Effects of Diet and Nutrition on Chronic Kidney Disease (CKD)—"Greedy Kidney" in Health and Diseases

Dear Colleagues,

There is an old Chinese saying that “medicine and food come from the same origin”, meaning that a balanced diet leads to a healthy body. Indeed, it is a well-known fact that calorie restriction (CR) prolongs life-span and prevents age-related diseases in many animals, from lower organisms to primates. Furthermore, the molecules related to longevity include insulin, mTOR, and surtuins/NAD+, all of which are nutritional state sensors or signal mediators and are involved in the regulation of carbohydrate, lipid, and protein metabolism. The kidney is sometimes referred as an “aging clock”, since a decline in kidney function faithfully reflects the aging of the whole body. The kidney is one of the most metabolically active organs. The renal proximal tubules are rich in mitochondria and are engaged in the re-absorption of nutrients and minerals, which requires a lot of ATP. When we consume a large amount of nutrients, the kidney functions to retain them within the body as much as possible. I describe this feature of the kidney as “Greedy Kidney” (“Greedy Organ Hypothesis”: Itoh H. et al. Metabol Open. 2022,13:10016). As as result of this process, the kidney easily becomes exhausted. This characteristic is similar to that of intestinal epithelial cells (“Greedy Guts”) (Kawano Y., Itoh H., et al. Cell Metab. 2016, 24:295-310). Protein over-load is well-recognized to be an aggravating factor in advanced-stage chronic kidney failure patients. We showed that the exhaustion of NAD+ in proximal tubules triggers diabetic nephropathy (Hasegawa K., Itoh H., et al. Nat Med. 2013, 19:1496-5042016) and induces intra-renal inflammation to initiate CKD (Itoh H et al. Nat Metab. 2023, 5:357-359). SGLT (sodium-glucose co-transporter)-1 inhibitors are demonstrated to not only reduce high blood glucose levels but also repair renal damage and prevent heart failure. Obesity is a predisposing condition of not only liver and pancreatic cancer but also renal cancer. The condition of “Greedy Kidney” leads to the dysfunction of other organs, including “Greedy Guts” (for example, dysbiosis, that is, the disturbance of gut microbiota) through hormones, metabolites, and other humoral factors, as well as the dysfunction of the autonomic nervous system. Renal nerve denervation is shown to be effective in alleviating high blood pressure in resistant hypertension.

With this context, we welcome any papers related to this Special Issue in the following aspects:

• The mechanism/pathophysiology of CKD from nutritional and metabolic perspectives;
• The nutri-genomics of CKD;
• Organ–organ interactions with the kidney as the hub-organ in non-communicable diseases (NCDs), especially from the perspective of the excessive intake of sugar/salt etc.;
• Dysbiosis and CKD;
• Gastrointestinal symptoms, including constipation and CKD/cardiovascular events;
• The significance of nutrition in the relationship between frailty, sarcopenia, and CKD;
• Evidence related to nutritional interventions, including dietary fibers or plant-dominant low-protein diet.

Prof. Dr. Hiroshi Itoh
Prof. Dr. Shu Wakino
Guest Editors

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• CKD
• sarcopenia
• aging
• mitochondria
• gut microbiome