Sarah Rice BSC. (Hons), Mcoptom (UK), MHP, NNP
Import
Diseases of cardiovascular, kidney and metabolic (CKM) share a common pathophysiology to develop terminology to reflect common pathways (1). A recent study analyzing sample population data shows that almost 90% of US adults may qualify for CKM syndrome, defined as at least Stage 1, which indicates a CKM risk factor of excess or dysfunctional fat (1).
Metabolic health is involved in the operation of the kidneys through the association of obesity and type 2 diabetes with chronic renal disease (CKD). Obesity plays a direct role in the development of CKD through increased inflammation due to the pronounced lipocytocin production associated with visceral oil. Insulin resistance is also involved through co -operation such as type 2 diabetes and hypertension. These factors support CKM syndrome and insulin resistance, as involved in vascular pathology and play a key role in the effect of kidney function due to its condition as a final organ (2). The final organs usually reflect chronic diseases and are affected by vascular and neurological lesions that often occur in diabetes. Eyes and kidneys are examples of final organs. Diabetic kidney disease is a CKD subset that is believed to occur in about 40% of people with type 2 diabetes. A decrease in kidney function, as reflected in a decrease in estimated glomerular filtration rate (EGFR) is associated with worse results and this measurement has been validated as a substitute for renal impairment (3).
Restriction of therapeutic carbohydrates
The therapeutic restriction of carbohydrates (TCRs) reliably improves obesity, metabolic syndrome, insulin resistance and type 2 diabetes, which are key guides of CKD (4). Historically, in the context of CKD, dietary protein levels have undergone a dispute over increased acid secretion, overflow and potentially negative effects on kidney function (5). However, a review of Athinarayanan et al. (2024) examined low carbohydrate studies and found that protein intake in the area from 0.6 g/kg to 1.4 g/kg were typical and below the threshold for anxiety (set to ≥2.0 g/kg). In fact, this range is similar to the one mentioned for the standard American diet (5).
TCR, which may include a state of nutritional ketosis, promotes metabolic changes beneficial to CKD that include general improvements in metabolic pathways through reduced insulin resistance as well as reduced inflammation, antioxidant effects, improved cellular energy (via body ketone) (5)
Recent studies on TCR for CKD
A recent study by Athinarayanan et al. (2025) undertook a post-HOC analysis that compares a continuous care intervention (CCI) using a low carbohydrate diet (UC) to evaluate the relationship between B-hydroxybert blood levels (BHB) (Egfr) (3). This study was inspired by the findings that the positive effects of SGLT2 inhibitors in kidney disease could be linked to a mild zest state caused by these drugs. The secondary analysis of the CCI data examined whether dietary ketosis can provide similar benefits. They found that CCI participants had a significant increase in EGFR’s inclination to the reduction of the UC group. The highest BHB levels were associated independently with greater improvement of EGFR. Dose-response relationship was observed, especially in those who had lower EGFR at start. Inflammatory indicators have also declined significantly in the CCI group, where the highest levels of dietary adhesion (ketosis) have caused a greater decrease. There were no significant changes in the nitrogen of blood urea (3).
Another study Retirement data was examined by a group of patients with metabolic syndrome and a diagnosis of CKD 3 and 4 (2) stages. They were given low carbohydrate nutrition tips (≤ 30 g/day), followed for at least 3 months. They found that the TCR was safe and effective, reducing BMI, HBA1C and BP along with a decrease in drug use. No patients treated EGFR and 15/18 patients showed increased EGFR (2).
Autosomal dominant polycystic kidney disease
Recent studies have indicated abnormal metabolism of energy as a key feature of autosomal dominant polycystic kidney disease (ADPKD), with emerging evidence showing that nutritional ketosis could play a role in slowing down the progression of the disease (6). Early studies indicate higher levels of ketone can offer more benefits, although more studies are needed to confirm these findings (7, 8). Regardless of these data, improving metabolic health in this population attributes benefits to weight loss and blood pressure, which are proposed as supportive measures for ADPKD (6).
Conclusion
Nutrition via TCR can be a non -pharmacological strategy for improving or stabilizing kidneys and reducing inflammation in adults with obesity, insulin resistance or type 2 diabetes. The first studies show a promise for ADPKD. Overall, these findings support further randomized controlled tests to validate the approach and investigate whether the synergistic effects of TCR and pharmacotheresis have a role in optimizing the effects of the disease.
References
1 Aggarwal, R., Ostrominski, JW and Vaduganathan, M. (2024) “The dominance of cardiovascular-Kidney-metabolic syndrome in US adults, 2011-2020”, Price [Preprint]. Available in: https://doi.org/10.1001/jama.2024.6892.
2. Colledge, bs et al. (2025) ‘is very low nutrition with carbohydrates safe for people with chronic kidney disease?’, Metabolic Health Journal8 (1), p. 10 Available in: https://doi.org/10.4102/jmh.v8i1.115.
3. Athinarayanan, SJ et al. (2025) “Effects of a continuous intervention of remote care, including nutritional ketosis on kidney function and inflammation in adults with type 2 diabetes: a post-hoc latent trajectory analysis”, Borders in diet12, p. 1609737 Available in: https://doi.org/10.3389/fnut.2025.1609737.
4. “Metabolic Disorders” (2025) Nutritional network. Available in: (Access: July 14, 2025).
5. Athinarayanan, SJ et al. (2024) “The case for a ketogenic diet in the management of kidney disease”, BMJ Open Research and Care of Diabetes12 (2), p. E004101. Available in: https://doi.org/10.1136/BMJDRC-2024-004101.
6. Li, J. et al. (2025) “Ketogenic diets and β-hydroxybUTy in the prevention and treatment of diabetic kidney disease: current progress and future prospects”, Bmc nephrology26 (1), p. 127. Available in: https://doi.org/10.1186/s12882-025-04019-0.
7. Cukoski, S. et al. (2024) ‘#2160 Kettosis mitigates the influence on kidney volume on adpkd dietary interventions – More information on the Keto ADPKD Test’, Transplantation of dialysis nephrology39 (supplement_1), p. GFAE069-0738-2160. Available in: https://doi.org/10.1093/ndt/gfae069.738.8. Knol, mge et al. (2023) “higher levels of beta-hydroxybutyry ketone associated with a slower decrease in renal function in ADPKD”, Transplantation of dialysis nephrologyp. Gfad239. Available in: https://doi.org/10.1093/ndt/gfad239.
