Protein and Kidney Function by Jamie Hale
How many times have you heard too much protein will destroy your kidneys? This is a common statement heard when speaking of high protein diets. You would think there should be mounds of evidence indicating this. After all, my doctor or dieteiatan said so. Like many other statements concerning nutrition the above statement cannot be verified by scientific or practical study. I have known hundreds of people who consume 300-400 gms of protein a day. Guess what, no kidney problems. I have searched through a multitude of studies and spoke to numerous coaches and nutrition consultants around the world and the resounding conclusion has been the same. There is no evidence whatsoever of protein intake causing kidney damage in individuals with normal renal functioning.
Below is some highlights from a paper taking an in depth look at Protein and it’s effects on Kidney Function.
Dietary protein intake and renal function William F Martin* 1 , Lawrence E Armstrong* Nancy R, Rodriguez
Dietary protein intake can modulate renal function and its role in renal disease has spawned an ongoing debate in the literature. At the center of the controversy is the concern that habitual consumption of dietary protein in excess of recommended amounts promotes chronic renal disease through increased glomerular pressure and hyperfiltration. Media releases often conclude that, “too much protein stresses the kidney.” The real question, however, is whether research in healthy individuals supports this notion.
The purpose of this paper is to review the available evidence regarding the effects of protein intake on renal function with particular emphasis on renal disease. This review will consider research regarding the role of dietary protein in chronic kidney disease, normal renal function and kidney stone formation and evaluate the collective body of literature to ascertain whether habitual consumption of dietary protein in excess of what is recommended warrants a health concern in terms of the initiation and promotion of renal disease.
Chronic Kidney Disease (CKD) is defined as either kidney damage or a decline in renal function as determined by decreased glomerular filtration rate (GFR) for three or more months. It is estimated that 1 in 9 adults in the United States meet this criteria, while an additional 1 in 9 adults are at increased risk for CKD. In the general population, a decline in renal function is considered an independent risk factor for both cardiovascular disease and all-cause mortality.
The relationship between dietary protein and renal function has been studied for over half a century. In 1923, Addis and Drury were among the first to observe a relationship between level of dietary protein and rates of urea excretion. Soon after, it was established that increased protein intake elevated rates of creatinine and urea excretion in the dog model. The common mechanism underlying increased excretion rates was eventually attributed to changes in GFR and Van Slyke et al., demonstrated that renal blood flow was the basis for GFR mediated changes in clearance rates in response to increased protein intake. Clearly dietary protein effects GFR, with both acute and chronic increases in protein consumption elevating GFR.
Observational data from epidemiological studies provide evidence that dietary protein intake may be related to the progression of renal disease. In the Nurses’ Health Study, protein intake, assessed with a semi-quantitative food frequency questionnaire, was compared to the change in estimated GFR over an 11-year span in individuals with pre-existing renal disease. Regression analysis showed an association between increased consumption of animal protein and a decline in renal function suggesting that high total protein intake may accelerate renal disease leading to a progressive loss of renal capacity. However, no association between protein intake and change in GFR was found in a different cohort of 1,135 women with normal renal function. The latter finding led the authors to conclude that there were no adverse effects of high protein intakes on kidney function in healthy women with normal renal status.
Research by Johnson et al., showed protein intake as a possible risk factor for progressive loss of remaining renal function in dialysis patients. Indeed, dietary protein restriction is a common treatment modality for patients with renal disease and practice guidelines exist regarding reduced dietary protein intakes for individuals with chronic renal disease in which proteinuria is present. The National Kidney Foundation (NKF) has extensive recommendations with regard to protein intake, which are a byproduct of the Dialysis Outcome Quality Initiative. Again, it is important to note that these recommendations are not indicated for individuals with normal renal function nor are they intended to serve as a prevention strategy to avoid developing CKD. Despite the clarity of these guidelines, their mere existence has resulted in concern regarding the role of dietary protein in the onset or progression of renal disease in the general population.
While the effect of hyperfiltration on renal function in those individuals with pre-existing renal disease is well documented, the application of these observations to healthy persons with normal renal function is not appropriate. To date, scientific data linking protein-induced renal hypertrophy or hyperfiltration to the initiation or progression of renal disease in healthy individuals is lacking. The possibility that protein-induced changes in renal function are a normal physiological adaptation to nitrogen load and increased demands for renal clearance is supported by changes noted in renal structure and function during pregnancy. GFR increases by as much as 65% in healthy women during pregnancy, typically returning to nonpregnant levels by three months postpartum. Despite these changes in renal function, pregnancy is not a risk factor for developing CKD.
Concerns about level of dietary protein and renal function are often presented in public health guidelines. In addition to the claims that high protein intake causes renal disease, some studies have suggested that renal function may be negatively affected by routine consumption of high protein diets. Although high protein diets cause changes in renal function (i.e., increased GFR) and several related endocrine factors that may be harmful to individuals with renal disease, there is not sufficient research to extend these findings to healthy individuals with normal renal function at this time.
Although the efficacy of high protein diets for weight loss has been evaluated, there have been no reports of protein-induced diminutions in renal function despite subject populations that are generally at risk for kidney disease (e.g., dyslipidemia, obesity, hypertension) A randomized comparison of the effects of high and low protein diets on renal function in obese individuals suggested that high protein diets did not present a health concern with regard to renal function their study population. In this study, 65 overweight, but otherwise healthy, subjects adhered to a low or high protein diet for six months. In the high protein group, both kidney size and GFR were significantly increased from that measured at baseline. No changes in albumin excretion were noted for either group and the authors concluded that, despite acute changes in renal function and size, high protein intake did not have detrimental effects on renal function in healthy individuals. Similar findings were recently reported by Boden et al., in a study of 10 subjects who consumed their typical diet for 7 days followed by strict adherence to a high protein diet for 14 days. No significant changes were noted in serum or urinary creatinine and albumin excretion, suggesting no ill-effects of a high protein diet on renal function.
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