A low-protein diet is beneficial with chronic kidney disease, but research suggests there are many reasons a vegan, high-soy diet may be problematic to renal patients. The possible effects include renal calcification, inhibited mineral absorption, and excessive levels of toxic minerals. Conversely, secondary nutrients such as conjugated linoleic acid (CLA) and L-carnitine found in animal products may have beneficial properties for renal patients.
A low-protein diet can be beneficial to a patient with chronic kidney disease (CKD), but the source of that protein is important as well. Many clinicians assume that a vegan diet is superior for kidney patients, but this may not be the case. With a vegan diet, the patient may be missing some potentially beneficial secondary nutrients found primarily in animal sources. Vegetarian protein sources may also contain substances such as phytates and aluminum that could potentially harm kidney patients.
It is essential for patients with CKD to consume adequate protein to prevent the body from entering a catabolic state. However, too much protein will put stress on the kidneys. Since a patient may be fighting a chronic condition for many years in an attempt to avoid dialysis, a low-protein diet should include enough protein to prevent cachexia, but at the same time protect the kidneys. For long-term use, a low-protein diet must not lead to a negative nitrogen balance, as muscle wasting increases the morbidity and mortality of CKD.1
When the patient is eating a low-protein diet, it is important that the protein being eaten is readily absorbable by the body.
When the patient is eating a low-protein diet, it is important that the protein being eaten is readily absorbable by the body. From 1919 until recently, the most common way to measure how well the body utilizes protein has been the protein efficiency ratio (PER). This has now been replaced by the Protein Digestibility Corrected Amino Acid Score (PDCAAS).2 When an individual has a low protein score on the PDCAAS, additional protein is necessary to obtain adequate nutrition. The following table shows PDCAAS values for common foods.
Protein Digestibility Corrected Amino Acid Scores for Common Foods3
A diet with protein sources that score high on the PDCAAS would include soy but not other legumes. However, although soy protein has a significantly better PDCAAS than other vegetable proteins, a number of studies indicate that there is no advantage to a high-soy diet in preserving renal function. One study that followed individuals with diabetic nephropathy found there was no advantage to soy as measured by proteinuria and renal function.4 Another study followed patients with non-diabetic nephropathy. The study included two groups of patients on a low-protein diet, but one obtained its protein from vegan sources and the other used animal sources. This study found no difference in creatinine clearance between the two groups.5 A later study of patients with non-diabetic nephrosis followed for 6 months showed all patients suffered a significant loss of renal function, whether they were vegan or not.6 This trend was also true for transplanted kidneys, as another study substituted 25 g of soy protein for 25 g of animal protein in a post-transplant population and found no difference in creatinine clearance and proteinuria. Lastly, in a review of literature on vegetable-based diets, Bernstein found that a high intake of protein, whether from animal or vegetable sources, will accelerate the underlying disease process of the kidneys.7
Soy is often considered beneficial for the cardiovascular system, and therefore a good choice for renal patients, as cardiovascular disease is the number one cause of mortality in patients with CKD.8 Elevation of total plasma cholesterol, triglycerides, very-low-density lipoprotein (VLDL) and low-density lipoprotein (LDL) are common features of nephrotic syndrome, and many CKD patients with nephrotic dyslipidemia are placed on statin medications.9 However, agents that address the loss of protein in the urine will reduce the hyperlipidemia, addressing the root cause of the problem.10 Although soy may have the ability to lower cholesterol, it presents with other independent risk factors.
Soy and Nutrient Levels
Consumption of soy is associated with an imbalance of amino acids. In one study, methionine deficiency was induced in rats by feeding soy and was associated with hypercholestrolemia and lipid peroxidation.11 An imbalance of the amino acid cysteine is also possible. Although soy is high in the amino acid cysteine, much of it is not bioavailable. Trypsin inhibitors, cystatins, and soyacystatins found in soy inhibit absorption of cysteine. In addition, cysteine is often irreparably damaged from modern processing methods.12
Trypsin inhibitors found in soy are considered to be an “antinutrient.” Trypsin inhibitors block the action of trypsin and other enzymes needed for the digestion of protein. This can lead to chronic amino acid deficiencies, especially when one is on a low-protein diet.13
In addition to inhibiting the digestion of protein, soy is capable of reducing the absorption of certain minerals. Phytic acid (phytates) in soy may inhibit calcium absorption as well as the absorption of zinc and iron.14 The reduction of calcium absorption is particularly worrisome since CKD patients are at a higher risk of osteoporosis than the general population.15 While all seeds and legumes have phytic acid, soy products such as tofu and soy milk are especially high in phytic acid.16 Inhibition of zinc is also a problem, as zinc deficiency is common the CKD population.17 Iron deficiency must also be addressed, as renal patients also face chronic anemia.
The problem with phytic acid is not limited to inhibition of mineral absorption, but it may in fact cause direct damage to the kidneys. In a Japanese study, phytic acid was shown to induce calcifications of the renal papillae in a dose-dependent manner when added to the drinking water of test animals. None of the control animals developed renal necrosis.18 With many forms of nephropathy involving renal papillary necrosis, the high phytic acid of soy may negate any potential benefits.
Another concern for a high-soy diet is excessive minerals including potassium, phosphorus, aluminum, and manganese. While soy may inhibit the absorption of some minerals, it is high in other minerals, which can be damaging to renal patients. Elevated potassium and phosphorus are particularly dangerous with advanced renal disease as the body loses the ability to eliminate these minerals. Soy has more potassium and phosphorus than similar amounts of red meat, poultry, or fish. This leads some experts to advise people with kidney disease to consult a renal dietician before including soy in the diet.19
Aluminum is inadequately excreted in patients with CKD, and so it can accumulate. Problems of aluminum toxicity include dialysis encephalopathy (dialysis dementia), osteomalacia (aluminum-related bone disease), and a microcytic anemia developed without iron deficiency.20 Soy is known to contain high levels of aluminum. In fact, the United Soybean Board acknowledges that soy infant formula contains 10 times as much aluminum as cow’s milk.21
Manganese, another mineral found in high concentrations in soy, is also seen to accumulate in dialysis patients.22 A Canadian study recommends not giving infants soy beverages because they are not only nutritionally inadequate, but they contain high levels of manganese, which increases the risk of neurological damage. Infants fed soy beverages had 7 to 56 times the serum levels of manganese of those fed a milk-based formula.23
From a more systemic perspective, soy’s goitrogenic effect on the thyroid may exacerbate underlying thyroid dysfunction in patients with CKD. The kidney is an organ of metabolism and excretion of thyroid hormones as well as a target organ. Nephrotic syndrome is known to cause changes in concentrations of thyroid hormone due to loss of protein in the urine. In addition, CKD is often accompanied by changes in the hypothalamus-pituitary-thyroid axis, and secretion of TSH is impaired by uremia. Considering that CKD alone increases the potential for thyroid dysfunction through these changes, it may be prudent to avoid all known goitrogens, including soy. As direct evidence, one study found that soy sterols directly reduced serum levels of T3 in an animal model.24 This is concerning, since there is also data to suggest that levels of T3 are an independent marker for survival with kidney disease.25
Therapeutic Nutritional Components for Renal Patients
Among the therapeutics I use with renal patients are L-carnitine, conjugated linoleic acid, fish oil, vitamin D, coenzyme Q10, vitamin B12, and vitamin K2— all of which are animal in origin.
L-carnitine, found in high concentrations in meat, is a conditionally essential nutrient obtained both from diet and endogenous production. Impaired renal synthesis of L-carnitine with CKD can lead to carnitine deficiency. Symptoms of this depletion are common among those in renal failure and include muscle weakness, fatigue, lipid abnormalities, and anemia that is resistant to treatment.26 Although supplementation is often necessary to adequately address carnitine deficiency, dietary sources may be advisable as well. Foods that are particularly high in carnitine include steak and ground beef, with 4 oz. portions containing up to 162 mg and 99 mg respectively. By comparison 4 oz. of chicken contains 5mg, and two slices of bread contains 0.2 mg.27
Conjugated linoleic acid (CLA), found in high concentrations in grass-fed meat, has been shown to have benefits for the kidneys. When proteinuria was induced in mice, the group fed CLA survived 1.7 times longer than the control group.28 CLA is known to reduce atherosclerosis and inflammation in animal models as well. Specifically, CLA reduces renal production of PGE2, demonstrating a reduction in the inflammation and fibrosis associated with the progression of renal disease.29
Another potential benefit of CLA is a reduction in parathyroid hormone (PTH) and the associated loss of bone mass. In one study, there was a 60% reduction in PTH with CLA in rats with polycystic kidney disease, compared to the control group.30 Elevated PTH is very common with advanced renal disease, and removal of the parathyroid gland is a common intervention among these patients. Reduction of PTH without surgery would be of enormous benefit to patients in renal failure.
There is also strong evidence that eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) found in fish oil benefit the kidneys. In one study from the Mayo Clinic, patients with IgA nephropathy were given either fish oil capsules or a vegetable oil placebo every day. After 2 years of treatment the placebo group had an increase in creatinine of 0.14 mg/dL annually, while the fish oil group had an annual increase of only 0.03 mg/dL. After 4 years of treatment, 40% of the placebo group had end-stage renal disease or were deceased, compared to only 10% of the fish oil group.31 Fish oil has also been demonstrated to reduce proteinuria.32
Animal products are useful to supply B vitamins and vitamin K2 to kidney patients. With advanced renal disease, low levels of erythropoietin will lead to chronic anemia, which is often treated with B vitamins and iron as well as prescription Epoetin alfa (Procrit®, Epogen®). Dialysis patients are often prescribed a B-vitamin supplement, which is especially useful for replacing the water-soluble vitamins lost during dialysis. Obtaining adequate B vitamins, including B12, from the diet is fundamental in addressing the anemia of CKD.
In addition to B vitamins, vitamin K2 is also useful to kidney patients. Vitamin K2 is found in egg yolks, beef, liver, and cheese.33 Among its benefits are improved bone density, which is especially important with CKD. Studies indicate K2 can prevent fracture and sustain bone mineral density,34 which may provide benefit to this population at risk for osteomalacia. K2 also benefits the cardiovascular system by reducing calcification and atherosclerotic plaque of the heart and blood vessels.35 This is especially important as elevated phosphorus in renal patients often causes calcium to leach out of the bones and deposit in soft tissue. The Rotterdam Heart Study, which followed 4,800 Dutch participants for 7 years, showed conclusively that those with the highest dietary intake of K2 had 57% fewer heart attacks than those who ingested the least.36
Another important consideration for patients with CKD is the composition of fats found in the kidneys themselves. Kidney fat is higher in saturated fat than other fats in the body and include myristic acid (14-carbon saturate), palmitic acid (16-carbon saturate), and stearic acid (18-carbon saturate). Cholesterol is also important to the cell membranes in the kidney. When the diet is switched and plant sterols found in vegetable oils are incorporated into the cell membrane, the result is weaker, more fragile cell membranes and a shorter life span. For these reasons, it is recommend that some animal fats be included in the diet and polyunsaturated fats high in omega-6 be limited.37
Although a vegan diet may appear beneficial to CKD patients due to its limiting of protein, soy is the only legume that comes close to providing adequate protein. Numerous problems with soy consumption, however, may cause problems for kidney patients. Animal products, particularly grass-fed meat, consumed in small amounts may offer benefits to the renal patient over a strict vegan diet.
- Workeneh BT, Mitch WE. Review of muscle wasting associated with chronic kidney disease. Am J Clin Nutr. 2010;(91):11285-11325.
- CBS Interactive Inc. Protein Efficiency Ratio. Search.com. www.search.com/reference/Protein_efficiency_ratio. Accessed July 22, 2010.
- Schaafsma G. The protein digestibility-corrected amino acid score. J Nutr. 2000;130(7):1865S-1867S.
- Anderson JW, Blake JE, Turner J, Smith BM. Effects of soy protein on renal function and proteinuria in patients with type 2 diabetes. Am J Clin Nutr. 1998; 68(6):1347S-1353S.
- Barsotti G, Morelli E, Cupisti A, Bertoncini P, Giovannetti S. A special supplemented ‘vegan’ diet for nephrotic patients. Am J Nephrol. 1991;11:380-385.
- Barsott G, Morelli E, Cupisti A, Meola M, Dani L, Giovannetti S. A low-nitrogen, low-phosphorus vegan diet for patients with chronic renal failure. Nephron. 1996;74:390-394.
- Renal & Urology News. Vegetarian Diets May Not Be Better. Renal and Urology News website. http://www.renalandurologynews.com/vegetarian-diets-may-not-be-better/article/24640/. Accessed July 22, 2010.
- Go AS, Chertow GM, Fan D, McCulloch CE, Hsu C. Chronic kidney disease and the risks of death, cardiovascular events, and hospitalizations. N Engl J Med. 2004;351:1296-1305.
- Wheel DC, Bernard DB. Lipid abnormalities in the nephrotic syndrome: causes, consequences and treatment. Am J Kidney Dis. 1994;23(3):331-346.
- Verseput GH, Provoost AP, Van Tol A, Koomans HA, Joles JA. Hyperlipidemia is secondary to proteinuria and is completely normalized by angiotensin-converting enzyme inhibition in hypertensive fawn-hooded rats. Nephron. 1997;77:346-352.
- Moundras C, Remesy C, Levrat MA, Demigne C. Methionine deficiency in rats fed soy protein induces hypercholesterolemia and potentiates lipoprotein susceptibility to peroxidation. Metabolism. 1995;44(9):1146-1152.
- Vitale Therapeutics Inc. The Effect of Soy Protein on Homocysteine. Vitale Therapeutics website. http://www.vitaletherapeutics.org/WAPSoyH4.pdf. Accessed July 23, 2010.
- Barth Ca, Lunding B, Schmitz M, Hagemeister H. Soybean trypsin inhibitor(s) reduce absorption of exogenous and increase loss of endogenous protein in miniature pigs. J Nutr. 1993;123:2195-2200.
- Zhao XF, Hao LY, Yin SA, Kastenmayor P, Barclay D. [A study on absorption and utilization of calcium, iron and zinc in mineral-fortified and dephytinized soy milk powder consumed by boys aged 12 to 14 years.] Zhonghua Yu Fang Yi Xue Za Zhi. 2003;37(1):5-8.
- Stehman-Breen C. Osteoporosis and chronic kidney disease. Semin Nephrol. 2004;24(1)78-81.
- Rose A. Phytic Acid Tips for Consumers. www.phyticacid.org. Accessed September 2, 2010.
- Eggert JV, Siegler RL, Edomkesmalee E. Zinc supplementation in chronic renal failure. Int J Pediatr Nephrol. 1982;3(1)21-24.
- Hiasa Y, Kitahori Y, Morimoto J, Konishi N, Nakaoka S, Nishioka H. Carcinogenicity study in rats of phytic acid ‘Daiichi’, a natural food additive. Food Chem Toxicol. 1992;30(2):117-125.
- University of Maryland Medical Center. Soy. University of Maryland website. http://www.umm.edu/altme/article/soy-000326.htm. Accessed July 23, 2010.
- National Kidney Foundation. KDOQI Clinical Practice Guidelines for Bone Metabolism and Disease in Chronic Kidney Disease. National Kidney Foundation website. http://www.kidney.org/professionals/kdoqi/guidelines_bone/Guide11.htm. Accessed July 23, 2010.
- United Soybean Board. Focus on Aluminum. Soy Connection website. http://www.soyconnection.com/newsletters/soy-connection/health-nutrition/article.php/Focus+On+Aluminum?id=99. Accessed July 22, 2010.
- Kiryluk K, Khan F, Valeri A. Acute chorea and bilateral basal ganglia lesions in a hemodialysis patient. Kidney Int. 2008;73(9):1087-1091.
- Cockell KA, Bonacci G, Belonje B. Manganese content of soy or rice beverage is high in comparison to infant formulas. J Amer Coll Nutr. 2004;23(2):124-130.
- Sunanda P, Kar A, Patil S. Soy sterols in the regulation of thyroid function, glucose homeostasis and hepatic lipid peroxidation in mice. Food Research International. 2009; 42(8):1087-1092.
- Iglesias P, Diaz JJ. Thyroid dysfunction and kidney disease. Eur J Endocrinol. 2009;150(4):503-15.
- Linus Pauling Institute at Oregon State University. L-Carnitine. Oregon State University website. http://lpi.oregonstate.edu/infocenter/othernuts/carnitine/. Accessed July 23, 2010.
- National Institutes of Health Office of Dietary Supplements website. http://ods.od.nih.gov/factsheets/carnitine.asp. Accessed September 1, 2010.
- Yang M, Cook ME. Dietary CLA decreased weight loss and extended survival following the onset of kidney failure in NZB/W F1 mice. Lipids. 2003;38(1):1558-9307.
- Ogborn MR, Nitschmann E, Bankovic-Calic N, Weiler HA, Fitzpatrick-Wong S, Aukema HM. Dietary conjugated linoleic acid reduces PGE2 release and interstitial injury in rat polycystic kidney disease. Kidney International. 2003;64:1214-1221.
- Weiler H, Austin S, Fitzpatrick-Wong S, et al. The role of conjugated linoleic acid in human health. Amer J Clin Nutr. 2004;79(6):1186S-1189S.
- Donadio JV, Bergstralh EJ, Offord KP, Spencer DC, Holley KE. A controlled trial of fish oil in IgA nephropathy. N Engl J Med. 1994;331:1194-1199.
- Weisse WJ, Natori Y, Levine JS, et al. Fish oil has protective and therapeutic effects on proteinuria in passive Heymann nephritis. Kidney Int. 1993;43(2):359-368.
- Plaza SM, Lamson DW. Vitamin K2 in bone metabolism and osteoporosis. Alternative Medicine Review. 2005;10(1):24-35.
- Shiraki M, Shiraki Y, Aoki C, Miura M. Vitamin K2 (menatetrenone) effectively prevents fractures and sustains lumbar bone mineral density in osteoporosis. J Bone Miner Res. 2000;15(3):515-521.
- Davis W. Vitamin K2: Newest heart-healthy supplement? Health Central Network Inc. website. http://www.healthcentral.com/heart-disease/c/1435/18016/k2-newest. Accessed August 29, 2010.
- Enig MG. Saturated fats and the kidneys. Wise Traditions in Food, Farming and the Healing Arts. 2000;14:31.