyperkalemia is limited. For CKD patients on a RAAS inhibitor, we were limited to reducing the dose or discontinuing the RAAS regimen altogether, even though keeping patients on this therapy is necessary to preserve renal function.
In the last two years, those treatment limitations were lifted with the introduction of a new class of potassium binders. Yet, even with the commercial availability of a non-absorbed polymer medicine, many hyperkalemic CKD patients are still not being treated optimally. A variety of factors account for this, but all of the challenges can be successfully addressed. For instance:
A large proportion of patients with hyperkalemia remain undiagnosed—mainly because the condition is often asymptomatic or first presents as sudden death due to arrhythmia. Because many CKD patients are at high risk for hyperkalemia, testing all patients for elevated serum potassium is essential.
Some nephrologists who treat hyperkalemic CKD patients on RAAS inhibitors think they need to modify or eliminate the patient’s RAAS inhibitor therapy in order to control their hyperkalemia. However, with new advances in treatment, hyperkalemia can be treated directly rather than requiring that the RAAS inhibitor the patient is taking for their underlying renal disease be regulated.
In some cases, hyperkalemic CKD patients are treated with SPS as a one-time only management strategy. Besides the GI risks associated with SPS, this approach may result in an increased sodium load—a special concern for CKD patients, especially those with hypertension. With new treatment advances that exchange potassium for calcium rather than sodium, this can be avoided.
I have found that many of my CKD patients fail to take their hyperkalemia medication as prescribed because they don’t understand the severity of the condition or the importance of chronic management. For those patients, I explain that having a high level of potassium in their blood can cause potentially fatal heart rhythm disturbances and even sudden death, and that a type of potassium is used in lethal injections because it stops the heart.
In summary, patients with reduced kidney function due to CKD are at risk for chronic hyperkalemia and their ability to maintain potassium homeostasis is increasingly impaired as their kidney disease progresses and renal function declines. Because hyperkalemia is a chronic problem for many CKD patients, this potentially life-threatening condition must be managed in all patients, including those on RAAS inhibitor therapy and those with end-stage renal disease. With the evolution in hyperkalemia treatments leading to advances in management, clinicians now have a viable option to treat hyperkalemia over the long term.
Jessica Coleman, MD, is a nephrology specialist at Nephrology & Hypertension Medical Associates, in Beaufort, South Carolina. She received her medical degree from Mercer University School of Medicine in Macon, Georgia, and completed a residency in internal medicine at the University of Kentucky. She is board certified in internal medicine and nephrology. Dr. Coleman is a paid consultant for Relypsa, Mallinckrodt Pharmaceuticals, and Otsuka.
Kovesdy CP. Management of hyperkalaemia in chronic kidney disease.
Nat Rev Nephrol. 2014; 10(11):653-662