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For many people living with chronic kidney disease, eating fruits, vegetables, legumes, or potatoes can quickly trigger caution, or even avoidance. Indeed, the potassium content of these foods is a source of concern, sometimes to the point of overshadowing their well-documented nutritional benefits. However, in recent years, research has challenged a long-held belief: that dietary potassium alone is a major determinant of hyperkalemia, meaning an elevation of blood potassium levels above the normal range (3.5-5.0 mmol/L).
Chronic kidney disease (CKD) is defined by a progressive and irreversible decline in kidney function, evidenced by a decrease in glomerular filtration rate (GFR) and/or the presence of persistent kidney abnormalities for more than three months. CKD is classified into different stages, from stage 1 (mildly impaired kidney function) to stage 5, corresponding to end-stage kidney disease, where the kidneys can no longer effectively filter the blood. Often asymptomatic in its early stages, CKD is associated with multiple metabolic disturbances, including hyperkalemia. Physicians closely monitor blood potassium due to its potential link with serious cardiac complications.
In this context, potassium restriction has long been a cornerstone of nutritional recommendations. However, this approach now deserves to be revisited in light of recent scientific evidence.
Historically, hyperkalemia in people with CKD has been largely attributed to excessive dietary potassium intake. This view often led to uniform nutritional recommendations aiming to limit all potassium-rich foods regardless of their source or the patient’s clinical profile. This approach was based on the idea that the amount of potassium consumed in the diet was the primary factor influencing blood potassium levels. What recent data reveal: a weaker correlation than anticipated.
Observational studies published in recent years have shown that the correlation between dietary potassium intake and blood potassium concentration is often weak in people with non-dialysis CKD. In several cohorts, higher dietary potassium consumption was not associated with a significant increase in the risk of hyperkalemia.
These findings suggest that, for many patients, hyperkalemia does not depend solely on dietary intake. It is influenced by multiple factors, including the stage of kidney disease, the presence of diabetes, acid-base balance, and the use of certain medications commonly prescribed in CKD, such as renin-angiotensin-aldosterone system inhibitors. Thus, two individuals with CKD consuming similar amounts of potassium may exhibit very different biological responses.
A key point from recent data is the distinction between different sources of potassium. Potassium naturally present in minimally processed foods, such as bananas, is often absorbed more slowly due to fiber content and the food’s structure, which can limit intestinal absorption. In contrast, potassium added as a food additive, frequently used in ultra-processed foods, is rapidly and almost completely absorbed. In practice, highly processed foods rich in potassium additives, as well as certain meats, dairy products, juices, and salt substitutes containing potassium chloride, can provide a higher and more readily absorbed potassium load than many fresh plant-based foods.
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