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May 15, 2022 6 min read
For quite some time, it has been theorized that high protein diets can lead to kidney disease. The school of thought is that if eating a high protein diet and generating a lot of urea, this could potentially cause kidney issues over time and lead to kidney disease.
Higher-protein diets are advocated for several reasons, including mitigation of sarcopenia, increased satiety, help with weight loss, etc., but their effects on kidney function are unclear.
Despite the proposed benefits of consuming a higher-protein diet to preserve muscle mass or promote muscle growth, higher-protein diets are often discouraged because of potential negative effects on kidney function, particularly glomerular filtration rate.
Broadly stated, the idea that protein affects kidney function is that with persistent consumption of a higher-protein diet, there will be an increase in renal solute load (as urea) and is an precursor leading to compensatory hyperfiltration, which then leads to glomerular damage and eventual kidney damage and failure(1).
This myth has largely been debunked by a recent meta-analysis conducted to determine the effect of HP intakes on kidney function in healthy adults(2).
Results of this meta-analysis suggest a nonexistent or trivial effect of higher-protein consumption on glomerular filtration rate in individuals with normal kidney function.
These findings are in line with statements from the World Health Organization and Institute of Medicine on protein intake and kidney function(3).
Furthermore, there is no suggestive link indicating that higher protein intake somehow leads to decrements in renal function in otherwise healthy persons and even in populations with greater risk for declines in renal function such as those with type 2 diabetes.
Given the proposed benefits of consuming higher protein diets to promote muscle growth during resistance training, high-quality weight loss during energy restriction, and maintenance of muscle mass with aging, the finding that a higher protein diet does not negatively affect kidney function is of relevance.
Essentially, if you have healthy kidneys, you don’t have to concern yourself with protein intake up to 3 g/kg of bodyweight. There is no evidence that it harms a healthy kidney.
A low protein diet reduces nitrogen waste products and decrease kidney workload by lowering intraglomerular pressure, which may protect the kidneys especially in patients with decreased renal function. It leads to favorable metabolic effects that can preserve kidney function and control of uremic symptoms as listed below and depicted in the figure below(4).
It’s also suggested that lower protein diets decrease urinary protein levels and to further reduce the risk of chronic kidney disease progression.
Protein restriction has been demonstrated to lower proteinuria by 20–50% in patients with chronic kidney disease, and a linear-relationship between reduction of protein intake and decrease in proteinuria is reported(5).
A lower protein diet is beneficial to improve metabolic acidosis in chronic kidney diseases. Acid is generated during metabolism of proteins including sulfur containing amino-acids, and pre-dialysis serum bicarbonate concentration was lower in patients with higher protein intake(6).
Low protein diets are still recommended to people with kidney disease. The idea behind this recommendation is that if there is damage to kidneys, you can reduce the load on the kidneys by reducing consumption of protein which will in turn, reduce urea.
There is not a lot of good data suggesting this reduces mortality in people who have chronic kidney disease.
In spite of the wealth of available evidence for benefits of a lower protein diet as described above; the renoprotective effect of a lower protein diet has been debated due to conflicting reports and concerns with malnutrition. In fact, several studies including the Modification of Diet in Renal Disease study demonstrated negative results regarding the effectiveness of a lower protein diet(7), and the benefit of a lower protein diet was not confirmed in diabetic patients.
It’s important to note that protein and calorie intake tend to decrease as renal function declines, and the gastrointestinal absorption and utilization of ingested protein may be hindered in advanced chronic kidney disease(8).
Given that adequate calorie intake (30–35 kcal/kg/day) is needed to avoid protein catabolism and
malnutrition under protein restriction ≤0.6 g/kg/day(9), uremic anorexia raises a question about safety of a lower-protein diet, which otherwise may induce malnutrition and aggravate protein-energy wasting among patients with chronic kidney disease(10).
In the Modification of Diet in Renal Disease study, the lower protein diet group, compared to the usual diet group, experienced unfavorable changes of anthropometric measurements account for nutritional status such as decrease in body weight, body fat percent, skinfold thickness, and arm muscle area(11).
Furthermore, although there were no differences in nutritional parameters except for 24–hour urinary creatinine between the very low protein diet vs. low protein diet group in the Modification of Diet in Renal Disease study, the long-term follow-up study showed higher mortality risk associated with very low protein diet
supplemented with amino-acids(12).
Over the past decades, the optimum protein intake for patients with chronic kidney disease has been an important, controversial issue.
Dietary protein restriction has been commonly recommended for patients with chronic kidney disease for preserving kidney function. However, evidence of the associations between long-term protein intake and mortality is not consistent in patients with chronic kidney disease. In support of this notion, a very recent study examined the associations between total protein intake and all-cause mortality in Korean adults with chronic kidney disease(13).
The available evidence showed no association between the level of protein intake and mortality in people with chronic kidney disease.
In fact, this large population cohort of Korean adults with chronic kidney disease, higher protein intake was not associated with all-cause mortality. Additionally, similar results were observed after stratifying based on chronic kidney disease stages and the presence of diabetes.
Interestingly, the highest protein intakes showed a trend to reduce mortality but this was not statistically different.
This data indicated no causal relationship between dietary protein intake and survival in the Korean population with chronic kidney disease. Higher protein intake was not associated with all-cause mortality in patients with chronic kidney disease, and similar results were obtained after stratifying patients based on chronic kidney disease stages and the presence of diabetes.
More evidence is needed to establish optimal dietary protein intake levels for this population with chronic kidney disease stage 3–5. Also, additional studies are needed to examine the impact of the dietary source of protein on various health outcomes and mortality.This data supports that severe protein restriction with less severe kidney failure may not have a clear beneficial effect for all-cause death events.