Dietary Management of CKD: Protein Restriction and Beyond
Dietary Management of CKD: Protein Restriction and Beyond
Purpose of review: More kidney protective strategies are needed to reduce the burden of complete kidney failure from chronic kidney disease (CKD). Clinicians sometimes use protein restriction as kidney protection despite its demonstrated lack of effectiveness in the only large-scale study. Small-scale studies support that dietary acid reduction is kidney-protective, including when done with base-inducing foods like fruits and vegetables. We review these studies in light of current kidney-protective recommendations.
Recent findings: Animal models of CKD show that acid-inducing dietary protein exacerbates and base-inducing protein ameliorates nephropathy progression, and that increased intake of acid-inducing but not base-inducing dietary protein exacerbates progression. Clinical studies show that dietary acid reduction with Na-based alkali reduces kidney injury and slows nephropathy progression in patients with CKD and reduced glomerular filtration rate (GFR); base-inducing fruits and vegetables reduce kidney injury in patients with reduced GFR; and base-inducing fruits and vegetables improve metabolic acidosis in CKD.
Summary: Protein type rather than amount might more importantly affect nephropathy progression. Base-inducing foods might be another way to reduce dietary acid, a strategy shown in small studies to slow nephropathy progression. Further studies will determine if CKD patients should be given base-inducing food as part of their management.
Chronic kidney disease (CKD) is a major public health burden with diabetes and hypertension contributing to most incident cases in the US. Unfortunately, kidney-protective strategies such as blood pressure reduction and antiangiotensin II drugs slow but do not stop progressive glomerular filtration rate (GFR) decline in individuals with CKD due to macroalbuminuric type 2 diabetes and hypertensive nephropathy with reduced GFR. Dietary management of CKD has generally focused on limiting intake of substances that might accumulate to toxic levels such as K and phosphorus, limiting Na intake for better blood pressure and volume control, and providing protein in amounts sufficient to maintain adequate nutrition. By contrast, dietary management of CKD has less frequently focused upon GFR preservation. Although high protein diets might exacerbate nephropathy progression and some small studies suggest that dietary protein restriction might slow progression, the largest such study showed that general protein restriction did not slow nephropathy progression. Indeed, dietary protein restriction in CKD risks protein malnutrition in these patients who have increased protein catabolism. More recent studies suggest that the type of protein, rather than its absolute amounts, might help reduce kidney injury that is associated with GFR decline. This review examines the effect of dietary protein on nephropathy progression; whether the type of protein rather than its dietary amount is an important determinant of protein effect on progression; and a general approach to dietary protein prescribing for patients with CKD.
Animal models of CKD are most commonly constructed by surgical infarction or removal of kidney mass in two stages: complete removal of one kidney and partial removal of the remaining kidney days later. The classic model is 5/6 nephrectomy in which 2/3 of the remaining kidney is infarcted or removed, typically in a rat. The GFR of this model is about 1/3 rather than 5/6 of baseline because remaining nephrons hyper-function. These 5/6 nephrectomy rats typically have metabolic acidosis when ingesting casein-based, acid-inducing standard rat chow. Investigators have also used the 2/3 nephrectomy model in which 1/3 of nephron mass of the remaining kidney is removed, yielding GFR that is about 2/3 of baseline, due to hyper-functioning of the remaining nephrons. Two-thirds nephrectomy models CKD in patients with less severely reduced GFR who have no metabolic acidosis by plasma acid–base parameters yet have progressive GFR decline.
Animals with 5/6 nephrectomy and 2/3 nephrectomy have progressive GFR decline on standard rat chow that is exacerbated by increased amounts of standard rat chow protein and is ameliorated by its reduction. This progressive GFR decline induced by casein-based rat chow is ameliorated by drugs that inhibit production or action of angiotensin (AII), supporting a mediating role for AII in nephropathy progression induced by casein after nephrectomy.
Abstract and Introduction
Abstract
Purpose of review: More kidney protective strategies are needed to reduce the burden of complete kidney failure from chronic kidney disease (CKD). Clinicians sometimes use protein restriction as kidney protection despite its demonstrated lack of effectiveness in the only large-scale study. Small-scale studies support that dietary acid reduction is kidney-protective, including when done with base-inducing foods like fruits and vegetables. We review these studies in light of current kidney-protective recommendations.
Recent findings: Animal models of CKD show that acid-inducing dietary protein exacerbates and base-inducing protein ameliorates nephropathy progression, and that increased intake of acid-inducing but not base-inducing dietary protein exacerbates progression. Clinical studies show that dietary acid reduction with Na-based alkali reduces kidney injury and slows nephropathy progression in patients with CKD and reduced glomerular filtration rate (GFR); base-inducing fruits and vegetables reduce kidney injury in patients with reduced GFR; and base-inducing fruits and vegetables improve metabolic acidosis in CKD.
Summary: Protein type rather than amount might more importantly affect nephropathy progression. Base-inducing foods might be another way to reduce dietary acid, a strategy shown in small studies to slow nephropathy progression. Further studies will determine if CKD patients should be given base-inducing food as part of their management.
Introduction
Chronic kidney disease (CKD) is a major public health burden with diabetes and hypertension contributing to most incident cases in the US. Unfortunately, kidney-protective strategies such as blood pressure reduction and antiangiotensin II drugs slow but do not stop progressive glomerular filtration rate (GFR) decline in individuals with CKD due to macroalbuminuric type 2 diabetes and hypertensive nephropathy with reduced GFR. Dietary management of CKD has generally focused on limiting intake of substances that might accumulate to toxic levels such as K and phosphorus, limiting Na intake for better blood pressure and volume control, and providing protein in amounts sufficient to maintain adequate nutrition. By contrast, dietary management of CKD has less frequently focused upon GFR preservation. Although high protein diets might exacerbate nephropathy progression and some small studies suggest that dietary protein restriction might slow progression, the largest such study showed that general protein restriction did not slow nephropathy progression. Indeed, dietary protein restriction in CKD risks protein malnutrition in these patients who have increased protein catabolism. More recent studies suggest that the type of protein, rather than its absolute amounts, might help reduce kidney injury that is associated with GFR decline. This review examines the effect of dietary protein on nephropathy progression; whether the type of protein rather than its dietary amount is an important determinant of protein effect on progression; and a general approach to dietary protein prescribing for patients with CKD.
Dietary Protein and Nephropathy Progression
Animal models of CKD are most commonly constructed by surgical infarction or removal of kidney mass in two stages: complete removal of one kidney and partial removal of the remaining kidney days later. The classic model is 5/6 nephrectomy in which 2/3 of the remaining kidney is infarcted or removed, typically in a rat. The GFR of this model is about 1/3 rather than 5/6 of baseline because remaining nephrons hyper-function. These 5/6 nephrectomy rats typically have metabolic acidosis when ingesting casein-based, acid-inducing standard rat chow. Investigators have also used the 2/3 nephrectomy model in which 1/3 of nephron mass of the remaining kidney is removed, yielding GFR that is about 2/3 of baseline, due to hyper-functioning of the remaining nephrons. Two-thirds nephrectomy models CKD in patients with less severely reduced GFR who have no metabolic acidosis by plasma acid–base parameters yet have progressive GFR decline.
Animals with 5/6 nephrectomy and 2/3 nephrectomy have progressive GFR decline on standard rat chow that is exacerbated by increased amounts of standard rat chow protein and is ameliorated by its reduction. This progressive GFR decline induced by casein-based rat chow is ameliorated by drugs that inhibit production or action of angiotensin (AII), supporting a mediating role for AII in nephropathy progression induced by casein after nephrectomy.
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