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Journal of Traditional and Complementary Medicine logoLink to Journal of Traditional and Complementary Medicine
. 2017 Jan 10;7(4):375–379. doi: 10.1016/j.jtcme.2016.12.004

Food strategies of renal atrophy based on Avicenna and conventional medicine

Marjan Mahjour a,e, Arash Khoushabi b,f, Maryam Miri Ghale Novi c,g, Zohre Feyzabadi d,
PMCID: PMC5634736  PMID: 29034182

Abstract

Kidneys have an important role in the body. Any damage to kidney role can damage many organs of the body. Traditional Persian Medicine (TPM) or Iranian traditional medicine (ITM) is an ancient temperamental medicine with many literatures about kidney diseases and Avicenna (980–1025 AD) describes kidney diseases in details. This is a review study by searching of the most important clinical and pharmaceutical TPM textbooks such as The Canon of Medicine by Avicenna and scientific data banks using keywords such as “Hozal-e-Kolye”, renal atrophy, tubular atrophy, kidney, chronic kidney disease, and end stage renal disease. This paper found that “Hozal-e-Kolye” in TPM texts is the same tubular atrophy in conventional medicine due to some similar symptoms between them. Lifestyle modification and use of proposed foodstuffs can be considered as a complementary medicine in addition to conventional treatments to manage these patients. TPM scholars prescribed some foodstuffs such as camel milk, sheep's milk and Ficus carica for this disease as a complementary management. This study aimed to explain HK (the same tubular atrophy considering their similar symptoms) and introduce some foodstuffs. It seems using of foodstuffs affecting tubular atrophy based on TPM literatures can has a role as a supplemental method in company with conventional medicine management.

Keywords: Renal atrophy, Food, Avicenna, Traditional Persian Medicine, Hozal

Graphical abstract

graphic file with name fx1.jpg

1. Introduction

Chronic kidney disease (CKD) can lead to end stage renal disease (ESRD).1 Renal atrophy is one of the kidney diseases occurring due to shrinkage of the kidney in which the nephrons are lost and tubular atrophy is the loss of parenchymal renal cells characterizing in CKD.2 Tubular atrophy is a hallmark of chronic kidney disease.3 The prevalence of CKD is increasing and estimated to be 8–16% worldwide.4, 5 Treatment of CKD considering the stages of the disease is various and the relationship between nutrition and kidney disease has a main effect on outcomes.6 Using complementary medicine (CAM) in treatment of chronic disease is growing in the past 10 years in the U.S.7 The management of CKD based on herbal traditional medicine is recommended as a preventive and therapeutic strategy8 and medicinal plants with kidney protective activities is prescribed.9

Traditional Persian Medicine (TPM) is an ancient temperamental medicine with a history of over one thousand years. Temperament is made of a normal interaction between four basic elements, named hot, cold, wet, and dry elements. And dystemperament occurs when the whole body or an organ's temperament changes.10 The kidney dystemperament occurs when the kidney temperament is changed and its function is disturbed. These conditions can lead to “Hozal-e-Kolye” (HK). HK in TPM occurs when the kidney becomes thin means its fat gets low or eliminates.11, 12, 13, 14 This study aimed to explain HK (the same tubular atrophy considering their similar symptoms) and introduce some foodstuffs as a complementary food management based on TPM.

2. Materials & methods

This is a review study by searching of the most important clinical and pharmaceutical TPM textbooks (That is not derived from the other books) such as The Canon of Medicine by “Avicenna” (10th and 11th centuries), Exir-e-Azam by Chishti (19th century), Tuhfat Al-momenin by Tonkaboni (17th century) and Makhzan-Al-advie by Aqili (18th century), with the keyword of “Hozal-e-Koleye” (the same tubular atrophy). Then, all of the foodstuffs extracted from this study were searched to find the related activity concerning the kidney function improvement by searching in scientific data banks such as Medline with these keywords: renal atrophy, tubular atrophy, kidney, chronic kidney disease, end stage renal disease. Finally, the results were inserted into a table.

3. Results

3.1. CKD in conventional medicine

CKD occurs when the impaired kidney function persists for three months or more. In this disorder, there is a decrease kidney function based on the presence of kidney damage. Glomerular filtration rate (GFR) has a central role in the pathophysiology of CKD complications. There are five stages in CKD classification on the basis of GFR: stage1 (more than 90 ml/min/1.73 m2), stage2 (60–89 ml/min/1.73 m2), stage3 (30–59 ml/min/1.73 m2), stage4 (15–29 ml/min/1.73 m2), stage5 (less than 15 ml/min/1.73 m2). Proteinuria has an important role in the pathogenesis CKD progression. When GFR is less than 15 ml/min/1.73 m2, kidney failure occurs and it needs dialysis or transplantation for treatment.15

Manifestations of CKD include: fluid and electrolyte imbalance (impaired ability to excrete leading to sensitive hypertension and edema due to reduce GFR), acid base abnormalities, carbohydrate intolerance, calcium and phosphate abnormalities and metabolic bone disease, hematologic abnormalities, gastrointestinal abnormalities, dermatological abnormalities, neuromuscular abnormalities. These patients are at risk of cardiovascular diseases.16 Also, there is a nocturnal polyuria in renal insufficiency that is a precocious symptom in CKD.17

3.2. Phosphorus and tubular defect

The main homeostasis of phosphorus occurs in the kidney and the small intestine. A large part of phosphate from eating is excreted in the urine. There is a hypophosphatemia in the renal tubular defect.18 80% of the phosphorus reabsorption occur in the proximal tubule of the kidney, but in a tubular defect such as tubular atrophy this process doesn't occur so in this condition there is a hypophosphatemia and phosphaturia.19 The urine color is white because of phosphaturia.20

3.3. Renal atrophy in conventional medicine

3.3.1. Renal atrophy

Renal atrophy caused by many diseases such as acute or chronic pyelonephritis and obstruction of the urinary tract, the systemic atherosclerosis, metabolic syndrome, sickle cell disease,21 atherosclerotic renal artery stenosis,22 after hereditary renal cell carcinoma surgery,23 xanthogranulomatous pyelonephritis (Cortical renal atrophy),24 posttraumatic (injury).25 Etiology of unilateral renal atrophy includes hydronephrosis, tumor, tuberculosis, Calculouse, chronic pyelonephritis,26, 27 congenital hypoplastic kidney, renal infarction, radiation, renal artery stenosis,26 partial nephrectomy.23 The classic signs of renal atrophy in modern medicine include high blood pressure, low calcium, acidosis, anorexia, malnutrition (serious deficiency minerals and vitamins),28 elevations in the serum creatinine concentration.29 Acute kidney injury (AKI) can lead to renal atrophy by incomplete tubular repair, tubulointerstitial inflammation, and interstitial fibrosis.30 Insufficient blood flow of kidney, can result in the renal atrophy too.31

3.3.2. Renal tubular disorder

Renal tubules are very important in the body homeostasis. The proximal tubules play a main role in the transport of phosphate, glucose, amino acid, bicarbonate and sodium. The dysfunctions of these tubules are primary or secondary. When these tubules are injured, some disorders occur, such as hypophosphatemia, and aminoaciduria. Common symptoms of most renal tubulopathies include polyuria and also growth failure and resistant rickets (in children). If tubular dysfunction occurs, phosphaturia will be present.32 Phosphaturia cause white urine.20 (Table 1).

Table 1.

Comparing symptoms of HK and tubular atrophy.

Symptoms of tubular disorders in conventional medicine Ref Symptoms of HK in TPM Ref
Polyuria
White urine (because of phosphaturia)
Growth failure
Resistant rickets
17
20
32
32
Polyuria
White urine
Weight loss
Permanent low Back pain
Low libido
11, 12, 13, 14
Hypophosphatemia in the laboratory test 18 There was not laboratory test at Avicenna's time

3.3.3. Etiologies of tubular atrophy

After allografts, persistent glomerulonephritis and proteinuria, antiglomerular basement membrane disease, medullary cystic kidney disease type I (a mutation in the mucin 1 gene), chronic tubulointerstitial diseases, allergic interstitial nephritis, granulomatous interstitial nephritis, vesicoureteral reflux and reflux nephropathy, lithium salts, the calcineurin inhibitor (CNI) immunosuppressive agent's cyclosporine and tacrolimus, prolonged and severe hypokalemic nephropathy, diphtheria toxin.33

3.4. HK in Traditional Persian Medicine

TPM scholars believed that any organ of the body has a typical temperament. In an ideal healthy state, the individual function is very good and dystemperament occurs when the whole body or an organ's temperament changes. In other words, it grows up in the imbalance of the quality or quantity of humors including phlegm, bile, blood and black bile.13 The kidney dystemperament occurs when the kidney temperament is changed and its function is disturbed. This kidney dystemperament can lead to “Hozal-e-Kolye” (HK). HK in TPM occurs when the kidney becomes thin (its fat gets low or eliminates), hot or cold.13, 14 In high kidney temperature, the kidney fat is lost because of the warmness and in low kidney temperature, the kidney equalizer is disturbed. TPM scholars believed that HK occurred by several reasons such as dystemperament of the kidney, evacuation (in TPM, evacuation means excretion of many fluids from the body, such as excessive hemorrhage, diarrhea, severe vomiting, expelling excess semen and excess usage of purgative or diuretic drugs resulting severe dehydration). Symptoms of HK include white urine, polyuria, weight loss, permanent low back pain and low libido.11, 12, 13, 14 (Table 1). Some TPM scholars believed that eye weakness and headache are caused due to the kidney fat loss in HK process. It was written in the other book that one of the symptoms of HK is mild pain in the back of head.34, 35

3.5. Food strategies in CKD in conventional medicine

Nutrition has a main role in the treatment of CKD. Nowadays in America, diet and lifestyle behaviors are important. There are food strategies recommending in CKD such as:

  • Intake of protein and energy (Considering the risk of malnutrition in CKD) is recommended. However, protein-restricted diets are used to decrease uremic symptoms.36

  • A calorie of at least 30–35 kcal/kg is recommended.

  • Adequate Intake of vitamin supplements (vitamin C, Thiamin, Riboflavin, Niacin, Folate, Pyridoxine, Cobalamin, Biotin, and Pantothenic acid) is recommended.

  • Use of vitamin D to prevent bone loss is needed.36

  • Low phosphorus intake (ideally 700 mg/day) especially in ESRD is needed. However, adequate protein intake must be maintained.37

  • Low fat diets including nonhydrogenated and unsaturated fats are recommended to prevent and treat the progression of cardio vascular disease (CVD) in these patients. Intake of whole grains, fruits, vegetables, and omega-3 fatty acids to correct dyslipidemias.36

  • Control of hypertension with DASH plans (Dietary Approaches to Stop Hypertension) including lower in fat and sodium and high in potassium, magnesium, calcium, fiber and antioxidant is necessary.36

  • Considering the risk of diabetes, diabetic regimen is needed.36

  • Allergen foods such as gluten, nuts, dairy foods, citrus foods such as oranges and grapefruit, cantaloupe, honeydew, berries, chocolate, shellfish, eggs, and sulfites should be restricted.36

3.6. Food strategies in HK in Traditional Persian Medicine

The principle of treatment of any disease is the elimination of its main causes and modifying the lifestyle.13 The management of HK is based on the etiologies too. Avicenna and the other TPM scholars prescribed fattening foods for patients with HK (Table 2):

Table 2.

Fattening foods and herbal or animal-derived compounds in tubular atrophy based on TPM resources.

Common name Local name11, 13, 14 Scientific name38 Family38 Fattening cause in conventional medicine Reference
Herbal-derived compounds Safflower Ghortom Carthamustinctorius Asteraceae The source of fat 39
Fig Tin Ficus carica Moraceae Excellent source of mineral, vitamin & carbohydrates 40
Raisin Zabib Vitis vinifera Vitaceae A rich source of carbohydrate 41
Banana Mauz Musa spp Musaceae High carbohydrate & energy 42
Manna of Alhagi with milk Taranjabin High caloriea 43
Chickpea Hemmas Cicer arietinum Fabaceae A good source of carbohydrate & protein 44
Kidney bean Loubia Phaseolus vulgaris Fabaceae High carbohydrate & protein 45
Rice flour Ard-e-brenj Oryza sativa Poaceae High carbohydrate 45
Flixweed Bazr al Katan Descurainia sophia Brassicaceae Stomach strengthening, appetizer 46
Sesame oil Dohn al Samsem Sesamumin dicum Pedaliaceae High fat 45
Coconut Nargil Cocos nucifera Arecaceae High calorie 47
Almond Louz Prunus dulcis L Rosaceae High calorie 48
Animal-derived compounds Camel milk Laban al Baghar Rich in protein 49
Sheep's milk Laban al Ghanam High protein 50
Poultry meat Lahm al Bot High protein 45
Lamb meat Lahm al Hamalan Bos Taurus – Ovis aries High protein 45
Honey Asal Honey The carbohydrate-rich meal 51
Egg Bayz Gallus domesticus High quality protein, vitamin B, minerals 49
a

Dava al taranjabin is a compound of manna of alhagi (high calorie) with milk (high protein).

3.6.1. Herbal-derived compounds

Herbal drugs mentioned in TPM literature include Ficus carica, Dava-Al-Taranjabin (milk + Manna of Alhagi), safflower, raisin, banana, chickpea, kidney bean, rice flour, flixweed, sesame oil, coconut and almond.11, 12, 14

3.6.2. Animal-derived compounds

Animal-derived compounds prescribed in TPM to fatten the thin kidney include poultry meat, lamb meat, camel milk, sheep's milk and the other food materials like honey, egg.11, 12, 14

3.7. Foodstuffs forbidden in CKD in conventional medicine

Eating of some foodstuffs are forbidden in CKD such as: Alfalfa, Aloe, Aristolochic acid, Artemisia absinthium (wormwood plant), Autumn crocus, Bayberry, Blue cohosh, Broom, Buckthorn, Capsicum, Cascara, Chaparral, and Chuifongtuokuwan (Black Pearl), Coltsfoot, Comfrey, Dandelion, Ephedra (Ma Huang), Ginger, Gingko, Ginseng, Horse chestnut, Horsetail, Licorice, Lobelia, Mandrake, Mate, Nettle, Noni juice, Panax, Pennyroyal, Periwinkle, Pokeroot, Rhubarb, Sassafras, Senna, St. John's wort, Tung shueh, Vandeliacordifolia, Vervain, Yohimbe.52

4. Discussion

According to this study, HK is the same tubular atrophy in the early stages of CKD. There is oliguria in CKD; however, there is polyuria in the early stage of CKD.16, 17 Tubular atrophy is a hallmark of CKD3 and polyuria is one of its symptoms,32 so HK is the same tubular atrophy at the beginning of CKD.

The management of tubular atrophy is based on the causes in both CM and TPM. In both of these medicines, the diet is important.53 In CM, restriction of protein in the diet is discussed. Some researchers believed that restriction in the intake of protein and energy is not necessary to prevent of the risk of malnutrition.54 In a clinical trial, restricted protein diet was more effective.55 Some scientists believed that restriction of protein is needed to decrease of uremic symptoms.56 Although some scientists have proven that a restricted protein diet supplemented with keto analogues (a diet of essential amino acids such as phenylalanine and Valine) can delay the progression of CKD without malnutrition.57 In TPM, correction of the kidney dystemperament by some foodstuffs prescribed in addition to fattening foodstuffs, including some nuts and seeds, meats, and natural drugs is done.13 In CM some chemical drugs prescribe instead of that, in addition to recovering of the complications and comorbidities. Nutrition therapy in CM is recommended for prevention of malnutrition and decreasing the progression of CKD. In CM, some foodstuffs should be avoided as mentioned in the results. Albeit neither of them is mentioned in TPM as a prescribed food strategy.36

In CM, low phosphorus intake is recommended. Of course phosphorus is not typically restricted until hyperphosphatemia is present.58

Low sodium intake to control of hypertension and low phosphorus intake for prevention of progressive CKD are recommended in CM.36 At TPM scientist's time, there were not laboratory tests to control of these cases. Then, they detected diseases by clinical symptoms and observing touching the skin surface of involved organ to find organ's temperament.

It needs to be cared about using of egg yolk and almond. They are not forbidden in tubular atrophy due to low phosphorus and high protein (an adequate phosphorus-to-protein ratio: 24.7 in egg yolk and 22.3 in almond).37 But increasing in their usage can cause a problem. Also using of some allergen foods as mentioned in this paper should be cared and it needs to be sure that the consumer has not allergy to these foodstuffs.

5. Conclusion

It seems using of foodstuffs affecting tubular atrophy based on TPM literatures can have a role as a supplemental method in company with CM management. However, more studies about these foods and their effects on these cases are needed.

Conflict of interest

The authors declare that there are no conflicts of interest.

Acknowledgments

We would like to thank Dr Salari for her guidance.

Footnotes

Peer review under responsibility of The Center for Food and Biomolecules, National Taiwan University.

Contributor Information

Marjan Mahjour, Email: Mahjourmm2@mums.ac.ir.

Arash Khoushabi, Email: Khooshabia1@gmail.com.

Maryam Miri Ghale Novi, Email: mirighm@mums.ac.ir.

Zohre Feyzabadi, Email: Feyzabadiz@mums.ac.ir.

References

  • 1.Hanif M., Javed H., Jallani U., Ranjha N.M. Prevalence of end stage renal disease in diabetic obese and hypertensive patients and cardiovascular risk in dialysis patients. Pak J Pharm Res. 2016;2:42–48. [Google Scholar]
  • 2.Moreno J.A., Ramos A.M., Ortiz A. 22 apoptosis in the kidney. Apoptosis Physiol Pathol. 2011:240. [Google Scholar]
  • 3.Schelling J.R. Tubular atrophy in the pathogenesis of chronic kidney disease progression. Pediatr Nephrol. 2016;31:693–706. doi: 10.1007/s00467-015-3169-4. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 4.McCarthy J.T. Mayo Clinic Proceedings. 1999. A practical approach to the management of patients with chronic renal failure; pp. 269–273. [DOI] [PubMed] [Google Scholar]
  • 5.Jha V., Garcia-Garcia G., Iseki K. Chronic kidney disease: global dimension and perspectives. Lancet. 2013;382:260–272. doi: 10.1016/S0140-6736(13)60687-X. [DOI] [PubMed] [Google Scholar]
  • 6.Choi P., Stevenson J. Nutrition and kidney disease. In: Harber M., editor. Practical Nephrology. Springer London; London: 2014. pp. 621–628. [Google Scholar]
  • 7.Clarke T.C., Black L.I., Stussman B.J., Barnes P.M., Nahin R.L. Trends in the use of complementary health approaches among adults: United States, 2002–2012. Natl Health Stat Rep. 2015:1. [PMC free article] [PubMed] [Google Scholar]
  • 8.Wijesinghe W., Pilapitiya S., Hettiarchchi P., Wijerathne B., Siribaddana S. Regulation of herbal medicine use based on speculation? A case from Sri Lanka. J Tradit Complement Med. 2017;7(2):269–271. doi: 10.1016/j.jtcme.2016.06.009. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 9.Tsai W.-H., Yang C.-C., Li P.-C., Chen W.-C., Chien C.-T. Therapeutic potential of traditional chinese medicine on inflammatory diseases. J Tradit Complement Med. 2013;3:142. doi: 10.4103/2225-4110.114898. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 10.Feyzabadi Z., Jafari F., Feizabadi P.S., Ashayeri H., Esfahani M.M., Aval S.B. Insomnia in Iranian traditional medicine. Iran Red Crescent Med J. 2014;16:e15981. doi: 10.5812/ircmj.15981. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 11.Aghili Alavi Khorasani M.H. Sabz Arang and Tehran University of Medical Sciences; Tehran: 2011. Makhzan-al-Adwiah. [Google Scholar]
  • 12.Hakim Mommen M. Noor vahy; Qom: 2010. Tuhfat-al Momenin. [Google Scholar]
  • 13.Ibn Sina H. Dar Ehya al-tarath al-arabi; Beirut: 2005. Canon of Medicine. [Google Scholar]
  • 14.Nazem Jahan M.A. Iran University of Medicine; Tehran: 2008. Exire Azam. [Google Scholar]
  • 15.Levey A.S., Coresh J. Chronic kidney disease. Lancet. 2012;379:165–180. doi: 10.1016/S0140-6736(11)60178-5. [DOI] [PubMed] [Google Scholar]
  • 16.Sudarshan Ballal H., Augostine R., Vishvanath S. Manual of Nephrology. Jaypee Brothers, Medical Publishers Pvt. Limited; 2016. Chronic kidney disease; pp. 128–147. [Google Scholar]
  • 17.Fukuda M., Motokawa M., Miyagi S. Polynocturia in chronic kidney disease is related to natriuresis rather than to water diuresis. Nephrol Dial Transplant. 2006;21:2172–2177. doi: 10.1093/ndt/gfl165. [DOI] [PubMed] [Google Scholar]
  • 18.Barratt J., Topham P., Harris K.P.G. Nephrology Oxford University Press; 2008. Oxford Desk Reference. [Google Scholar]
  • 19.Amanzadeh J., Reilly R.F. Hypophosphatemia: an evidence-based approach to its clinical consequences and management. Nat Clin Pract Nephrol. 2006;2:136–148. doi: 10.1038/ncpneph0124. [DOI] [PubMed] [Google Scholar]
  • 20.Aycock R.D., Kass D.A. Urine: abnormal color. South Med J. 2012;105:43–47. doi: 10.1097/SMJ.0b013e31823c413e. [DOI] [PubMed] [Google Scholar]
  • 21.Davran R., Helvaci M.R., Davarci M. Left renal atrophy. Int J Clin Exp Med. 2014;7:1603. [PMC free article] [PubMed] [Google Scholar]
  • 22.Textor S.C., Wilcox C.S. Renal artery stenosis: a common, treatable cause of renal failure? Annu Rev Med. 2001;52:421–442. doi: 10.1146/annurev.med.52.1.421. [DOI] [PubMed] [Google Scholar]
  • 23.Herring J.C., Enquist E.G., Chernoff A., Linehan W.M., Choyke P.L., Walther M.M. Parenchymal sparing surgery in patients with hereditary renal cell carcinoma: 10-year experience. J Urol. 2001;165:777–781. [PubMed] [Google Scholar]
  • 24.Loffroy R., Guiu B., Watfa J., Michel F., Cercueil J., Krausé D. Xanthogranulomatous pyelonephritis in adults: clinical and radiological findings in diffuse and focal forms. Clin Radiol. 2007;62:884–890. doi: 10.1016/j.crad.2007.04.008. [DOI] [PubMed] [Google Scholar]
  • 25.Clark D., Georgitis J., Ray F. Renal arterial injuries caused by blunt trauma. Surgery. 1981;90:87–96. [PubMed] [Google Scholar]
  • 26.McAfee J.G. Radionuclide Imaging in the assessment of primary chronic pyelonephritis 1. Radiology. 1979;133:203–206. doi: 10.1148/133.1.203. [DOI] [PubMed] [Google Scholar]
  • 27.Emmett J.L., Alverez-Ierena J.J., McDonald J.R. Atrophic pyelonephritis versus congenital renal hypoplasia. J Am Med Assoc. 1952;148:1470–1477. doi: 10.1001/jama.1952.02930170010003. [DOI] [PubMed] [Google Scholar]
  • 28.Brull L., Dumont-Ruyters L., Firket J. Rickets and renal infantilism. Rev Belge Sci Medicales. 1941;13:129–150. [Google Scholar]
  • 29.Caps M.T., Zierler R.E., Polissar N.L. Risk of atrophy in kidneys with atherosclerotic renal artery stenosis. Kidney Int. 1998;53:735–742. doi: 10.1046/j.1523-1755.1998.00805.x. [DOI] [PubMed] [Google Scholar]
  • 30.Adachi T., Sugiyama N., Yagita H., Yokoyama T. Renal atrophy after ischemia–reperfusion injury depends on massive tubular apoptosis induced by TNFα in the later phase. Med Mol Morphol. 2014;47:213–223. doi: 10.1007/s00795-013-0067-3. [DOI] [PubMed] [Google Scholar]
  • 31.Chen Y.-p. Experiences on the integrative medical diagnosis and treatment of acute kidney injury. Chin J Integr Med. 2010;16:207–212. doi: 10.1007/s11655-010-0207-z. [DOI] [PubMed] [Google Scholar]
  • 32.Goodyer P. Manual of Pediatric Nephrology. Springer; 2014. Tubular disorders; pp. 231–248. [Google Scholar]
  • 33.Kasper D.L., Fauci A.S., Hauser S.L., Longo D.L., Jameson J.L., Loscalzo J. 19th ed. McGraw-Hill Companies; United States: 2015. Harrison's Principles of Internal Medicine. [Google Scholar]
  • 34.Jorjani E.I.H. Ehyaye Tebe Tabiee; Ghom: 2012. Zakhireye Khwarazmshahi. [Google Scholar]
  • 35.Shah Arzani Mir Mohammad A.M. Ehyaye Tebe Tabiee; Qom: 2009. Teb-e-Akbari; p. 1182. [Google Scholar]
  • 36.Harvey K.S. Nutrition in Kidney Disease. Springer; 2008. Nutrition and pharmacologic approaches; pp. 191–226. [Google Scholar]
  • 37.Kalantar-Zadeh K. Patient education for phosphorus management in chronic kidney disease. Patient Prefer Adherence. 2013;7:379–390. doi: 10.2147/PPA.S43486. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 38.Ghahraman A.O.A. Tehran University Publisher; Tehran: 2004. Matching the Old Medicinal Plant Name with Scientific Terminology. [Google Scholar]
  • 39.Neuringer M., Connor W.E., Van Petten C., Barstad L. Dietary omega-3 fatty acid deficiency and visual loss in infant rhesus monkeys. J Clin Investig. 1984;73:272. doi: 10.1172/JCI111202. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 40.Mawa S., Husain K., Jantan I. Ficus carica L. (Moraceae): phytochemistry, traditional uses and biological activities. Evid Based Complement Altern Med. 2013;2013 doi: 10.1155/2013/974256. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 41.Ghrairi F., Lahouar L., Brahmi F., Ferchichi A., Achour L., Said S. Physicochemical composition of different varieties of raisins (Vitis vinifera L.) from Tunisia. Ind Crops Prod. 2013;43:73–77. [Google Scholar]
  • 42.Kumar K.S., Bhowmik D. Traditional and medicinal uses of banana. J Pharmacogn Phytochem. 2012;1 [Google Scholar]
  • 43.Thomson I., Asadi karam G.R., Salem Z. Biochemical Compounds and Nutritional Roles of the Foods Explained in the Qur'an. Pak J Nutr. 2009;8:13–19. [Google Scholar]
  • 44.Jukanti A.K., Gaur P.M., Gowda C., Chibbar R.N. Nutritional quality and health benefits of chickpea (Cicer arietinum L.): a review. Br J Nutr. 2012;108:S11–S26. doi: 10.1017/S0007114512000797. [DOI] [PubMed] [Google Scholar]
  • 45.McDougall J. McDougall Newsletter. November 2009. Nuts come in hard shells—for reasons. [Google Scholar]
  • 46.Aghaabasi K., Baghizadeh A. Investigation of genetic diversity in flixweed (Descurainia sophia) germplasm from Kerman province using inter-simple sequence repeat (ISSR) and random amplified polymorphic DNA (RAPD) molecular markers. Afr J Biotechnol. 2015;11:10056–10062. [Google Scholar]
  • 47.Kritchevsky D., Weber M.M., Klurfeld D.M. Dietary fat versus caloric content in initiation and promotion of 7, 12-dimethylbenz (a) anthracene-induced mammary tumorigenesis in rats. Cancer Res. 1984;44:3174–3177. [PubMed] [Google Scholar]
  • 48.Brufau G., Boatella J., Rafecas M. Nuts: source of energy and macronutrients. Br J Nutr. 2006;96:S24–S28. doi: 10.1017/bjn20061860. [DOI] [PubMed] [Google Scholar]
  • 49.McCord B.A. Crystal Clarity Publishers; 2002. Vegetarian Cooking for Starters. [Google Scholar]
  • 50.Bencini R., Pulina G. The quality of sheep milk: a review. Anim Prod Sci. 1997;37:485–504. [Google Scholar]
  • 51.Raben A., Agerholm-Larsen L., Flint A., Holst J.J., Astrup A. Meals with similar energy densities but rich in protein, fat, carbohydrate, or alcohol have different effects on energy expenditure and substrate metabolism but not on appetite and energy intake. Am J Clin Nutr. 2003;77:91–100. doi: 10.1093/ajcn/77.1.91. [DOI] [PubMed] [Google Scholar]
  • 52.Reilly Lukela J., Van Harrison R., Jimbo M., Mahallati A., Saran R., Sy A.Z. Guidelines for Clinical Care Ambulatory. 2014. Management of chronic kidney disease; pp. 1–27. University of Michigan: Clinical alignment & performance excellence. Taubman Medical Library. [Google Scholar]
  • 53.Harvey K.B., Blumenkrantz M.J., Levine S.E., Blackburn G.L. Nutritional assessment and treatment of chronic renal failure. Am J Clin Nutr. 1980;33:1586–1597. doi: 10.1093/ajcn/33.7.1586. [DOI] [PubMed] [Google Scholar]
  • 54.Yuvaraj A., Vijayan M., Alex M., Abraham G., Nair S. Effect of high-protein supplemental therapy on subjective global assessment of CKD-5D patients. Hemodial Int. 2016;20:56–62. doi: 10.1111/hdi.12330. [DOI] [PubMed] [Google Scholar]
  • 55.Ihle B.U., Becker G.J., Whitworth J.A., Charlwood R.A., Kincaid-Smith P.S. The effect of protein restriction on the progression of renal insufficiency. N Engl J Med. 1989;321:1773–1777. doi: 10.1056/NEJM198912283212601. [DOI] [PubMed] [Google Scholar]
  • 56.Kovesdy C.P., Kalantar-Zadeh K. Back to the future: restricted protein intake for conservative management of CKD, triple goals of renoprotection, uremia mitigation, and nutritional health. Int Urol Nephrol. 2016;48:725–729. doi: 10.1007/s11255-016-1224-0. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 57.Jiang Z., Zhang X., Yang L., Li Z., Qin W. Effect of restricted protein diet supplemented with Keto analogues in chronic kidney disease: a systematic review and meta-analysis. Int Urol Nephrol. 2016;48:409–418. doi: 10.1007/s11255-015-1170-2. [DOI] [PubMed] [Google Scholar]
  • 58.Beto J.A., Schury K.A., Bansal V.K. Strategies to promote adherence to nutritional advice in patients with chronic kidney disease: a narrative review and commentary. Int J Nephrol Renovascular Dis. 2016;9:21. doi: 10.2147/IJNRD.S76831. [DOI] [PMC free article] [PubMed] [Google Scholar]

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