Do Low-Carbohydrate or High-Protein Diets Harm the Kidneys? What the Research Actually Shows

Patients are often warned that low-carbohydrate diets are dangerous for the kidneys because they supposedly contain too much protein. The warning is repeated so often that many people assume it is a settled fact.

It is not.

Controlled human trials have not demonstrated that higher protein intake causes chronic kidney disease in people with healthy kidneys. Trials lasting one to two years have found no harmful effect on measured kidney function, albumin excretion or electrolyte balance compared with higher-carbohydrate or low-fat diets—even when the low-carbohydrate group ate more protein.[4–10]

This does not mean that protein intake never matters. A person with advanced or high-risk chronic kidney disease may need a deliberately moderate protein target, and that target should be coordinated with a physician or nephrologist and a renal dietitian. People receiving dialysis may have higher protein needs, not lower ones. The important distinction is between claiming that protein causes kidney disease in healthy kidneys and using protein moderation as a therapeutic tool after significant kidney disease is present.

Low-carbohydrate nutrition also deserves to be evaluated on its actual composition. A well-formulated ketogenic diet is usually moderate in protein, not an unlimited-protein diet. Its defining feature is carbohydrate restriction and the resulting shift toward fat and ketones as major fuels.

Three kidney questions that should not be confused

Discussions about “keto and the kidneys” often collapse three different questions into one:

1. Does a low-carbohydrate or higher-protein diet damage otherwise healthy kidneys? Controlled trials have not demonstrated that it does.[4–10]
2. Can carbohydrate restriction be used in people who already have chronic or diabetic kidney disease? Clinical studies show stable kidney markers and substantial metabolic improvements when the intervention is individualized and medically supervised.[1,2,5,8,11–14]
3. Can ketogenic metabolic therapy influence autosomal-dominant polycystic kidney disease (ADPKD)? Thomas Weimbs and collaborators have developed a translational research program extending from animal models to pilot trials, a randomized human trial and longer-term real-world reports.[15–25]

Kidney stones are a fourth, related issue. They involve urine chemistry, fluid intake, genetics, medications and dietary factors. Stone risk should not be treated as proof that a diet is causing chronic loss of kidney function.

The claim that protein causes kidney disease is unsubstantiated in healthy kidneys

Protein digestion increases the work of filtration, and higher protein intake can produce a rise in glomerular filtration. This response is often called hyperfiltration. But observing an acute or adaptive increase in filtration is not the same as demonstrating progressive kidney injury.

To prove that protein causes chronic kidney disease, researchers would need to show that higher protein intake produces sustained loss of kidney function or structural kidney damage in people who begin with healthy kidneys. Controlled human trials have not shown that outcome.

• In a two-year randomized trial of 307 adults with obesity but without serious kidney disease, a low-carbohydrate, high-protein diet produced no harmful effect on filtration markers, albuminuria, fluid balance or electrolytes compared with a low-fat diet.[4]
• In the two-year DIRECT trial, 318 adults were assigned to low-fat, Mediterranean or low-carbohydrate diets. Protein intake increased to 22% of energy in the low-carbohydrate group. Estimated glomerular filtration rate, or eGFR, improved across all three groups, including among participants with type 2 diabetes and those who began with an eGFR below 60.[5]
• A one-year trial in 68 adults with abdominal obesity found no adverse change in creatinine, eGFR or albumin excretion with a very-low-carbohydrate diet containing 35% of energy from protein.[6]
• A one-year randomized trial in 115 adults with type 2 diabetes found that the very-low-carbohydrate group consumed approximately 1.3 grams of protein per kilogram per day without an adverse difference in creatinine, eGFR or albumin excretion compared with the higher-carbohydrate group.[7]
• A randomized trial in people with type 2 diabetes and early renal disease found no difference in measured GFR, estimated GFR or cystatin C between moderate- and standard-protein weight-loss diets after one year.[8]
• In a one-year crossover study, healthy resistance-trained men consuming approximately 2.5–3.3 grams of protein per kilogram per day did not develop harmful changes in the kidney or liver markers measured.[9]
• A meta-analysis of nine randomized trials involving 1,687 participants found no deterioration in renal function from low-carbohydrate diets compared with control diets.[10]

These trials do not establish that there is no conceivable upper limit to protein intake. They do directly challenge the blanket assertion that eating more protein causes kidney disease in people with healthy kidneys.

Where trials and kidney guidelines disagree

The research and the guidelines are answering related but different questions.

Controlled diet trials ask whether higher-protein or low-carbohydrate diets cause measurable kidney injury in selected participants over a defined period. In people with normal kidney function—and in several studies that included mild-to-moderate impairment—these trials have not shown the predicted harm.[2,4–10]

Kidney guidelines are written for people who already have diagnosed CKD and may be at risk for progression. The 2024 KDIGO guideline suggests approximately 0.8 grams of protein per kilogram per day for adults with CKD stages G3–G5 and advises against intake above 1.3 grams per kilogram per day in those at risk of progression. It also emphasizes nutritional status and warns against restrictive diets in metabolically unstable people.[26]

That recommendation is conservative and is partly informed by physiological theory, observational associations and the need to reduce the accumulation of protein-derived waste as kidney function declines. It is not proof that dietary protein caused the kidney disease in the first place.

The practical reconciliation is straightforward:

• Healthy kidneys: There is no controlled human-trial proof that higher protein intake causes chronic kidney disease.
• Mild kidney impairment: Do not assume that a low-carbohydrate diet is prohibited or that every patient needs aggressive protein restriction. Evaluate the cause, trajectory, albuminuria, medications, blood pressure, diabetes control, nutritional status and actual protein intake.
• Advanced, progressive or otherwise high-risk CKD: A moderate or lower protein target may be appropriate. It should be prescribed and monitored with the treating physician or nephrologist and a renal dietitian so that the patient does not lose muscle or become malnourished.
• Dialysis: Protein requirements commonly rise because amino acids and proteins can be lost during treatment.[26]

This is the discordance: guidelines remain cautious in established CKD, while controlled trials do not support using that caution to tell the general population that protein causes kidney disease.

Low-carbohydrate nutrition in chronic and diabetic kidney disease

The kidneys are harmed by many of the metabolic problems that carbohydrate restriction can improve: chronic hyperglycemia, insulin resistance, high blood pressure, visceral obesity and inflammation. A useful kidney analysis therefore has to consider the whole metabolic effect of the intervention—not protein in isolation.

The original Toward Health article cited a randomized trial of 30 people with type 2 diabetes and mild-to-moderate diabetic kidney disease. For 12 weeks, participants followed either a very-low-carbohydrate diet or a standard low-protein, low-salt diet. The very-low-carbohydrate intervention did not worsen kidney function and improved glycemic control, body weight, abdominal adiposity and interleukin-6.[2]

A 2025 real-world study followed 18 people with metabolic syndrome and CKD stages 3–4 who used a very-low-carbohydrate diet under close medical supervision for an average of approximately one year. eGFR and bicarbonate remained stable, creatinine and urea decreased, and no participant progressed to a more advanced CKD stage. Fifteen of the 18 had a higher eGFR at follow-up, while BMI, HbA1c and medication burden improved.[1]

This does not mean that every CKD patient should copy a ketogenic diet from the internet. Medication doses, blood pressure, hydration, potassium, acid-base balance, uric acid, protein intake and nutritional status may all require individual management. It does mean that CKD should not automatically disqualify someone from a clinically supervised low-carbohydrate approach.

What Virta’s long-term kidney data show

Virta Health’s continuous-care intervention combines a very-low-carbohydrate ketogenic diet with remote medical management, biomarker monitoring, health coaching and medication adjustment. Its studies are particularly useful for addressing the claim that kidney markers must worsen over time on ketogenic nutrition.

They did not.

Two years: no kidney deterioration and a favorable eGFR trajectory

Virta’s original two-year nonrandomized controlled trial followed 262 adults receiving the intervention and 87 receiving usual care. Kidney markers were included among the safety outcomes while participants achieved sustained improvements in diabetes, weight, blood pressure, inflammation and medication use.[11]

A 2025 post-hoc kidney analysis of the same cohort examined eGFR trajectories in greater detail. The intervention group had an average eGFR slope of +0.91 mL/min/1.73 m² per year, compared with −0.68 in usual care. Higher measured beta-hydroxybutyrate was independently associated with greater improvement in eGFR, with the clearest relationship among participants whose baseline eGFR was below 90. Inflammatory markers also declined.[12]

Three years: creatinine, eGFR and urine albumin did not worsen

In the Veterans Health Administration–Virta observational cohort, 310 participants remained enrolled for two years and 197 for three years. The program used a low-carbohydrate, high-fat, moderate-protein ketogenic diet with continuous remote care.[13]

At two years, eGFR changed from 83.4 to 82.6, creatinine from 0.94 to 0.95 and urine albumin-to-creatinine ratio from 44.8 to 56.0. At three years, eGFR changed from 85.2 to 83.2, creatinine from 0.91 to 0.95 and urine albumin-to-creatinine ratio from 33.4 to 42.6. None of these changes was statistically significant. The investigators reported that eGFR, creatinine and urine albumin remained unchanged while HbA1c, weight, medication use and several cardiometabolic markers improved.[13]

This is the long-term kidney-marker result that is often missing from public discussions: there was no worsening signal across the measured kidney markers through three years.

Five years: lower observed CKD incidence and no excess renal adverse events

In 2026, investigators reported a five-year real-world study matching 11,077 participants in Virta’s low-carbohydrate telehealth intervention with 11,077 usual-care controls. Participation was associated with lower rates of newly diagnosed CKD: 10.1 versus 15.6 cases per 1,000 person-years, corresponding to a hazard ratio of 0.64. The hazard ratios were 0.57 for CKD stage 3 or greater and 0.38 for CKD stage 4 or greater.[14]

The intervention was not associated with increased kidney stones, metabolic acidosis, diabetic ketoacidosis or gout.[14]

Because this was a retrospective matched-cohort study, it establishes a strong real-world association rather than random assignment. Together with the two- and three-year biomarker studies, however, it directly contradicts the prediction that sustained carbohydrate restriction should worsen kidney function.

Several authors in these studies were employed by or affiliated with Virta Health. That relationship should be disclosed, but it does not erase the measured results. Study design, population, endpoints and reproducibility should determine how the evidence is interpreted.

Thomas Weimbs’ research: from kidney metabolism to human ADPKD studies

Autosomal-dominant polycystic kidney disease is an inherited disorder in which fluid-filled cysts progressively replace healthy kidney tissue. The work of Thomas Weimbs and collaborators has reframed ADPKD partly as a disease of altered cellular metabolism.

Affected cyst-lining cells demonstrate impaired mitochondrial function, increased reliance on glucose and growth signaling involving pathways such as mTOR. Ketosis reduces glucose and insulin exposure while producing beta-hydroxybutyrate, or BHB, which acts not only as a fuel but also as a signaling molecule.[15,19,20,23]

2019: ketosis slowed or reversed cystic disease in animal models

In rat, mouse and cat models of PKD, time-restricted feeding, fasting, ketogenic diets and BHB supplementation inhibited disease progression. A ketogenic diet led to regression of renal cystic burden in the animal model, while BHB strongly inhibited progression.[15]

This established the central biological hypothesis: cystic cells may be metabolically inflexible and vulnerable when glucose availability falls and ketone signaling rises.

2021–2023: the program moved into human feasibility studies

A retrospective study collected the experiences of 131 people with ADPKD who had independently used a ketogenic diet, time-restricted eating or caloric restriction for a median of approximately six months. Participants commonly reported weight loss, better blood pressure and improved ADPKD-related symptoms; 45 reported a slight improvement in eGFR. The study established real-world feasibility and generated the case for prospective trials.[16]

RESET-PKD then prospectively studied ten adults with rapidly progressive ADPKD using either a 14-day ketogenic diet or a three-day water fast. Both interventions produced ketosis. Total liver volume decreased significantly during the intervention period, and the protocol demonstrated short-term feasibility under clinical monitoring.[17]

2023: KETO-ADPKD randomized 66 patients

The exploratory KETO-ADPKD randomized controlled trial assigned 66 people with ADPKD to a ketogenic diet, monthly three-day water fasting or usual diet for three months. Ninety-five percent of the ketogenic group and 85% of the fasting group considered the intervention feasible.[18]

The ketogenic group lost body fat and had a significant reduction in liver volume. Kidney volume also decreased, although the main comparison did not reach statistical significance. Kidney function improved at the end of treatment in the ketogenic group while it declined in the control and water-fasting groups.[18]

This trial is why the article should not reduce the ADPKD discussion to animal evidence. Human randomized data now demonstrate feasibility, metabolic effects and a favorable kidney-function signal, with a promising but not statistically definitive main kidney-volume result.

2024: BHB and citrate produced complementary effects in laboratory models

Weimbs’ group reported that BHB and citrate each slowed cystic disease in a rat model and worked synergistically when combined. In adult animals with established disease, the combination produced partial regression, reduced cyst number and cystic area, preserved glomerular health and reduced markers of kidney injury.[19]

A separate 2024 study tested repeated fasting, time-restricted feeding and BHB in multiple rodent PKD models. BHB reproduced major benefits of fasting while influencing mitochondrial biogenesis, oxidative-stress defenses, fibrosis and proliferative signaling. These findings strengthened the case that BHB is an active signaling mediator rather than merely a byproduct of carbohydrate restriction.[20]

2026: real-world ADPKD outcomes and longer-term imaging

A 2026 study evaluated 103 adults with ADPKD who completed a three-month Ren-Nu program combining a very-low-carbohydrate ketogenic diet, dietitian support and a BHB-, citrate-, mineral- and alkali-containing medical food. Mean eGFR increased 6.3%, from 58.4 to 61.6 mL/min/1.73 m². BMI improved, antihypertensive-medication use declined, kidney pain and headaches decreased, and lipid, electrolyte and acid-base markers remained stable.[21]

In June 2026, a case series described four adults with genetically confirmed PKD1 variants who had used carbohydrate restriction, intermittent fasting and exogenous BHB/citrate for periods ranging from six months to approximately four years. Serial imaging showed stabilization or reduction in total kidney volume relative to each person’s prior growth trajectory, with preserved kidney function. One participant moved from Mayo imaging class 1C to 1B, and the others shifted downward within their existing imaging trajectories.[22]

This four-person series is not a substitute for a large randomized trial, but it adds the kind of long-term human imaging that the earlier trials could not provide.

At the 2026 World Congress of Nephrology, investigators also presented 12-month interim results from the first ten participants in an ongoing Japanese ADPKD study. Median total kidney volume changed by −3.0%, median liver volume by −5.1%, and eGFR slope was −5.2 mL/min/1.73 m² per year. Higher ketone levels at three months correlated with less kidney- and liver-volume expansion. The team reported a planned enrollment of 200 participants, including a control group. These are conference-level interim findings and should remain labeled as such until the full controlled study is published.[27]

Weimbs and colleagues also published a 2026 mechanistic review proposing BHB as a renoprotective hormone because it can influence inflammation, oxidative stress, mitochondrial function and growth signaling. It integrates the laboratory and human work and describes ketogenic metabolic therapy as complementary to—not automatically a replacement for—established pharmacologic treatment.[23]

The Ren-Nu and case-series authors disclosed affiliations with Santa Barbara Nutrients and intellectual-property or financial interests related to the studied medical food. Those relationships should remain visible whenever the findings are discussed.[21–23]

What can now be said about ADPKD?

The evidence supports several clear statements:

• Ketosis, ketogenic diets, fasting and BHB have repeatedly slowed or partially reversed cystic disease in animal models.[15,19,20]
• Human pilot studies show that ketogenic interventions can be implemented in people with ADPKD.[16–18]
• The randomized KETO-ADPKD trial demonstrated improved kidney function and a directionally favorable kidney-volume result in the ketogenic group.[18]
• Recent real-world human studies report improved or preserved eGFR, symptom improvement and stabilization or reduction of total kidney volume during longer-term ketogenic metabolic therapy.[21,22]

The key distinction is that the strongest cyst-regression evidence comes from animal experiments. Human structural findings are now promising and include favorable randomized and longitudinal imaging results, but they should be described according to their actual study designs.

People with ADPKD should not begin prolonged fasting, a ketogenic diet, BHB, citrate or mineral supplements without coordinating with a clinician who understands their kidney function, blood pressure, medications, stone history and electrolyte requirements. Tolvaptan and other prescribed treatments should not be stopped without the treating nephrologist.

Kidney stones: a different risk that can be anticipated

The original Toward Health article correctly treated kidney stones separately from chronic kidney-function decline.

A 2021 systematic review pooled 36 studies involving 2,795 people using ketogenic diets and estimated an overall kidney-stone incidence of 5.9%. Many participants were children receiving highly restrictive therapeutic ketogenic diets for epilepsy, which differ from the moderate-protein ketogenic nutrition commonly used for obesity or type 2 diabetes.[3]

Stone risk depends on the person and the type of stone. Relevant factors can include low fluid intake, low urine citrate, changes in urine pH, higher calcium or uric-acid excretion, rapid weight loss, sodium intake, supplements, medications and a previous stone history.

Practical prevention may include:

• Maintaining adequate fluid intake unless a clinician has prescribed fluid restriction
• Avoiding dehydration during the early natriuretic phase of carbohydrate restriction
• Reviewing prior stone composition and urine studies when available
• Individualizing sodium, calcium, oxalate, citrate, magnesium and uric-acid management
• Monitoring people with recurrent stones, ADPKD or reduced kidney function more closely

Drinking enough to produce pale urine is a useful general cue, but people with advanced CKD, heart failure, edema or a prescribed fluid limit should follow their clinician’s fluid target rather than forcing water.

Who needs medical supervision before reducing carbohydrates?

Medical guidance is especially important for people who have:

• CKD stage 3 or greater, rapidly changing eGFR or substantial albuminuria
• ADPKD or another inherited kidney disorder
• Recurrent kidney stones
• A single kidney or a kidney transplant
• Dialysis treatment
• Diabetes treated with insulin, sulfonylureas or an SGLT2 inhibitor
• Blood-pressure medication or diuretics
• Heart failure, edema, electrolyte abnormalities or acid-base disorders
• Pregnancy, frailty, undernutrition or a history of an eating disorder

Carbohydrate restriction can rapidly lower glucose and blood pressure. Medication reduction may be necessary to prevent hypoglycemia, hypotension or volume depletion. This is one reason medically supervised programs can produce different safety outcomes from an unsupervised diet.

The takeaway

The idea that protein causes kidney disease in people with healthy kidneys is not supported by controlled human trials. Higher-protein and low-carbohydrate diets have repeatedly shown no adverse effect on kidney filtration, albumin excretion or major safety markers in studied populations.[4–10]

For people with type 2 diabetes or established kidney disease, improving glucose, insulin resistance, blood pressure, obesity and inflammation can be kidney-protective. Clinical studies of carbohydrate restriction—including Virta’s two-, three- and five-year analyses—show no long-term worsening of kidney markers and, in several analyses, more favorable kidney outcomes than usual care.[1,2,11–14]

Protein moderation belongs in the management of advanced, progressive or otherwise high-risk CKD—not as a blanket warning to everyone considering low-carbohydrate nutrition. It should be individualized with a physician or nephrologist and renal dietitian, with special attention to preserving muscle and adequate nutrition.

Thomas Weimbs’ ADPKD research extends this discussion further. The program now includes mechanistic experiments, multiple animal models, human feasibility studies, an exploratory randomized trial, real-world clinical outcomes, longer-term imaging and a larger ongoing clinical study. The combined record supports ketogenic metabolic therapy as a serious area of kidney research and a clinically relevant option to discuss with a knowledgeable care team.[15–25,27]

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13. Adams RN, Athinarayanan SJ, Zoller AR, McKenzie AL, Ratner RE. Sustained metabolic improvements in a remotely delivered ketogenic nutrition programme for veterans with type 2 diabetes: A 3-year observational study. Diabetes Obes Metab. 2025;27(9):4825–4835. doi: 10.1111/dom.16525. PubMed Central.

14. Athinarayanan SJ, Bjornstad P, Shanmugam PV, et al. Effectiveness of Telehealth Low-Carbohydrate Intervention in Preventing Chronic Kidney Disease: A Real-World, Retrospective, Matched Cohort Study. Diabetes Obes Metab. Published online July 16, 2026. doi: 10.1111/dom.71086. PubMed.

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19. Torres JA, Holznecht N, Asplund DA, et al. A combination of beta-hydroxybutyrate and citrate ameliorates disease progression in a rat model of polycystic kidney disease. Am J Physiol Renal Physiol. 2024;326:F352–F368. doi: 10.1152/ajprenal.00205.2023. PubMed.

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21. Muensterman E, Torres JA, Weimbs T. Real-world outcomes of managing autosomal-dominant polycystic kidney disease using a medical food as part of a nutrition and lifestyle program to improve renal and metabolic health. Front Nutr. Published January 21, 2026;12:1624639. doi: 10.3389/fnut.2025.1624639.

22. Messing M, Muensterman E, Marcon S, Weimbs T. Halting cyst progression in ADPKD using long-term ketogenic metabolic therapy and supplementation with exogenous ketones and alkaline citrate—a case series. Front Nutr. 2026;13:1843178. doi: 10.3389/fnut.2026.1843178.

23. Torres JA, Sharpe EH, Weimbs T. Beta-hydroxybutyrate: a renoprotective hormone in polycystic kidney disease. Am J Physiol Endocrinol Metab. 2026;331(3):E300–E311. doi: 10.1152/ajpendo.00067.2026.

24. Weimbs T, Saville J, Kalantar-Zadeh K. Ketogenic metabolic therapy for chronic kidney disease—the pro part. Clin Kidney J. 2024;17(1):sfad273. doi: 10.1093/ckj/sfad273. PubMed.

25. Athinarayanan SJ, Roberts CGP, Vangala C, et al. The case for a ketogenic diet in the management of kidney disease. BMJ Open Diabetes Res Care. 2024;12(2):e004101. doi: 10.1136/bmjdrc-2024-004101. PubMed.

26. Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. Kidney Int. 2024;105(Suppl 4S):S117–S314. Official guideline PDF.

27. Weimbs Laboratory, UC Santa Barbara. 12-month interim results of ketogenic metabolic intervention in Japanese ADPKD patients. Presented at the World Congress of Nephrology 2026, Yokohama, Japan. Study summary and conference link.