Can Novel Potassium Binders Liberate People with Chronic Kidney Disease from the Low-Potassium Diet?: A Cautionary Tale : Clinical Journal of the American Society of Nephrology

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Can Novel Potassium Binders Liberate People with Chronic Kidney Disease from the Low-Potassium Diet?

A Cautionary Tale

St-Jules, David E.1; Clegg, Deborah J.2; Palmer, Biff F.3; Carrero, Juan-Jesus4

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CJASN 17(3):p 467-472, March 2022. | DOI: 10.2215/CJN.09660721
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People with CKD are at risk for hyperkalemia, a potentially life-threatening condition. Awareness of risk of hyperkalemia in CKD began in the 1940s with kinetic studies demonstrating that ingesting large doses of potassium salts increased plasma potassium concentrations to a much greater extent in people with CKD compared with healthy controls (1,2). At the time, the findings were interpreted with regard to the use of potassium-based diuretics rather than dietary potassium restriction. However, hyperkalemia was a common complication of the very low–protein diets that were introduced in the 1960s for conservative management of kidney failure, and restricting dietary potassium intake to 1000 mg/d (25 mEq/d) was proposed as a way of managing this problem (3,4). Since this time, low-potassium diets (2000–3000 mg/d [50–75 mEq/d]) have been standard first-line therapy for preventing and treating hyperkalemia in people with CKD (5,6).

In healthy individuals, absorbed dietary potassium is rapidly taken up by cells and excreted by the kidneys, preventing any notable changes in plasma potassium concentrations (7). This process appears to be mediated, in part, by a yet to be characterized feed-forward mechanism that increases kaliuresis as much as five-fold in response to dietary potassium (8–10). As kidney function declines in CKD, there is a corresponding decline in the ability of the kidneys to increase kaliuresis postprandially (8,9), and eventually, kaliuresis is no longer sufficient to maintain external potassium balance. Loss of kaliuresis in kidney failure is partially offset by adaptations, such as increased colonic secretion of dietary potassium in stool (11). These adaptations appear adequate to maintain external potassium balance, even in patients reporting high–dietary potassium intakes (12–14). However, this mechanism does not prevent postprandial increases in plasma potassium concentrations in people with kidney failure (1,2,7–9,15,16), perhaps because it lacks the ability to increase potassium secretion in response to dietary potassium intakes, as the kidneys do (Figure 1) (8–10).

Figure 1.:
Novel potassium binders may not reduce postprandial hyperkalemia risk in people with kidney failure. (A) Healthy individuals. Following a meal, plasma potassium values are maintained in the normal range by shifting potassium intracellularly through insulin-mediated increases in sodium-potassium ATPase (Na/K-ATPase) activity on cells and by increasing potassium excretion in the kidneys (kaliuresis) via a potassium-sensing feed-forward mechanism (7,8,10). (B) Kidney failure (without potassium binders). Similar to healthy individuals, potassium is shifted intracellularly after a meal. However, loss of kidney function precludes an increase in kaliuresis (8,9). Some potassium can be secreted through the bowels (11), but this mechanism lacks the feed-forward regulation of the kidneys, and therefore, the rate of secretion corresponds to that needed to maintain external potassium balance (e.g., 2400 mg K diet =100 mg/h). As a result, plasma potassium values increase postprandially (7). (C) Kidney failure (with potassium binders). Potassium binders increase the rate of potassium secretion in the bowels (30), which may attenuate the increase in plasma potassium values postprandially. However, the onset of action of potassium binders is not timed to coincide with dietary potassium intake. The increase in the rate of potassium secretion in the bowels is limited and cannot replicate the feed-forward mechanism of functioning kidneys. Importantly, potassium binders have been found to decrease plasma aldosterone levels (35), which may decrease Na/K-ATPase activity and potassium uptake by cells postprandially (36). ECF, extracellular fluid; ICF, intracellular fluid; K, potassium.

We feel there are two distinct goals behind the so-called low-potassium diet therapy in CKD: one is preventing postprandial hyperkalemia, and the other one is preventing potassium bioaccumulation (chronic hyperkalemia). Exploring both goals is outside the scope of this review, and we will focus primarily on the effect of dietary potassium on postprandial kalemia. Briefly, postprandial hyperkalemia occurs when dietary potassium is absorbed at a rate exceeding cellular uptake and body excretion, causing it to temporarily accumulate in the extracellular compartment. Numerous kinetic studies in people with CKD have shown that plasma potassium concentrations increase within 30 minutes of ingesting potassium and remain elevated for up to 3 hours (1,2,7–9,15,16). The sustained increase in plasma potassium levels in people with CKD suggests a potential for piggybacking kalemic responses and need to consider the temporal distribution of dietary intakes. The postprandial rise in plasma potassium levels may be blunted by insulin-stimulating and base-forming compounds in food, which promote potassium uptake by cells (15), and by dietary fiber, which may lower the rate and amount of potassium absorbed (13). In contrast, chronic hyperkalemia occurs when the total amount of potassium absorbed from the diet exceeds body excretion (external balance disorders) and/or when the distribution of body potassium shifts from the intracellular to extracellular compartment (internal balance disorders). It is important to recognize that postprandial and chronic hyperkalemia are related but distinct conditions in people with CKD. Although they share common risk factors, such as impaired urinary potassium excretion and metabolic acidosis, a large bolus of ingested potassium can cause postprandial hyperkalemia in patients with CKD without chronic hyperkalemia (2).

The long-standing recommendation to prevent hyperkalemia in people with CKD has been to limit or avoid high-potassium foods (5,6). This approach might be suitable if the only dietary consideration was postprandial hyperkalemia and if the postprandial kalemic response was only determined by dietary potassium intake. However, we now know that this is not the whole story and offers an incomplete picture of the clinical context. For one, plasma potassium levels are generally measured in the predialysis (hemodialysis [HD]) and fasting (non-HD) states, not the postprandial state. These timings are better suited to evaluate chronic hyperkalemia risk. Although dietary factors, such as dietary acid load and dietary fiber intake, may affect chronic hyperkalemia risk (13), potassium intake does not appear to be an important determinant of predialysis and fasting plasma potassium concentrations. In fact, evidence for the bioaccumulation of dietary potassium as a major cause of hyperkalemia is, if any, weak or lacking (12–14), likely reflecting the capacity of bowel adaptation to maintain external potassium balance (11,17). These findings have spurred considerable interest in the potential benefits of liberalized, plant-rich diets in people with CKD (17). However and central to this review, patients with advanced CKD are at risk of postprandial hyperkalemia, regardless of their diet or their basal plasma potassium levels. Although eliminating the ban on high-potassium plant foods may be justified and bring other benefits associated to the nutrients that often accompany potassium-rich foods (18), certain elements of the low-potassium diet may still be important for people with CKD, and potassium exchange resins may not necessarily overcome this need.

The postprandial rise in plasma potassium from ingested potassium can be consequential. In the early 1990s, Allon et al. (7) conducted a series of potassium kinetic studies in patients on maintenance HD without diabetes mellitus and healthy controls (n=8 per group) that analyzed plasma potassium levels before and at 30-minute intervals for 3 hours after ingesting a 0.25-mEq/kg solution of potassium chloride in a fasted state. The mean peak increase in plasma potassium concentrations was 0.9 mEq/L in patients on HD compared with 0.5 mEq/L in controls (P<0.001), and crucially, potassium levels remained roughly four times higher than those in controls at 3 hours (approximately +0.78 versus +0.18 mEq/L on the basis of visual assessment of the graph). When 50 g of dextrose was included with the potassium load, mean plasma potassium levels remained at basal levels throughout the 3-hour monitoring period in the control group but gradually increased in the HD group by approximately 0.4 mEq/L at the 150- and 180-minute time points, highlighting the role of meal composition and temporal distribution in determining postprandial hyperkalemia risk in people with CKD. Importantly, this amount of potassium (684 mg for a 70-kg patient) is moderate, particularly when compared with some processed food products containing potassium additives. Indeed, although food composition data on potassium additives are limited, one study identified a sodium-reduced ham that contained more than double this amount of potassium (1500 mg/100 g [3.5-oz] portion) (19).

Since 2015, the US Food and Drug Administration and the European Medicines Agency approved two new potassium exchange resins: patiromer (Veltassa) and sodium zirconium cyclosilicate (Lokelma). Classic potassium exchange resins (sodium and calcium polystyrene sulphonate) have had tolerability issues and the very rare complication of life-threatening bowel necrosis that limited their widespread use as chronic therapy (20–22). In contrast, these new exchange resins appear relatively safe and efficacious for long-term use (23,24). Thus, the promise for these drugs to allow for liberalization of the low-potassium diet in people with CKD has been theorized (25,26).

What Is in a Name?

New potassium exchange resins effectively reduce circulating potassium levels in people with CKD (27), but the term potassium “binder” may be misleading. The name binder suggests a parallel mechanism of action to phosphate binders, which are taken with meals to bind to dietary phosphate, preventing its absorption. Similar to phosphate binders, potassium exchange resins target external potassium balance by increasing fecal excretion of potassium from the body. However, unlike phosphate binders, potassium exchange resins are cation-exchange resins that may have a limited effect on dietary potassium absorption, particularly as prescribed.

The ability of potassium exchange resins to lower plasma potassium concentrations in people with CKD is independent of dietary potassium intake. In fact, one of the early clinical trials demonstrating efficacy of patiromer for lowering plasma potassium concentrations in patients with CKD and hyperkalemia included a 3-day controlled feeding run-in period of a low-potassium diet (approximately 2400 mg/d) and instructions to remain on a low-potassium diet during the study (approximately 2000–3000 mg/d) (28). Of interest, following the run-in feeding period of a low-potassium diet, the vast majority of enrolled participants (n=25/27; 93%) continued to have hyperkalemia, highlighting the limited effect of total dietary potassium intake on chronic hyperkalemia. Because potassium exchange resins bypass the normal homeostatic mechanisms to increase fecal potassium excretion, regardless of potassium intake (29), they may be ideally targeted toward disorders that impair potassium excretion from the body, which are common in CKD, such as conditions and medications that inhibit the renin-angiotensin-aldosterone system (e.g., hyporeninemic hypoaldosteronism, renin-angiotensin-aldosterone system inhibitors, spironolactone). At the same time, potassium exchange resins have been shown to be effective in lowering plasma potassium concentrations in anuric patients with hyperkalemia (30), suggesting that potassium bioaccumulation from inadequate fecal potassium excretion may contribute to hyperkalemia in this population, despite the apparent lack of association with dietary potassium intakes (12–14). Supporting this concept, constipation has been found to be associated with hyperkalemia in at least one observational study of patients on HD (31), and laxative use in people with advanced CKD was associated with significantly lower risk of hyperkalemia (odds ratio, 0.79; 95% confidence interval, 0.76 to 0.84) (32). In addition, in a small pilot study of patients with kidney failure (n=13), treatment with Bisacodyl (Dulco-lax) was associated with a significant decrease in plasma potassium concentrations (5.9±0.2–5.5±0.2 mEq/L; P<0.001) (33). What remains unclear is the extent to which increasing fecal potassium excretion from potassium exchange resins is sufficient to blunt postprandial kalemic response.

The amount of additional potassium excreted in stool from potassium exchange resins depends on the drug dose, but effective doses have been found to remove 1000 mg or more potassium per day in stool (34). Importantly, the reduction in plasma potassium lowers plasma aldosterone concentration (35), which is thought to reduce aldosterone-dependent increases in bowel potassium secretion, and limits potassium depletion and hypokalemia. Despite the apparent benefits of suppressing plasma aldosterone concentrations on external potassium balance, this shift may impair cellular adaptations that protect against postprandial hyperkalemia. In a landmark series of experiments, Alexander and Levinsky (36) demonstrated that rats fed a high-potassium diet had lower postprandial kalemic response to a potassium bolus, even after nephrectomy, and that this adaptation was mediated by aldosterone-dependent increases in cellular uptake of potassium (i.e., not bowel secretion of potassium) (36). Subsequently, this phenomenon has been demonstrated to be achieved by increasing the activity of Na/K-ATPases on cells, which facilitates insulin-mediated potassium uptake in the postprandial state (37,38).

As previously mentioned, unlike phosphate binders, the timing of potassium exchange resins is not intended to have an onset of action coinciding with dietary potassium intake. For example, potassium exchange resins are given once daily typically at lunch to avoid interactions with other medications in the morning and evening. Given their onsets of action ranging from 1 to 7 hours (28,39), increases in potassium excretion from potassium exchange resins are unlikely to coincide with potassium intake from diet. Consequently, similar to the homeostatic mechanisms in the bowels that take over regulation of external potassium balance as the kidney fails, potassium exchange resins may lack the feed-forward increase in potassium excretion that protects against postprandial hyperkalemia in intact kidneys. If the increase in stool potassium excretion from potassium exchange resins is roughly evenly distributed across the day, then the amount of additional potassium removed postprandially would average roughly 50 mg/h. For comparison, the increase in kaliuresis from a potassium bolus in healthy kidneys was found to be >300 mg/h in one study (8).

Potassium Exchange Resins and Postprandial Hyperkalemia

New potassium exchange resins are an important breakthrough in the chronic management of hyperkalemia risk in people with CKD. Many researchers and clinicians (ourselves included) have viewed these new medications as a possible means to safely transition patients away from the low-potassium diet to a more healthful eating pattern (25,26). However, it is important to recognize that the need to restrict dietary potassium is largely related to the risk of postprandial hyperkalemia, whereas these medications primarily target hyperkalemia caused by potassium retention and bioaccumulation, which have not been clearly linked to reported dietary potassium intakes (12–14).

Even if potassium exchange resins could be timed with meals, it is not clear that they would have a significant effect on postprandial hyperkalemia. The majority of ingested potassium is absorbed alongside endogenously secreted potassium in the small intestines through solvent drag via the paracellular pathway (40). Patiromer is specifically designed to function beyond this point in the large intestine, having an onset of action of about 7 hours (28). Sodium zirconium cyclosilicate has a relatively rapid onset of action (1 hour), suggesting that potassium binding may begin in the small intestine (39). However, the actual concentration of potassium in the small intestine is relatively low compared with that of the large intestine (5–20 versus 70–80 mEq/L), and it is not clear that potassium binding at this low concentration would significantly overcome the convective flux of potassium drag to significantly reduce dietary potassium absorption.

It is possible, but currently unknown, that lowering the premeal plasma potassium concentrations will lower the absolute peak postprandial plasma potassium concentrations in patients taking potassium exchange resins. Yet, the problem remains that normal fasting plasma potassium concentrations may not prevent postprandial hyperkalemia and corresponding cardiac arrhythmia in people with CKD (2). For example, in a study of eight nondiabetic, anuric patients on HD (16), there was a strong negative correlation between fasting plasma potassium concentrations and peak changes in plasma potassium concentrations following a potassium-glucose bolus in carrot juice (20 mg potassium and 0.5 g glucose per 1 kg). Specifically, the peak change in plasma potassium concentrations was approximately two-fold higher at fasting plasma potassium concentrations of 4 mEq/L compared with 6 mEq/L (r=−0.79; P=0.02). Importantly, participants’ body weights and, therefore, the doses of potassium and glucose were not reported in this study and could have affected these results.


Potassium exchange resins appear to be safe and efficacious for lowering plasma potassium concentrations in people with CKD. Whenever possible and indicated, clinicians should consider their use. However, there is uncertainty regarding the effects of potassium exchange resins on the absolute and relative changes in plasma potassium concentrations following a high-potassium meal. This represents a major knowledge gap that warrants being addressed. Until these questions are answered, clinicians and patients may wish to be cautious, as normal basal plasma potassium levels may offer a false sense of safety regarding dietary potassium.


J.-J. Carrero reports consultancy agreements with AstraZeneca and Bayer; receiving research funding from Astellas, AstraZeneca, the Swedish Heart and Lung Foundation, the Swedish Research Council, and ViforPharma; serving as a scientific advisor or member of the advisory committee of AstraZeneca and the editorial boards of Journal of Nephrology and Nephrology Dialysis Transplantation; speakers bureau for Abbott Laboratories, AstraZeneca, Fresenius, and ViforPharma; and other interests/relationships with the European Renal Nutrition Working Group at the European Renal Association and the International Society of Renal Nutrition and Metabolism. D.E. St-Jules reports receiving research funding from Relypsa, Inc.; receiving speaking fees from Ardelyx, manufacturers of novel potassium binders; and serving on the editorial board of Journal of Renal Nutrition. All remaining authors have nothing to disclose.



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cation exchange resins; diet; potassium; chronic renal insufficiency; chronic kidney disease

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