Gang Jee Ko, MD, PhD,1,2 Yoshitsugu Obi, MD, PhD,1 Amanda R. Tortoricci, RD,1 and Kamyar Kalantar-Zadeh, MD, MPH, PhD1,3,4 Show
Gang Jee Ko1Harold Simmons Center for Kidney Disease Research and Epidemiology, University of California Irvine, School of Medicine, Orange, CA, USA 2Department of Internal Medicine, Korea University School of Medicine, Seoul, Korea Find articles by Gang Jee Ko Yoshitsugu Obi1Harold Simmons Center for Kidney Disease Research and Epidemiology, University of California Irvine, School of Medicine, Orange, CA, USA Find articles by Yoshitsugu Obi Amanda R. Tortoricci1Harold Simmons Center for Kidney Disease Research and Epidemiology, University of California Irvine, School of Medicine, Orange, CA, USA Find articles by Amanda R. Tortoricci Kamyar Kalantar-Zadeh1Harold Simmons Center for Kidney Disease Research and Epidemiology, University of California Irvine, School of Medicine, Orange, CA, USA 3Department of Medicine, Long Beach Veteran Affairs Health System, Long Beach, CA, USA 4Los Angeles Biomedical Research Institute at Harbor-UCLA, Torrance, CA, USA Find articles by Kamyar Kalantar-Zadeh Author information Copyright and License information Disclaimer 1Harold Simmons Center for Kidney Disease Research and Epidemiology, University of California Irvine, School of Medicine, Orange, CA, USA 2Department of Internal Medicine, Korea University School of Medicine, Seoul, Korea 3Department of Medicine, Long Beach Veteran Affairs Health System, Long Beach, CA, USA 4Los Angeles Biomedical Research Institute at Harbor-UCLA, Torrance, CA, USA Correspondence: Kamyar Kalantar-Zadeh, MD, MPH, PhD, Professor of Medicine, Pediatrics & Epidemiology, Harold Simmons Center for Kidney Disease Research and Epidemiology, Division of Nephrology & Hypertension, University of California Irvine (UCI) School of Medicine, 101 The City Drive South, City Tower, Suite 400 - ZOT: 4088, Orange, California 92868-3217, Tel: (714) 456-5142, Fax: (714) 456-6034, ude.icu@zkk Copyright notice The publisher's final edited version of this article is available at Curr Opin Clin Nutr Metab Care AbstractPurpose of reviewHigh protein intake may lead to increased intraglomerular pressure and glomerular hyperfiltration. This can cause damage to glomerular structure leading to or aggravating chronic kidney disease (CKD). Hence, a low protein diet (LPD) of 0.6–0.8 g/kg/day is often recommended for the management of CKD. We reviewed the effect of protein intake on incidence and progression of CKD and the role of LPD the CKD management. Recent findingsActual dietary protein consumption in CKD patients remain substantially higher than the recommendations for LPD. Notwithstanding the inconclusive results of the Modification of Diet in Renal Disease (MDRD) study, the largest randomized controlled trial to examine protein restriction in CKD, several prior and subsequent studies and meta-analyses including secondary analyses of the MDRD data appear to support the role of LPD on retarding progression of CKD and delaying initiation of maintenance dialysis therapy. LPD can also be used to control metabolic derangements in CKD. Supplemented LPD with essential amino acids or their keto-analogs may be used for incremental transition to dialysis especially in non-dialysis days. An LPD management in lieu of dialysis therapy can reduce costs, enhance psychological adaptation, and preserve residual renal function upon transition to dialysis. Adherence and adequate protein and energy intake should be ensured to avoid protein-energy wasting. SummaryA balanced and individualized dietary approach based on LPD should be elaborated with periodic dietitian counselling and surveillance to optimize management of CKD, to assure adequate protein and energy intake and to avoid or correct protein-energy wasting. Keywords: Low protein diet, progression of chronic kidney disease, Glomerular hyperfiltration, incremental hemodialysis, Protein energy wasting IntroductionThe crucial role of the kidney in amino acid and protein metabolism including breakdown and excretion of protein metabolites heralds paramount impact of dietary protein intake on metabolic processes regulated by kidney and on kidney function itself. High protein diet may cause damage to kidney and may lead to accumulation of toxic protein metabolites, while a low protein diet (LPD) offers a variety of clinical benefits in patients with renal insufficiency. However, interests and effort to adopt the merit of LPD in the management of chronic kidney disease (CKD) remain variable. This review focuses on the reasons as to why a high dietary protein intake may cause harm to the kidney, how lower protein intake may prolong kidney longevity, and why dietary protein restriction should be considered for and how it works in the management of CKD. Impact of High Protein Diet on Renal FunctionHigh protein diet, usually defined as >1.2 grams of dietary protein per kilogram of body weight per day (g/kg/day), is known to induce significant alterations in renal function and kidney health.[1] In contrast to dietary intake of fat and carbohydrates, higher protein intake modulates renal hemodynamic by increasing renal blood flow and elevating intraglomerular pressure leading to higher glomerular filtration rate (GFR) and more efficient excretion of protein-derived nitrogenous waste products, while an increase in kidney volume and weight may ensue.[2] The so-called “glomerular hyperfiltration” that is induced by high protein diet has been well reported in both animal models and in different clinical studies in human subjects (Table 1), [3–8] and confirmed in a recent meta-analysis including 30 randomized controlled trials (RCTs).[9] High protein diet associated glomerular hyperfiltration, together with resultant increase in urinary albumin excretion, may have deleterious consequences on kidney and other organs in long term.[1] Experimental studies have revealed that glomerular injury by an increase in intraglomerular pressure and flow can lead to progressive glomerular damage and sclerosis.[2,10] Table 1Recent randomized controlled trials of high protein diet on renal function with over 24-week follow-up period including more than 50 participants. ReferencesSample sizeMean age (years)Duration (weeks)Protein amount (% of total energy amount or g/kg/day)Renal function changesLi et al, 2010[3]10049.352HP-30%, 2.2g/kg/d Open in a separate window Abbreviations: HP-high protein diet; NP/LP-normal protein/low protein diet, LC diet-low carbohydrate diet; Cr-creatinine; eGFR-estimated glomerulofiltration rate; mAlb-microalbuminuria; CCr-creatinine clearance rate; CKD-chronic kidney disease. Hence, whereas the GFR may increase in short-term, kidney damage may ensue and the renal function will decline with long-term exposure to high dietary protein intake. This is important in the contemporary life style where a high protein diet for weight management has gained increasing popularity. It is not clear whether the potentially deleterious effects of high protein intake are equally observed in people with normal kidney function when compared to those with pre-existing kidney disorders. In the Nurses’ Health Study, high protein diet was associated with a faster decline in estimated GFR in people with subnormal kidney function, but not in those with normal kidney function.[11] It was the first large-scale observational study followed-up more than 10 years about the impact of high protein diet on renal function in general population. There are additional studies with conflicting results for the impact of high protein diet on renal function decline in the general population.[12,13] A recent prospective study of the general population in Singapore indicated that the impact of protein consumption on the risk of end-stage renal failure (ESRD) may depend on the type of protein sources.[14] Specifically, red meat intake was strongly associated with ESRD risk in a dose dependent manner, while other protein sources such as poultry, fish, eggs, or dairy products did not show such a deleterious association. Higher acid load induced by sulfur-containing amino acids and end products from animal protein may exert detrimental effect on renal function. Meanwhile, another community-based cohort study showed the association of high protein intake with cardiovascular events but not with loss of kidney function.[12] Additional studies to examine these differences are warranted. Relevant data from selected observational studies are summarized in Table 2.[15,16] Table 2Recent observational studies about high protein diet on renal function. ReferencesSample sizeMean age (years)Duration (years)HP dietBaseline eGFR (ml/min per 1.73 m2)Renal function changesKnight et al. 2003[11]1,62455.411Divided into quintiles Open in a separate window Abbreviations: CKD-chronic kidney disease; HP-high protein diet; eGFR-estimated glomerulofiltration rate; OR-odd ratios; CI-confidence interval; yr-year; n.d-not described; ESRD-end stage renal disease Dietary Protein Intake in North Americans with and without Chronic Kidney DiseaseLPD as a means of slowing CKD progression is not largely prescribed in the current clinical setting in North America.[1] Besides inconclusive data on the effectiveness of LPD (see below) and concerns about aggravation of protein-energy wasting (PEW), [2] one of main obstacles to the implementation of LPD is the big gap in protein intake between the amount of recommendations from guidelines and what is consumed contemporarily in the USA.[17] According to the National Health and Nutrition Examination Survey (NHANES) between 2001 and 2008, average dietary protein intake was 1.34 g/kg ideal body weight (IBW) per day or 1.09 g/kg actual body weight (ABW) per day in the US general population, [18] which is higher than the recommended protein intake for normal healthy adults (i.e., 0.8g/kg·ABW/day).[19] There were also variabilities in protein intake depending on CKD stages, and average protein intake was 1.04 g/kg·IBW/day or 0.81 g/kg·ABW/day in those with advanced stages of CKD.[18] Benefits of Protein Restriction in Patients with Chronic Kidney DiseaseLPD reduces nitrogen waste products and decrease kidney workload by lowering intraglomerular pressure, which may protect the kidneys especially in patients with decreased nephron capital and renal function. It leads to favorable metabolic effects that can preserve kidney function and control of uremic symptoms as listed below and depicted in Figure 1.[2,10,20]  Open in a separate window Figure 1 Diagram of the role of low protein diet in the management of chronic kidney disease. Effect of Protein Restriction on Proteinuria and AlbuminuriaUrinary protein or albumin excretion, a surrogate of the progression of CKD, increases with damages in podocytes and proximal tubular cells.[21] In turn proteinuria induces apoptosis of renal tubules and impairs podocyte regeneration, which leads to tubular atrophy and progressive renal failure (Figure 2).[22] Protein restriction has been demonstrated to lower proteinuria by 20–50% in patients with CKD, and a linear-relationship between reduction of protein intake and decrease in proteinuria is reported.[23] LPD may exert its vasoconstrictive effect at afferent arterioles while the renin-angiotensin system (RAAS) inhibition treatment preferentially decreases efferent resistance. Indeed LPD shows additive anti-proteinuric effect over the RAAS inhibition treatment.[2] Thus, the combined treatment with LPD and the RAAS blockade may be warranted to achieve lower urinary protein levels and to further reduce risk of CKD progression. Open in a separate window Figure 2 Effect of high dietary protein intake on kidney Effect of LPD on the Progression of Chronic Kidney DiseaseExperimental studies in 1980s demonstrated that LPD imposed on animal models of CKD led to a greater preservation of GFR.[10] Since then, the renoprotective effect of LPD had been supported by several clinical trials.[23] However, the Modification of Diet in Renal Disease (MDRD) study, which has thus far been the largest controlled trial of dietary protein management in CKD, failed to show the definite effectiveness of LPD on retarding CKD progression.[2,10] It contributed to form a conception that dietetic therapy plays a marginal role in the management of CKD. Yet secondary analysis of the MDRD study showed that each 0.2 g/kg/day decrease in protein intake was associated with a small amelioration in GFR decline over time, i.e., 1.15 ml/min/1.73m2/year, and with a halved risk of renal failure or death.[24] Indeed, the relatively short period of the MDRD study and the unusually large proportion of polycystic kidney patients who often have very slow CKD progression might have reduced the study power. Renoprotective effect of LPD may be reinforced proportionally with the extent of protein restriction. A recent RCT demonstrated that very low vegetarian protein diet (VLPD, 0.3g/kg/day) supplemented with keto-analogs, compared to conventional LPD (0.6g/kg/d), mitigated kidney function decline and reduced the number of patients requiring renal replacement therapy.[25] A meta-analysis of RCTs including the MDRD study also confirmed the risk reduction of the development of ESRD by protein restriction among non-diabetic patients with CKD.[26] It is postulated that LPD prevents uremic symptoms and avoids dialysis therapy despite the small effect on kidney function decline. Effect of Low Protein Diet on Metabolic ControlLPD is beneficial to improve metabolic acidosis in CKD. 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.[27–29] There is a tendency toward acid retention with kidney function declines and resultant chronic metabolic acidosis in CKD impairs protein metabolism, increases muscle catabolism and wasting, and aggravates decline in renal function and uremic symptoms.[30] Indeed, LPD ameliorated metabolic acidosis among patients with advanced CKD. In a study of supplemented VLPD, mean serum bicarbonate levels remained <19 mmol/L in the control (LPD) group while it increased to the normal levels in the VLPD group.[25] Interestingly, a RCT of correcting metabolic acidosis with sodium bicarbonate supplementation among patients with stage 4 CKD showed that after 2 years of study period, participants in the intervention group experienced slower decline in kidney function, much lower incidence of ESRD, and improvements in nutritional status although they increased dietary protein intake.[31] LPD also offers better control of CKD-mineral and bone disorder (MBD). Dietary control is essential in the management of hyperphosphatemia in CKD, because dietary protein, especially animal protein, is the major source of phosphorus.[32–34] LPD, especially with plant protein, is efficacious on lowering serum phosphorus, which results in reduction in serum levels of parathyroid hormone (PTH) and fibroblast growth factor (FGF)-23.[35,36] Although the benefits of LPD in CKD-MBD may include slowing the progression of vascular calcification and improving cardiovascular outcome, [37] it should be noted that the risk may outweigh if LPD is solely used to control hyperphosphatemia.[38,39] Additionally, LPD may attenuate insulin resistance and oxidative stress, the common features that may play roles in accelerating atherosclerosis among patients with CKD.[2,40]. VLPD supplemented with keto-analogs also ameliorated erythropoietin responsiveness.[23,41] These metabolic advantages of LPD in CKD aid better control of uremic symptoms, decrease in cardiovascular risk, and less medications leading to better adherence.[42] Conservative Management with Low Protein Diet in End-Stage Renal DiseaseLess accumulation of protein waste products relieves clinical manifestations of uremia even in very late stage of CKD, and indeed LPD can be used effectively to delay the initiation of dialysis therapy.[10] Given that earlier dialysis initiation does not appear to offer any survival benefit, [1] conservative approaches are warranted in managing patients with advanced CKD. A RCT among elderly patients with GFR 5–7 ml/min demonstrated that VLPD supplemented with keto-analogs and vitamins delayed the initiation of dialysis by a mean period of 10.7 months without negative consequences. Estimated economic benefit for health care system based on this study was €21,180/patient in the first year.[43] Financial saving with delayed dialysis by LPD was also confirmed in another study.[44] Delaying dialysis with LPD could also save time for maturation of arteriovenous fistula and avoid the insertion of central venous catheter.[45] Furthermore, LPD may play a role in incremental transition to dialysis therapy; once-weekly dialysis combined with LPD was found beneficial compared to thrice-weekly hemodialysis with respect to frequency of hospitalization, dose of erythropoietin, phosphorus binder, and cinacalcet therapy, without a significant difference in patient survival.[46] The importance of incremental dialysis has been revisited to preserve residual kidney function in dialysis patients, [47–51] because rapid decline in residual kidney function is associated with increased mortality.[52] Implementation of LPD regimen by dietary counselling combined with low phosphorus and high energy intake may support incremental transition to thrice a week hemodialysis.[53] Conflicting Data and Safety Issue about Low Protein Diet in CKDIn spite of many available evidences for benefits of LPD described above, renoprotective effect of LPD has been debated due to conflicting reports and concerns with malnutrition. In fact, several studies including the MDRD study showed negative results regarding the effectiveness of LPD, [2,10] and the benefit of LPD was not confirmed in diabetic patients.[54,55] Several studies of protein restriction in CKD in patients without other serious illnesses have shown acceptable safety and a low rate of malnutrition even with VLPD. A 0.6 g/kg/day of protein intake may meet protein requirement among clinically stable, non-dialysis-dependent CKD patients.[40] In a 48-month RCT of LPD in patients with CKD stages 3–5, dietary intervention was given under careful monitoring for nutritional status, and only 3 subjects developed malnutrition, [10] suggesting that close monitoring for nutritional status was more important to avoid malnutrition rather than the amount of protein intake itself. Some studies reported preserved body composition and skeletal muscle mass and function in CKD patients on LPD.[56] However, 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 CKD.[57] Given that adequate calorie intake (30–35 kcal/kg·AW/day) is needed to avoid protein catabolism and malnutrition under protein restriction ≤0.6 g/kg·ABW /day, [19,58] uremic anorexia raises a question about safety of LPD, which otherwise may induce malnutrition and aggravate protein-energy wasting (PEW) among patients with CKD.[59,60] In the MDRD study, the LPD 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.[61] Furthermore, although there was no differences in nutritional parameters except for 24–hour urinary creatinine between the VLPD vs. LPD group in the MDRD study, the long-term follow-up study showed higher mortality risk associated with VLPD supplemented with amino-acids.[62] However, the energy intakes of participants were substantially low (≈22 kcal/kg/day), which may have increased the risk og malnutrition risk and PEW with VLPD. This is so far the only study that followed up participants with VLPD for up to 7 years. In a recent 18-month RCT comparing ketoanalogue-supplemented VLPD with LPD, participants in both groups showed average energy intakes ≈30 kcal/kg•IBW/day and preserved nutritional status.[25] Although the VLPD group showed a lower risk of ESRD compared to the LPD group, studies with longer follow-ups are necessary to evaluate the safety underlying VLPD. The Challenge of Adherence to Low Protein DietDespite the established benefits of LPD in CKD management, adherence to LPD is a key element to gain its renoprotective effect. Although psychosocial factors such as knowledge, attitude, and support, are among the most important determinants of adherence, [10] successful adherence was hardly predictable.[41] Good patient-physician communication, self-monitoring of protein intake, and periodic feedback by the dietitian strengthens adherence through improved recognition of the importance of diet.[63] Education with simplified diet approach could also assist in robust adherence.[64–66] In a RCT with CKD stage 3 patients, renal nutrition education program including individual class, hands-on sessions about food types, and recipe distribution improved adherence to LPD.[67] Better knowledge about patient’s preference for food types and continuous effort to find new solutions for better tolerability would be essential for successful dietary treatment.[68] Given the high frequency of poor adherence with dietary protein restriction in some CKD management centers, there has been criticism against the role of LPD in the real-world clinical practice. In a meta-analysis of 13 RCTs the mean of protein intake in restricted group was 0.68g/kg/day, which was higher than target values and marginally below the recommended protein intake in the general population.[69] Indeed, even 0.1 to 0.2 g/kg/day reduction in protein intake from baseline appears to result in significant metabolic improvement and longer preservation of kidney health.[2] The VLPD may offer incremental renal protection and beneficial metabolic effects compared to LPD despite a more challenging adherence and somewhat higher risk of PEW (see Figure 1).[70] We believe some reduction in dietary protein intake from baseline is warranted across virtually all stages of CKD but the protein intake target range should be individualized, e.g. we suggest <1.0 g/kg.IBW/day for non-proteinuric CKD stages 1 and 2 such as in those after nephrectomy with a solitary kidney or elderly people with Stage 3b and very slow progression, and 0.6–0.8 g/kg.IBW/day for patients with eGFR<45 mg/ml/1.73m2BSA or proteinuria. Good adherence to LPD is defined as an actual intake within ±20% of the prescribed target range in 80% of the time.[1] It should be noted again that adherence to adequate energy intake (i.e., 30–35 kcal/kg·ABW/day) is also essential for the success in protein restriction, especially with more healthy and complex carbohydrates and mono- and poly-unsaturated fat.[71] Nutritional Assessment in Low Protein DietProtein and energy requirement varies with clinical conditions and across severity of disease, and actual intake could also be affected with psychosocial aspects and comorbid conditions. Therefore, frequent periodic follow-up visits, e.g. every 3–4 months, for monitoring dietary intake and nutritional status is essential in the implementation of LPD. To verify if actual protein intake is in prescribed range, the amount of protein intake should be periodically evaluated preferably by nitrogen appearance via serial 24-hour urine collections.[1] Dietary intake can be assessed with dietary recalls or interviews, and food frequency questionnaires.[65] One caveat is that dietary protein intake is overestimated by UNA-based calculation if patients are on hypercatabolic states including malnutrition, inflammatory conditions, post-operative period, and burns. Because such patient would appear “non-adherent” to LPD even if they actually follow the prescribed protein intake, careful monitoring of both disease conditions and nutritional status together with other diet assessment tools is necessary before reinforcing protein restriction. Physical measurements such as body weight and anthropometries, [72,73] or biochemical parameters such as transthyretin, cholesterol and normalized protein nitrogen appearance provide additional data on patient nutritional status.[2,74–76] However, it should be noted that in the MDRD study, the VLPD group, compared to the LPD group, did not show any significant difference in these nutritional parameters except for 24-hour urinary creatinine despite the increased mortality risk in the follow-up study in VLDP but not LPD.[62] Further studies are still necessary to develop a sensitive method to detect inadequate nutrient intake of either protein or energy. Essential Amino-acid and Ketoanalog Supplemented Very-Low Protein DietTo attain proper nutritional status and avoid PEW, nutritional supplementation with essential amino-acids (EAAs) and keto-analogs has been proposed primarily for VLPD.[41] EAAs need to be obtained from food, because it could not be generated in the body. Meanwhile, keto-analogs, formed by transamination of EAAs except lysine and threonine, can be utilized through their conversion to respective EAAs without providing nitrogen products.[39] Potential benefits of EAAs and keto-analogs supplementation include (1) maintaining protein-energy status without increase in nitrogen waste products; (2) reducing phosphorus and acid load given no phosphorus in purified EAA or their ketoanalogs; and (3) decreasing protein degradation and enhancing protein synthesis.[39] However, it can be argued that >25% less protein intake than recommended in the general population (given the <0.6 g/kg•ABW/day is the lowest protein requirement to avoid negative nitrogen balance) on a long-term basis might eventually compromise metabolic balance and survival through gradually deteriorating nutritional status if patients may suffer from hypercatabolic conditions such as infections. Such considerations have led to the emergence of a camp in the field of renal nutrition representing the opinion that even a protein intake of 0.6 g/kg/day needs to be supplemented by EAAs or keto-analogs.[19] Indeed in both LPD and VLPD, at least 50% of the dietary protein intake should be provided by high biologic value proteins.[24] Although the efficacy of keto-analogs combined with VLPD, compare to standard LPD, for retarding the progression of CKD was not significant in the MDRD study, it was observed in other studies including several RCTs and meta-analyses.[2,26,38] Supplemented VLPD with keto-analogs and EAAs also had benefits for better metabolic control in hyperphosphatemia, and anemia.[38] Further studies are required to explore how to combine protein restriction and supplementation for minimizing the risk of malnutrition while maximizing the benefits of LPD. Protein Intake in Maintenance Dialysis PatientsDialysis treatment may stimulate protein catabolism, which aggravates PEW in ESRD patients. In a recent study, whole-body skeletal muscle metabolism appeared to increase to lead net loss of muscle protein during hemodialysis treatment.[58] Guidelines recommends much higher protein intake (1.2–1.4 g/kg.IBW/day) in ESRD patients treated with dialysis than in pre-dialysis CKD patients, [17,32] because dialysis itself is sufficient to correct uremic symptoms and metabolic derangements without LPD, and proper protein intake should be assured to avoid aggravation of PEW caused by loss of nutrients and hypermetabolism during dialysis treatment.[58,77] Low dietary protein intake is associated with higher morbidity, hospitalization and mortality in hemodialysis patients.[78] Interestingly, elements of over-nutrition such as increased body mass index or high serum cholesterol levels, which are deleterious in the general population, are paradoxically protective in dialysis patients, which is known as “obesity paradox” or “reverse epidemiology”.[79] Strict diet restrictions may cause unfavorable outcome in dialysis patients. Careful relaxation for dietary restrictions and adoption of more balanced diet regimen with individualized approach should be considered in patients treated with dialysis.[80,81] ConclusionThe aim of LPD for handling accumulation of protein waste products conservatively and delaying the need for dialysis treatment has been hampered by the fear of PEW. Implementation of LPD as proper dietary regimen is recommended to retard decline of GFR and initiation of dialysis. Multi-directional approach including dietary approach should be considered to ensure the best outcome for CKD patients. Key Points
AcknowledgmentsFunding Sources: Supported by research grants from the National Institute of Diabetes, Digestive and Kidney Disease of the National Institutes of Health K24-DK091419 and philanthropic grants from Dr Joseph Lee and Mr. Lois Chang. FootnotesImportant Disclosure KKZ serves as a part-time physician in a US Department of Veterans Affairs medical center as a part-time employee of a US Department of Veterans Affairs medical center. Opinions expressed in this paper are those of the authors’ and do not represent the official opinion of the US Department of Veterans Affairs. Potential Conflict of Interests Dr. K. Kalantar-Zadeh has received honoraria and/or support from Abbott, Abbvie, Alexion, Amgen, ASN (American Society of Nephrology), Astra-Zeneca, Aveo, Chugai, DaVita, Fresenius, Genentech, Haymarket Media, Hofstra Medical School, IFKF (International Federation of Kidney Foundations), ISH (International Society of Hemodialysis), International Society of Renal Nutrition & Metabolism (ISRNM), JSDT (Japanese Society of Dialysis Therapy), Hospira, Kabi, Keryx, Novartis, NIH (National Institutes of Health), NKF (National Kidney Foundations), Pfizer, Relypsa, Resverlogix, Sandoz, Sanofi, Shire, Vifor, UpToDate, ZS-Pharma. How much protein can your kidneys handle in a day?Studies now show that limiting protein to 0.55-0.60 grams per kilogram of your body weight can delay decline in kidney function. For example, if your weight is 150 lbs or 68 kg, your protein needs are: 68 x 0.6 – 0.8 g/kg = 40-54 grams per day.
Can too much protein cause kidney problems?High dietary protein intake can cause intraglomerular hypertension, which may result in kidney hyperfiltration, glomerular injury, and proteinuria. It is possible that long-term high protein intake may lead to de novo CKD. The quality of dietary protein may also play a role in kidney health.
Can you overload your kidneys with protein?Having too much protein can cause waste to build up in your blood, and your kidneys may not be able to remove all the extra waste. If protein intake is too low, however, it may cause other problems so it is essential to eat the right amount each day. The amount of protein you need is based on: your body size.
Is kidney damage from too much protein reversible?People who are unaware they have mild chronic kidney disease and who are following a high-protein diet risk 'taking the fast lane to irreversible kidney failure'. Three new studies published in the journal Nephrology Dialysis Transplantation, link high-protein diets with kidney damage.
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How much protein is too much for kidneys
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