What Should You Eat With Chronic Kidney Disease? Why There Is No Single ‘Kidney Diet’
One of the most common things I see in clinical practice is someone who has been diagnosed with chronic kidney disease (CKD), searched online for what they should eat, and subsequently placed themselves on a very restrictive ‘kidney diet’.
Typically, they have reduced protein, potassium and phosphorus—sometimes quite substantially—because these are the dietary restrictions most commonly associated with kidney disease.
The problem is that there is no single kidney diet that is appropriate for everyone with CKD.
Kidney disease describes a very broad group of conditions. Someone with early-stage diabetic kidney disease may have very different nutritional priorities from someone with IgA nephropathy, autosomal dominant polycystic kidney disease (ADPKD), advanced stage 4 CKD or someone receiving haemodialysis.
Even within the same stage of kidney disease, two people may require quite different diets depending on their blood results, medications, blood pressure, proteinuria, nutritional status, gastrointestinal health and other medical conditions.
This is why automatically following a low-protein, low-potassium and low-phosphorus diet simply because you have been diagnosed with CKD can sometimes be unnecessary and, in certain circumstances, potentially detrimental.
Where did the traditional ‘kidney diet’ come from?
Many of the restrictions people associate with a renal diet have an important clinical purpose.
As kidney function declines, the kidneys can become less effective at maintaining electrolyte and acid–base balance and eliminating metabolic waste products. Depending on the individual, this may contribute to hyperkalaemia, phosphate retention, metabolic acidosis and accumulation of nitrogenous waste.
However, the presence of kidney disease does not automatically mean all of these problems are occurring.
Current KDIGO guidance recommends that dietary adjustments involving sodium, phosphorus, potassium and protein are tailored according to the individual's needs, severity of CKD and comorbidities rather than prescribed as a standardised diet for everybody with kidney disease (KDIGO CKD Work Group, 2024).
A person with stage 2 CKD, normal potassium, normal phosphate and good nutritional status does not necessarily need to eat as though they have kidney failure. Likewise, a dietary approach suitable for someone approaching dialysis may be inappropriate once dialysis has commenced.
Protein is a good example of why stage matters
Protein restriction is probably one of the best-known components of the traditional renal diet.
There are physiological reasons for avoiding excessive protein intake in CKD. Protein metabolism produces nitrogenous waste products, and high protein intake can increase glomerular filtration and intraglomerular pressure. However, this does not mean that the lowest possible protein intake is automatically better.
The 2024 KDIGO CKD guideline suggests approximately 0.8 g of protein per kilogram of body weight per day for adults with CKD stages G3–G5 who are not receiving dialysis, while advising against high intakes above approximately 1.3 g/kg/day in people at risk of progression (KDIGO CKD Work Group, 2024).
KDOQI has proposed lower protein intakes for selected metabolically stable patients with non-dialysis CKD, illustrating that the appropriate degree of protein restriction depends on the individual and how the diet is supervised (Ikizler et al., 2020).
More intensive restriction may have a role in selected people with advanced CKD. In a randomised controlled trial, Garneata and colleagues compared a vegetarian very-low-protein diet supplemented with ketoanalogues against a conventional low-protein diet. In carefully selected patients who were able to adhere to the diet, the very-low-protein approach was associated with delayed initiation of renal replacement therapy without deterioration in measured nutritional parameters (Garneata et al., 2016).
This type of diet, however, requires adequate energy intake, careful food selection, appropriate supplementation and close monitoring. It should not be interpreted as evidence that people with CKD should simply eat as little protein as possible.
Once someone commences dialysis, the situation changes again. Dialysis is associated with amino acid and protein losses and an increased risk of protein-energy wasting. Protein requirements therefore generally increase rather than decrease. KDOQI recommends approximately 1.0–1.2 g/kg/day for metabolically stable adults receiving maintenance dialysis (Ikizler et al., 2020).
So telling everyone with kidney disease simply to ‘eat less protein’ misses an important part of the picture.
Potassium does not always need to be restricted
Potassium is another area where overly restrictive kidney diets can become problematic.
Hyperkalaemia can be dangerous and dietary potassium sometimes does need to be reduced. However, potassium should generally be managed in response to the individual's serum potassium, kidney function, medications, acid–base status, bowel function and other factors that influence potassium balance.
Current KDIGO guidance recognises that the relationship between food potassium and serum potassium is more complicated than was historically assumed (KDIGO CKD Work Group, 2024).
Potassium from whole plant foods is not necessarily absorbed in the same way as potassium salts used as additives in processed foods. Highly processed foods containing potassium additives, potassium-based salt substitutes and some animal foods can provide more readily absorbable potassium than many intact plant foods.
This means that automatically removing fruit, vegetables, legumes, nuts and whole grains because they contain potassium may unnecessarily reduce fibre, phytochemicals and overall dietary quality.
A small randomised proof-of-concept study published in 2025 examined a whole-food plant-based dietary education programme in people with stage 3–4 CKD and hypertension. Despite a substantial increase in plant foods, serum potassium did not increase significantly compared with controls (Liebman et al., 2025).
The study was small and short in duration, so it does not demonstrate that a high-potassium diet is safe for everyone with CKD. It does, however, reinforce why potassium recommendations should be individualised rather than based solely on lists of ‘high-potassium foods’.
If someone is experiencing persistent hyperkalaemia, potassium restriction may certainly form part of treatment. The important distinction is that the restriction should have a clinical reason.
Phosphorus is also more complicated than a list of foods to avoid
As kidney function declines, phosphate regulation can become increasingly difficult. However, the amount of phosphorus listed in a food does not tell us everything about how much will actually be absorbed.
Phosphorus naturally present in plant foods is often bound within phytate and is generally less bioavailable than phosphorus from animal foods, while inorganic phosphate additives used in processed foods are particularly readily absorbed.
KDOQI therefore recommends considering the source and bioavailability of phosphorus, rather than focusing on total phosphorus intake alone (Ikizler et al., 2020).
In a controlled crossover study of people with CKD, Moe and colleagues compared equivalent protein intake from predominantly vegetarian and meat-based diets. After one week, the vegetarian diet resulted in lower serum phosphorus and lower fibroblast growth factor-23 despite similar total phosphorus content (Moe et al., 2011).
This is why I generally consider the source and bioavailability of phosphorus, rather than simply adding up the phosphorus content of individual foods.
For some people with early CKD and normal phosphate regulation, aggressively restricting naturally phosphorus-containing whole foods may provide little advantage while substantially reducing dietary variety. In advanced CKD, particularly where phosphate is rising or CKD-mineral and bone disorder is developing, phosphorus management can become considerably more important.
Again, the blood results and clinical context should determine the diet.
The type of kidney disease matters too
CKD stage tells us how much kidney function has been lost. It does not necessarily tell us why it has been lost.
This distinction can substantially change the nutritional priorities.
For someone with diabetic kidney disease, the dietary plan also needs to consider glucose regulation, insulin resistance, cardiovascular risk, blood pressure and body composition. KDIGO's diabetes and CKD guidance incorporates protein and sodium intake within a broader strategy addressing glycaemic and cardiovascular risk rather than treating CKD as an isolated nutritional problem (KDIGO Diabetes Work Group, 2022).
With hypertensive kidney disease, sodium intake, blood pressure, vascular health, weight and broader cardiometabolic factors may take greater priority than unnecessarily restricting potassium-rich whole foods in a person whose serum potassium is normal.
With IgA nephropathy and other proteinuric glomerular diseases, proteinuria, blood pressure and sodium become particularly important considerations. The current KDIGO IgA nephropathy guideline includes dietary sodium restriction below 2 g/day as part of management of the consequences of nephron loss (KDIGO IgAN/IgAV Work Group, 2025).
With ADPKD, there are additional disease-specific considerations around sodium, hydration and, for some people, the use of tolvaptan. The 2025 KDIGO ADPKD guideline highlights lower sodium intake and individualised hydration advice, while warning that people with advanced CKD or conditions predisposing them to fluid retention or hyponatraemia should not simply increase water intake without clinical assessment (KDIGO ADPKD Work Group, 2025).
There remains considerable overlap between these diets, but the emphasis changes according to the underlying disease process. This is one of the reasons I do not think a generic downloadable ‘renal diet’ adequately addresses the nutritional management of CKD.
Food quality matters—not just potassium, phosphorus and protein
Renal nutrition has moved considerably beyond simply restricting individual nutrients.
The 2024 KDIGO guideline advises people with CKD to consume a healthy, diverse diet with a greater proportion of plant-based foods and fewer ultra-processed foods (KDIGO CKD Work Group, 2024).
This is important because diet also influences blood pressure, glycaemic control, cardiovascular risk, dietary acid load, bowel function and the gastrointestinal microbiome.
Dietary acid load is one example. In a three-year randomised study involving people with stage 3 CKD, Goraya and colleagues compared usual care with either sodium bicarbonate or increased base-producing fruits and vegetables. Both interventions improved acid–base measures and were associated with preservation of kidney filtration compared with usual care (Goraya et al., 2014).
This provides another reason not to remove plant foods indiscriminately, although the amount and type of fruit and vegetables still need to be considered in people with impaired potassium handling.
Food processing also deserves particular attention.
Many ultra-processed foods contain substantial sodium as well as inorganic phosphate and potassium additives. These added forms can be considerably more bioavailable than the phosphorus or potassium naturally contained within many whole foods.
KDIGO specifically advises lower consumption of ultra-processed foods and, in people with CKD stages G3–G5 who have hyperkalaemia, recommends focusing attention on foods containing highly bioavailable potassium, including processed foods containing potassium additives (KDIGO CKD Work Group, 2024).
Observational data also suggest that this may matter clinically. In the Chronic Renal Insufficiency Cohort study, greater ultra-processed food intake was associated with higher all-cause mortality and with CKD progression, particularly in participants with earlier-stage disease (Sullivan et al., 2023).
As an observational study, this cannot establish cause and effect. However, it supports shifting some of the focus away from simply restricting individual whole foods and towards improving the quality and degree of processing of the diet overall.
The gut–kidney connection
Another area I consider relevant when developing a nutritional plan for CKD is gastrointestinal and microbiome health.
Certain intestinal bacteria metabolise dietary substrates into compounds that are subsequently converted into uraemic solutes such as indoxyl sulphate and p-cresyl sulphate. As kidney clearance declines, these compounds can accumulate.
Dietary fibre may influence this process by shifting microbial metabolism away from predominantly proteolytic fermentation and towards carbohydrate fermentation, while also supporting short-chain fatty acid production and bowel regularity.
Rossi and colleagues found that a higher dietary protein-to-fibre ratio was associated with higher circulating concentrations of indoxyl sulphate and p-cresyl sulphate in people with CKD (Rossi et al., 2015).
Interventional research is also developing. An eight-week randomised controlled trial in haemodialysis patients found that fermentable resistant starch reduced p-cresol, although it did not significantly change indoxyl sulphate (Khosroshahi et al., 2019).
The gut–kidney axis is a promising area of renal nutrition, but it would be premature to claim that correcting the microbiome can reverse CKD.
What the research does support is taking gastrointestinal health seriously. Adequate fibre where clinically appropriate, plant diversity, bowel regularity and reducing reliance on ultra-processed foods may all form part of a broader renal dietary strategy.
For me, this is more useful than simply creating an increasingly long list of foods that somebody is no longer allowed to eat.
What should actually be assessed before developing a kidney diet?
Before making significant changes to someone's diet, I would generally want to understand much more than their eGFR.
Relevant considerations include:
the underlying kidney diagnosis
current CKD stage and trajectory of kidney function
urine protein or albumin levels
serum potassium
bicarbonate and acid–base status
phosphate, calcium and relevant mineral–bone markers
blood pressure
diabetes or insulin resistance
cardiovascular and metabolic health
current medications
body weight, muscle mass and overall nutritional status
gastrointestinal function and bowel regularity
current protein, sodium, fibre and overall food intake
other medical conditions that may alter nutritional requirements
whether the person is approaching dialysis, receiving dialysis or has received a kidney transplant.
For someone receiving dialysis, residual urine production, dialysis frequency and adequacy, fluid balance and the pattern of blood results between treatments become additional considerations.
It is only after looking at these factors together that it is possible to decide whether protein, potassium, phosphorus, sodium, fluid or other components of the diet actually need to be modified.
There is no single ‘renal diet’
The main point I try to convey to people with CKD is that a kidney-friendly diet should not simply be a restrictive diet.
The goal is to develop the least restrictive diet that appropriately manages the person's current renal and metabolic needs while maintaining nutritional adequacy and dietary quality.
For one person, this may involve reducing excessive protein and sodium. For another, the priority may be improving blood glucose regulation and replacing ultra-processed foods. Someone else may require active potassium or phosphorus restriction.
Another person may actually need their diet liberalised because unnecessary restrictions have resulted in inadequate energy, protein, fibre or micronutrient intake.
And once dialysis commences, priorities can change again.
This is why I recommend having renal nutrition assessed individually rather than relying on generic kidney diet information found online. Ideally, this should be undertaken by a qualified practitioner who regularly works with kidney disease, understands the nutritional differences between the various stages and causes of CKD, and can interpret dietary requirements in the context of current pathology results, medications and the person's broader health.
A well-designed renal diet is not about restricting everything that could potentially become a problem.
It is about identifying what is actually relevant to the individual in front of you and developing the diet around that.
References
Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. Kidney International. 2024;105(4S)–S314.
Ikizler TA, Burrowes JD, Byham-Gray LD, et al. KDOQI Clinical Practice Guideline for Nutrition in CKD: 2020 Update. American Journal of Kidney Diseases. 2020;76(3 Suppl 1)–S107.
Garneata L, Stancu A, Dragomir D, Stefan G, Mircescu G. Ketoanalogue-Supplemented Vegetarian Very Low-Protein Diet and CKD Progression. Journal of the American Society of Nephrology. 2016;27(7):2164–2176.
Kidney Disease: Improving Global Outcomes (KDIGO) Diabetes Work Group. KDIGO 2022 Clinical Practice Guideline for Diabetes Management in Chronic Kidney Disease. Kidney International. 2022;102(5S)–S127.
Kidney Disease: Improving Global Outcomes (KDIGO) IgAN/IgAV Work Group. KDIGO 2025 Clinical Practice Guideline for the Management of Immunoglobulin A Nephropathy and Immunoglobulin A Vasculitis. Kidney International. 2025;108(Suppl 4S)–S71.
Kidney Disease: Improving Global Outcomes (KDIGO) ADPKD Work Group. KDIGO 2025 Clinical Practice Guideline for the Evaluation, Management, and Treatment of Autosomal Dominant Polycystic Kidney Disease. Kidney International. 2025;107(Suppl 2S)–S239.
Moe SM, Zidehsarai MP, Chambers MA, et al. Vegetarian compared with meat dietary protein source and phosphorus homeostasis in chronic kidney disease. Clinical Journal of the American Society of Nephrology. 2011;6(2):257–264.
Goraya N, Simoni J, Jo CH, Wesson DE. Treatment of metabolic acidosis in patients with stage 3 chronic kidney disease with fruits and vegetables or oral bicarbonate reduces urine angiotensinogen and preserves glomerular filtration rate. Kidney International. 2014;86(5):1031–1038.
Rossi M, Johnson DW, Xu H, Carrero JJ, Pascoe E, French C, Campbell KL. Dietary protein–fibre ratio associates with circulating levels of indoxyl sulphate and p-cresyl sulphate in chronic kidney disease patients. Nutrition, Metabolism and Cardiovascular Diseases. 2015;25(9):860–865.
Khosroshahi HT, Abedi B, Ghojazadeh M, Samadi A, Jouyban A. Effects of fermentable high-fibre diet supplementation on gut-derived and conventional nitrogenous products in patients on maintenance haemodialysis: a randomised controlled trial. Nutrition & Metabolism. 2019;16:18.
Liebman SE, Baran A, Barnett TD, et al. The effects of a whole-food plant-based nutrition education programme on blood pressure and potassium in chronic kidney disease: a proof-of-concept study. Nutrients. 2025;17(5):779.
Sullivan VK, Appel LJ, Anderson CAM, et al.; CRIC Study Investigators. Ultraprocessed Foods and Kidney Disease Progression, Mortality, and Cardiovascular Disease Risk in the CRIC Study. American Journal of Kidney Diseases. 2023;82(2):202–212.
This article provides general educational information and is not intended to replace individual medical or nutritional assessment. Dietary requirements in chronic kidney disease can change substantially according to kidney function, pathology results, medications and treatment stage.