The Hidden Impact of Ultra-Processed Foods on Chronic Kidney Disease; Much Needed Publicity

Andrew Kowalski, MD, FASN

An article by the Wall Street Journal (WSJ, Nov. 2023) titled Trouble With America’s Ultra-Processed Diet crossed my news feed this past week and greatly sparked my interest. My first thought was why didn't I see this sooner, but nevertheless I am seeing it now. My second thought was if this article was featured in the WSJ, then why haven't we seen more of a push towards educating readers or tidbits in the media?

Either way, the subject of UPF (ultra-processed foods) is one I frequently discuss with my patients as it has been strongly implicated as a prominent driver in the progression of diabetes, heart disease and of course CKD.

Aside from reading some of the disturbing facts and cautions in the above article, I was excited, and unnerved, to stumble upon another article on LinkedIn highlighting the impact of processed foods among children. In the paper by V. S. Chamarthi, P. Shirsat et al, they presented the startling fact of how UPF are effecting the children of Western nations. Quoting them, "UPFs now make up nearly 70% of US children's calories - driving obesity, cardiometabolic risk, mental health, liver disease..." and of course CKD.

UPFs are a runaway train contributing to practically all the current preventable diseases and it will take a culture change to reroute and begin the massive healing process that is so desperately needed.

Let begin with some definitions, UPFs are industrially manufactured products that undergo extensive modifications including chemical, physical, and biological that strip away their natural structure. Some key examples include sweetened cereals, packaged snack cakes, soda, flavored yogurts, hot dogs (I'm sad too), chicken nuggets (oh lovely childhood), and instant noodles. Unlike minimally processed foods (etc. canned beans or plain oats), UPFs are built from extracted or synthetic ingredients such as high-fructose corn syrup, hydrogenated oils, protein isolates, flavor enhancers, and preservatives (natural in every way...huff).

From a nephrology standpoint, this distinction is not trivial. Patients with CKD are particularly vulnerable to the effects of UPFs because of their high phosphate additive load, excess sodium, poor fiber content, and inflammatory potential. Studies have shown that many UPFs contain inorganic phosphate salts used to improve texture and shelf life that are absorbed far more readily than naturally occurring phosphorus, contributing to hyperphosphatemia, vascular calcification, and accelerated CKD progression. Furthermore, sodium-rich UPFs exacerbate hypertension and volume overload, two cornerstones of CKD progression and cardiovascular risk. All the while, offering lack of dietary fiber and the presence of emulsifiers and artificial sweeteners that will disrupt the gut microbiome, fueling low-grade systemic inflammation.

Ultra-Processed Foods, Inflammation, and Sarcopenia in CKD

The CKD triad of inflammation, muscle wasting (sarcopenia), and kidney disease progression is increasingly recognized as a central axis of poor outcomes. UPFs intersect with each of these domains:

• Inflammation: Chronic intake of UPFs is associated with elevated CRP and IL-6 (key markers of inflammation) levels in the general population. In CKD and dialysis patients, who already live in a pro-inflammatory state, this dietary pattern further amplifies the inflammatory burden. Inflammation not only accelerates glomerulosclerosis (scarring of the filter of the kidney) and loss of residual kidney function, but also worsens cardiovascular morbidity, anemia resistance, and malnutrition-inflammation-atherosclerosis (MIA) syndrome.

• Sarcopenia: Protein quality is another critical concern. While UPFs may be calorie-dense, they are often poor in high-biological-value (HBV) protein and micronutrients essential for muscle preservation. Instead, they contribute empty calories, leading to fat gain without muscle support. For CKD patients, this promotes sarcopenic obesity: a state of low muscle mass combined with excess adiposity, linked to frailty, falls, dialysis intolerance, and higher mortality.

• Kidney Disease Progression: The additive effects of phosphorus overload, sodium-driven hypertension, and inflammation accelerate kidney decline. Observational data suggest that diets rich in UPFs are linked with faster eGFR decline and greater risk of new onset CKD. This positions dietary processing as an unrecognized driver of renal outcomes.

  
  

Implications for Clinical Care and Policy

For all nephrology practices, the implications are significant. Patient counseling should not stop at “limit salt” or “cut back on sugar.” Instead, dietary conversations must address degree of food processing. A CKD patient choosing baked chicken with herbs, steamed vegetables, and brown rice is not only lowering sodium and phosphorus exposure but also reducing inflammatory triggers compared with choosing chicken nuggets, boxed macaroni, and a cola, even if the macronutrient totals appear similar.

From a policy perspective, the availability of UPFs are often cheaper and more accessible than fresh foods, and this presents significant barriers. CKD disproportionately affects populations with limited resources, meaning patients often rely on inexpensive ultra-processed foods that worsen their prognosis. Strategies must include labeling reforms (clear disclosure of phosphorus additives), subsidies for fresh produce, reformulation of UPFs, and culturally tailored nutrition education.

By linking UPF consumption to the CKD triad of inflammation and sarcopenia, the message becomes sharper: what patients eat is not only about calories or protein, it is about the biological impact of processing itself. Reducing UPFs represents a powerful, underutilized lever in slowing CKD progression, dampening inflammation, and preserving muscle mass and functional independence.

While looking at the literature for this post I found numerous published papers citing concern over UPFs.

What the evidence strongly suggests is...

• Many observational studies and meta-analyses link higher UPF intake with increased risks of obesity, type-2 diabetes, cardiovascular disease, various metabolic problems, mental health issues, and mortality.

• There is fairly consistent evidence that UPFs tend to have poorer nutritional profiles: more added sugar, salt, saturated fat; lower fiber; less nutrient density.

• Some studies have suggested other mechanisms beyond just “bad nutrients,” such as effects on appetite regulation, gut microbiome disruptions, or how ultra-processed items may lead to overconsumption due to palatability and convenience.

As is when reading the literature, you are bound to stumble upon lobbiests and criticism that have been put forth to stumble the average patient and even occasional clinician.

What are the limitations/criticisms and industry arguments?

Observational versus experimental evidence

• Much of the research is observational (cohort studies, case-control). Observational data can only show associations but not prove causation. Confounding variables (e.g. income, overall lifestyle, other dietary patterns) may account for some of the inconsistencies.

• There are few long-term randomized controlled trials (RCTs) that isolate UPF consumption vs other diets or trends. That being said, it’s harder to nail down exactly which features of UPFs cause harm, or how much modifying UPF intake alone helps.

Definition ambiguity and classification

• The NOVA (a commonly used classification of ultra-processed foods) and other schemes vary in how clearly they define “ultra-processed.” The boundaries are fuzzy, which can lead to misclassification of foods that are studied. For example, some foods that are “processed” but not “ultra-processed” are lumped together, or vice versa...tOmato, tomAto is what I say.

• There are even arguments that grouping very different foods (snacks, sodas, reformed meats, sweetened cereals, etc.) under “UPFs” throws away nuance. One argument stated that some UPFs are relatively benign (or even helpful if fortified, ie. bread and breakfast cereals). The “all or nothing” framing is grossly oversimplified.

  
  

Dose and effect sizes

• In many studies, the portion sizes are modest as risks of a disease or a event typically increases with greater intake of what is being measured. That means that moderate consumption may carry smaller risk. Therefore, eal world complications depend heavily on how much people are eating and as a result the evidence in some studies are far from impressive..

Mechanisms are still being worked out

• Unfortunatelly, we don’t fully understand how ultra-processing causes health harms. Some plausible mechanisms (additives, emulsifiers, physical structure, etc.) have been mentioned, but the conclusion is that inflammation is activated. One CLASSIC example is why many tobacco products are still on the market. Not everyone who smokes will die of lung cancer, although many will, and there are non-smokers that get lung cancer and die.

• There’s also the question of whether it's the processing or simply the end product’s diet quality (calories, sugar, fat, fiber) that matters most. Some of the negative health outcomes could be fully explained by those “classic” nutritional issues; ie. overeating, lack of exercise, high-fat diets and so forth.

Balancing it all Together

• The risk associated with high UPF intake is probably VERY real, particularly in diets where UPFs are a large fraction of intake (like a whole box of Twinkies).

• UPFs are likely on a spectrum of "ok-->please don't eat it." Some might play useful roles in food systems (shelf life, affordability, convenience). Although I doubt eating a hamburger that has been sitting around for years without mold would not contribute to something happening in your body.

• It may be more useful and even easier to focus on reducing the worst UPFs (high sugar, salt, low fiber, high calorie density) rather than demonizing all processed or ultra-processed foods.

• More RCTs, refined definitions, mechanistic studies are needed to clarify which features are most harmful, and what interventions (dietary, regulatory, behavioral) are most effective.