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Protein and Renal Function The federal Dietary Guidelines for Americans recommend an amount of 0.8 g/kg/body wt/d dietary protein intake for healthy adults [19].Although LPDs provide direct benefits to CKD patients, healthcare professionals are concerned about protein-energy malnutrition and protein-energy wasting (PEW) in CKD patients due to inadequate energy intake [26,27].The Modification of Diet in Renal Disease (MDRD) was the largest RCT to examine the hypothesis that dietary protein restriction delays the progression of CKD [PMID 10541304].This study concluded that an HPD might increase SNGFR and induce glomerular hyperfiltration; however, this study is unique by identifying that the analysis of human SNGFR is an exemplary parameter to alterations in renal hemodynamics at the single-nephron level [24].HPDs induce glomerular hyperfiltration, hyperemia, and increased hydraulic pressure, resulting in vasodilation of the afferent arteriole [22].HPDs contribute to progressive glomerular damage, which, combined with the renal deterioration from diseased kidneys may contribute to CKD progression.Oba et al. collected 43 healthy (non-diseased) kidneys from live human donors to examine the effect of an HPD on the single-nephron GFR (SNGFR) [24].Proteinuria declined by 20-50% in CKD patients who adhered to a LPD [26,27].

Protein and Renal Function
The federal Dietary Guidelines for Americans recommend an amount of 0.8 g/kg/body wt/d dietary protein intake for healthy adults [19]. Exceeding the recommended dietary allowance (RDA) may increase the risk of health complications even for healthy adults [19]. Protein intake recommendations for CKD patients are dependent on the stage of the disease, which is determined by declining GFR function [18].
The effects of high-protein diets (HPDs) on renal health have been investigated since the 1920s when rats given a HPD presented with increased kidney weight [20]. Data suggest that chronic protein intake (more than 1.2 g/kg/body weight/d) [21] leads to increased pressure and glomerular morphologic changes, resulting in renal dysfunction [22]. Glomerular hyperfiltration is defined as modifying renal hemodynamics through glomerular capillary hyperemia and increasing intraglomerular pressure [21]. HPDs induce glomerular hyperfiltration, hyperemia, and increased hydraulic pressure, resulting in vasodilation of the afferent arteriole [22]. HPDs contribute to progressive glomerular damage, which, combined with the renal deterioration from diseased kidneys may contribute to CKD progression. The Modification of Diet in Renal Disease (MDRD) was the largest RCT to examine the hypothesis that dietary protein restriction delays the progression of CKD [PMID 10541304]. The study found proteinuria to be one of the two strongest predictors in the rate of CKD progression in two studies [23]. Oba et al. collected 43 healthy (non-diseased) kidneys from live human donors to examine the effect of an HPD on the single-nephron GFR (SNGFR) [24]. This study concluded that an HPD might increase SNGFR and induce glomerular hyperfiltration; however, this study is unique by identifying that the analysis of human SNGFR is an exemplary parameter to alterations in renal hemodynamics at the single-nephron level [24]. The exact mechanism for renal hemodynamic responses to heightened protein intake is not yet understood [25].
Low-protein diets (LPDs) have been shown to improve hyperfiltration, reduce nitrogenous waste, and ease the renal workload by decreasing glomerular pressure [21]. Proteinuria declined by 20–50% in CKD patients who adhered to a LPD [26,27]. Although LPDs provide direct benefits to CKD patients, healthcare professionals are concerned about protein-energy malnutrition and protein-energy wasting (PEW) in CKD patients due to inadequate energy intake [26,27]. When determining the estimated energy requirements for CKD patients, 25–35 kcal/kg/body weight/d is recommended to maintain energy and nitrogen balance and avoid risk for malnutrition [16] (Table 1).