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The results suggested a correlation between the degree of weight loss and slower kidney growth . The interventions led to clinically significant weight loss and potentially slower than expected kidney growth. Interestingly, subgroup analysis showed that renal function improved most in individuals who achieved sustained nutritional ketosis (consistently ≈1 mM BHB), suggesting a dose-dependent relationship with endogenous ketone concentration . The eGFR slope was negative (worsened CKD) in the usual care group but was positive (improved CKD) in the ketogenic intervention group, with a significant difference between groups. In contrast, the Mediterranean diet had no significant effects and led to a continuing decline in eGFR . The lowering of insulin permits lipolysis by the adipose tissues to release fatty acids which are partially converted to the ketone BHB by the liver that releases BHB into circulation. The restriction of carbohydrate intake in KMT leads to normoglycemia and prevents glucose spikes, lowers insulin levels and reverses insulin-resistance and hypertension. In contrast, ketogenic metabolic therapy (KMT) reverses these underlying factors. Long-term, persistent hyperglycemia due to the standard American diet (SAD) high in sugar, carbohydrates, calories and highly processed foods leads to chronic hyperinsulinemia, insulin-resistance, hypertension, chronic inflammation, and renal tissue damage. KMT is an effective method of decreasing baseline blood glucose levels and reducing spikes. In this review, we will not focus on discussing whether animal or plant foods are preferable for CKD, although there is emerging data on PLADO and PLAFOND diets [7, 8]. 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