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However, their effectiveness is often limited, with a substantial proportion of patients experiencing only partial relief of symptoms or significant side effects such as weight gain, metabolic disorders, and extrapyramidal symptoms. Plasma concentrations of anticonvulsant medications may be decreased by KD, resulting in diminished efficacy and potential adverse effects [101,110,111]. It has been hypothesised that the drop in INRs could be caused by an increase in levels of serum albumin as well as cytochrome P450 activity, which could be achieved by increasing dietary protein intake. Beta-blockers and exercise are both involved in mediating ketosis, with beta-blockers playing a more significant role than exercise. This study investigates the effect of the low-protein diet supplemented with ketoacids (LPD+KA) on the RAAS in chronic kidney disease. This increase in aldosterone, with the direct association of the presence of ketone bodies, would strongly indicate a direct mechanistic link between the metabolic state of ketosis, induced by KDs, and an increase in aldosterone production. The relationship between the KD and drugs acting on the renin–angiotensin–aldosterone system (RAAS) is a very promising research field, especially for dietary interventions and their endocrine effects. Et al. suggested that ketone bodies produced by the KD may have various beneficial impacts on cardiovascular health. Urinary tract infections and diabetic ketoacidosis (DKA) are the most prevalent adverse effects . Sodium-glucose cotransporter-2 (SGLT-2) inhibitors, commonly referred to as gliflozins or flozins, are medications used extensively to treat type 2 diabetes (T2D) owing to their benefits in reducing glucose levels and improving cardiovascular and renal function . While not essential for metformin’s ability to lower blood sugar, activating 5′-AMP-activated protein kinase enhances insulin sensitivity primarily through the regulation of lipid metabolism [40,41]. Although highly acknowledged for its beneficial effects on health and in managing chronic conditions, the KD can cause severe health problems if followed without surveillance. Furthermore, KB affects ion channels and neurotransmitter carriers, impacting the glutamate-to-ketone percentage and potentially decreasing epileptic events [27,28]. Moreover, reducing dietary carbohydrates through the KD hinders the production of cholesterol, which is influenced by insulin and plasma glucose levels . During a shortage of glucose, the energy focus switches from glycolysis to the breakdown of fatty acids . Changes in lipid metabolism are notable when following the KD, with a common focus on its effects on blood lipids. 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