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-**Multiple Sclerosis (MS)** is an autoimmune disease affecting the central nervous system. The disease specifically affects the myelin and as a result inflammation occurs and the myelin is damaged. Myelin performs the crucial role of nerve impulse through nerve fibers. If myelin is damaged then there will be a decrease in the transmission of nerve impulses. When the damage is significant then scar tissue will replace the myelin. The symptoms of MS vary for each individual, some include fatigue, pain, bladder problems, walking problems, cognitive difficulties and optic neuritis. Canada currently has the highest rate of MS with approximately 100,000 Canadians currently diagnosed (Multiple Sclerosis Society of Canada, 2016).
+The Acceptable Macronutrient Distribution Ranges (AMDR) are the proportion of one’s caloric intake which should come from each macronutrient. It is recommended that 10-35% of daily energy intake should be provided by protein (Whitney, Rolfes, Hammond and Piche, 2013). In a typical Western diet, more than twice the recommended levels of protein are often consumed, and some research supports that this may be associated with the increased prevalence of chronic kidney disease in Western society (Hariharan, Vellanki and Kramer, 2015). Conversely, high protein diets are increasingly recommended for weight loss and weight management programs, and there is much controversy regarding the safety of such long-term diets. An article written by Kamal Patel, and featured on examine.com (2014), attempts to demystify the claim that high protein diets lead to increased glomerular filtration rate (GFR) which is a measure of the amount of blood that filters through the glomeruli every minute (mL/min). There is speculation that an increase in GFR leads to stress on the kidneys, resulting in kidney damage.
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-**Figure 1**: Renal function, MCP-1, and plasma homocysteine in pigs that consumed NP or HP diet for 4 or 8 months
+**Figure 1**: Renal function, MCP-1, and plasma homocysteine in pigs that consumed NP or HP diet for 4 or 8 months (Source: Jia et al, 2010)
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-**Jia and colleagues (2010)** tested the effects of a high protein diet on adult pigs. Pigs have very similar renal anatomy and physiology to that of humans, and thus are an appropriate test animal to use (Jia et al., 2010). Adult pigs were fed a diet consisting of either 15% of total calories from protein or 35% of total calories from protein for eight months. Protein came from a mixture of both plant and animal sources to closely resemble an average human diet. Between both the high and normal protein diets, lipid, fibre and micronutrient compositions were made equal to eliminate the presence of any confounding variables from diet. (Jia et al., 2010) After eight months, adult pigs fed the high protein diet had significantly higher kidney and glomerular volumes, however there was no significant difference in body mass between the high protein and normal protein groups. Additionally, after eight months, pigs fed the high protein diet exhibited more histological renal damage with 55% more fibrosis, and 30% more glomerulosclerosis in the kidney. There were also higher plasma homocysteine levels at 4 and 8 months. However, overall renal function as determined by inulin clearance, creatine clearance, or proteinuria was not affected by a high protein diet, as any increase in values at 4 months did not persist in the long term and differences overall were not statistically significant (Figure 1). Due to the similarity between pig and human renal physiology, this study presents evidence that suggests high protein diets may potentially be harmful to human renal function. (Jia et al., 2010)
+**Jia and colleagues (2010)** tested the effects of a high protein diet on adult pigs. Pigs have very similar renal anatomy and physiology to that of humans, and thus are an appropriate test animal to use (Jia et al., 2010). Adult pigs were fed a diet consisting of either 15% of total calories from protein or 35% of total calories from protein for eight months. Protein came from a mixture of both plant and animal sources to closely resemble an average human diet. Between both the high and normal protein diets, lipid, fibre and micronutrient compositions were made equal to eliminate the presence of any confounding variables from diet. (Jia et al., 2010) After eight months, adult pigs fed the high protein diet had significantly higher kidney and glomerular volumes, however there was no significant difference in body mass between the high protein and normal protein groups. Additionally, after eight months, pigs fed the high protein diet exhibited more histological renal damage with 55% more fibrosis, and 30% more glomerulosclerosis in the kidney. There were also higher plasma homocysteine levels at 4 and 8 months. However, overall renal function as determined by inulin clearance, creatinine clearance, or proteinuria was not affected by a high protein diet, as any increase in values at 4 months did not persist in the long term and differences overall were not statistically significant (Figure 1). Due to the similarity between pig and human renal physiology, this study presents evidence that suggests high protein diets may potentially be harmful to human renal function. (Jia et al., 2010)
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 for 4 months; Glomeruli from rats given c) NP or d) HP diet for 17 months
+(Source: Wakefield et al., 2011)
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 ====== High protein diet and obesity  ======
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-Zhaoping et al. (2010) conducted a research experiment which investigated the adverse effects of a high protein diet on kidney function during weight loss. The experiment integrated 100 obese men and women who were monitored for the duration of one year. During the experiment, high protein consumption was clearly defined at 2.2g/kg versus standard protein ingestion, which was at 1.1g/kg. As for results, researchers had not found a direct or indirect correlation between inhibited renal function and high protein diet. Furthermore, no variation was found in creatinine clearance, which suggests an unmodified GFR rate. Thus, it is evident that this study supports the idea that a high protein diet safely reduces an obese individual’s Body Mass Index with no adverse concerns regarding kidney function.
+**Zhaoping and colleagues (2010)** They conducted a research experiment which investigated the adverse effects of a high protein diet on kidney function during weight loss. The experiment integrated 100 obese men and women who were monitored for the duration of one year. During the experiment, high protein consumption was clearly defined at 2.2g/kg versus standard protein ingestion, which was at 1.1g/kg. As for results, researchers had not found a direct or indirect correlation between inhibited renal function and high protein diet. Furthermore, no variation was found in creatinine clearance, which suggests an unmodified GFR rate. Thus, it is evident that this study supports the idea that a high protein diet safely reduces an obese individual’s Body Mass Index with no adverse concerns regarding kidney function. </style>
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-Another controlled study conducted by Friedman et al. (2012) between the duration of 2003 and 2007 observed whether low-carbohydrate high protein diets led to any harmful renal effects. People that took part in the study were healthy obese individuals who followed the high protein diet for two years, as well as, another group who followed a low fat diet. The primary focus for the researchers was the GFR measured by creatinine clearance and albuminuria. The researchers found that even though the levels of solute excretion such as calcium and sodium were slightly raised in the high protein diet subjects, it was still lower than the low fat diets. In addition, they also measured urinary calcium excretion and found that despite an increase, there was no presence of new kidney stones. Besides that, small reductions in serum creatinine at three months (4.2% relative to low fat diet), as well as serum urea at two years (8.2%) were observed, indicating kidney adaptation. Upon review of all collected data, the researchers concluded that low carbohydrate and high protein diets in healthy obese individuals does lead to weight loss without causing renal damage to the kidney.
+**Friedman and colleagues (2012)** It was a controlled study that examined whether low-carbohydrate high protein diets led to any harmful renal effects. People that took part in the study were healthy obese individuals who followed the high protein diet for two years, as well as, another group who followed a low fat diet. The primary focus for the researchers was the GFR measured by creatinine clearance and albuminuria. The researchers found that even though the levels of solute excretion such as calcium and sodium were slightly raised in the high protein diet subjects, it was still lower than the low fat diets. In addition, they also measured urinary calcium excretion and found that despite an increase, there was no presence of new kidney stones. Besides that, small reductions in serum creatinine at three months (4.2% relative to low fat diet), as well as serum urea at two years (8.2%) were observed, indicating kidney adaptation. Upon review of all collected data, the researchers concluded that low carbohydrate and high protein diets in healthy obese individuals does lead to weight loss without causing renal damage to the kidney. </style>
-====== Treatment and Management ======
+====== Does Protein source Affect Renal Function? ======
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-Currently, there is no cure for multiple sclerosis as there are still many unclear aspects to the disease. (Hedley, 2012) There are several treatments available to aid with prolonging the remission period, to manage relapse, and to manage symptoms of the disease. Different treatments are recommended for different patterns of MS. For RRMS, SPMS, disease modifying drugs (DMDs) may be prescribed, whereas with PPMS, symptomatic treatment is the main approach as there has yet to be a proven disease modifying treatment. (Hedley, 2012) There are also complementary therapies available for MS.
+There are many different types of protein sources available to humans today. Perhaps some sources of protein provide better protection for renal function than others. Aukema et al. (2010) compared the effects of soy based protein diets to those of plant based protein diets on renal protection. They used Weanling Han rats who were afflicted with kidney disease, and subjected them to hemp, pea, soy, and casein protein sources. Upon review of the experimental data they found that hemp and soy protein sources resulted in the least amount of kidney inflammation, as well as a more normal serum creatinine level, and smaller cyst sizes. This allowed them to conclude that there was a difference in kidney disease protection when it came to the source of the protein. Despite using rat test subjects instead of humans, the study still provides valuable insight into human chronic kidney disease treatment. There is a strong misconception that vegetarian diets are the healthiest type of diet, and while acquiring the necessary nutrients from a vegetarian diet is possible, it is crucial to include soy based protein for chronic kidney disease patients. Limiting one’s self to a single source of protein would be an opportunity passed to slowing renal disease progression.
+Another study done by Moe et al. (2011) looked at animal based protein and plant based protein with respect to phosphorus homeostasis in chronic kidney disease. Increases in parathyroid hormone (PTH) and fibroblast growth factor-23 (FGF23) induce phosphaturia which maintains phosphorus levels in an appropriate range. Moe et al. (2011) performed a crossover trial involving nine patients who had an average GFR at 32 ml/min to allow for a fair comparison of both diets. They found that after a week of implementing the vegetarian diets, there was a decrease in serum phosphorus and FGF23 levels. Progressive deterioration of renal function is usually indicative in an increase in FGF23 levels. This study was able to show the significant effect on phosphorus homeostasis in patients which might be due to decreased bioavailability of phytate-bound phosphorus or the higher availability of protein in meat-based diets, placing strain on the kidney. High FGF23 were more prevalent in the meat based diet, and could have possibly inhibited PTH. These studies show the importance of phosphate and protein source that the phosphate comes from, especially regarding those with chronic kidney disease. Future studies should look at the long term effects of high protein intake on phosphorus levels.
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-**Maintaining Remission**
+**High Protein Diets Do Not Affect Kidney Function**
-There are treatments available to modify the disease course by helping to maintain remission and delay relapse in MS. For RRMS, SPMS, disease modifying drugs (DMDs) may be prescribed. There are many DMDs available for MS. Interferon beta and glatiramer acetate are the current front-line therapies for maintaining remission. These make up the ABC-R therapy of MS, which consists of Avonex (interferon b-1a), Betaseron (interferon b-1b), Copaxone (glatiramer acetate), and Rebif (interferon b-1a). (Hillman, 2014)
+Through systematic review and meta-analysis, Schwingshackl and Hoffman (2014) investigated the effects of high protein versus low/normal protein diets in relation to renal function on subjects who did not have any form of CKD. Many literatures were performed using the electronic databases MEDLINE, EMBASE, and the Cochrane Trial Register until February 27th, 2014. Thirty studies which included 2160 subjects were used. High protein diets resulted in a significantly higher GFR, serum urea, and calcium excretion in comparison to low protein/normal protein diets.  A limitation that exists in the present review consist of the limited number of studies and their heterogeneity of design. The many studies included in the analyses varied in terms of type(s) of diets used, definition of high protein and low protein/normal protein diets, study population, intervention time, as well as nutritional assessment. Additionally, the sample size of 2160 subjects in the current meta-analysis establishes statistically significant mean differences. Although, the subjects experienced an increase in GFR, nobody reported clinical symptoms of kidney pathology. These changes can be associated with physiological adaptive mechanisms induced by high protein diets without any clinical relevance.
-__ Interferon Beta __
->Interferon beta is in the family of cytokines, which possess antiviral and immunoregulatory activities. The mechanisms of interferon beta in MS, however, are not clearly understood. (Hedley, 2012) There are two types of interferon beta (interferon beta-1a and interferon beta-1b) that have no difference in effectiveness. They are only different in the way they are manufactured. Interferon beta use in MS patients reduces the number and severity of relapses, and improves MRI measures. (Hillman, 2014) Studies show that MS patients using interferon beta therapy showed 75% fewer brain lesions on a brain MRI compared with a placebo. (Hedley, 2012) The effect of the treatment on long-term progression is not clear. There are some serious side effects of interferon beta. These include flu-like symptoms such as myalgia, fever, chills, asthenia, headache, and nausea, as well as psychological symptoms such as depression. Interferon beta may also lead to the development of neutralizing antibodies that may lead to a decrease in the effectiveness of therapy. (Hillman, 2014)
+Poortmans and Dellalieux (2000) investigated the relationship between high protein intake and renal function in both body-builders and athletes. The range of protein intake for the two groups was between 1.35 to 2.8 g/kg•b•wt. Through blood and urine analysis, they found no significant differences between the test groups regarding concentrations of plasma protein, creatinine and uric acid. High concentrations of these variables are indicative of protein absorption and potential renal impairment. Despite high plasma variables in both groups, there was no accumulation of urea, thus indicating that they were within the upper limit of normal. In addition, the GFR assessed by creatinine clearance suggested no sign of glomerular hyperfiltration.  This supports that the high protein diet under 2.8 g/kg•b•wt does not adversely affect kidney physiology.
-__ Glatiramer Acetate __
->Glatiramer acetate is thought to alter the immune processes believed to be responsible for the pathogenesis of MS, however its mechanism is not fully known. (Hedley, 2012) Studies have shown that there is delay of progression from CIS to “clinically definite MS” in MS patients for up to three years with use of glatiramer acetate. (Hedley, 2012) This treatment reduces the number and severity of relapses, and the formation of new lesions on a brain MRI, however its effects on long-term progression are not clear. (Hedley, 2012) Adverse effects of glatiramer acetate minor and mainly consist of injection site reactions, seen in 70% of patients. (Hedley, 2012) Other less common side effects include lipoatrophy, flushing, shortness of breath, chest tightness, and palpitations. (Hillman, 2014)
-Deciding on which treatment to use (interferon beta or glatiramer acetate) depends on patient preference in type and frequency of injection. (See Figure 7)
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-&nbsp;**Figure 7**: The dosing, frequency, and route of administration for the ACB-R therapies. (Source: Hillman & Khorassani, 2014)
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-There are several other treatments available aside from the front-line ABC-R therapies.
-__Natalizumab__
->Natalizumab is a monoclonal antibody that is currently the best treatment for preventing relapses. (Hedley, 2012) 67% of patients using Natalizumab are relapse free (compared to 41% of patients with a placebo) after two years of treatment. (Hedley, 2012) This treatment is recommended for patients with rapidly evolving severe RRMS. There are however, several side effects including infections, urticaria, and headaches to name a few. (Hedley, 2012) One side effect that could possibly escalate to something serious is an increased risk of progressive multifocal leukoencephalopathy (PML). With PML, there is a progressive inflammation of white matter in the brain. Due to the morality of up to 50% with PML, Natalizumab is not a first-line therapy. (Hedley, 2012)
-__Mitoxantrone__
->Mitoxantrone is not used as often since the development of natalizumab. It is a DNA-reactive agent of which the mechanism of action is not yet known, but is approved in the US to treat SPMS and RRMS. (Hedley, 2012) It is cytotoxic, thus has serious side effects such as life threatening reactions and cardiac toxicity. Mitoxantrone has a maximum lifetime dose and thus is not used long-term. (Hedley, 2012)
-__Azathioprine__
->Azathioprine is an immunosuppressant that is used to try to prevent relapse and to slow disease progression. It is not commonly used as side effects include gastrointestinal disturbances, bone marrow suppression, and hepatic toxicity. (Hedley, 2012)
-__Fingolimod__
->Fingolimod is a sphingosine-1-phosphate receptor modulator that retains lymphocytes in lymph nodes. This prevents lymphocytes from reaching the CNS and causing damage. (Hedley, 2012) In RRMS patients where interferon beta is unsuccessful, fingolimod is used. It is administered orally (one capsule daily). (Hedley, 2012) The development of oral agents are exciting as it is a easier method of administration than injections.
-**Maintaining Relapse**
-There are also treatments to manage relapse MS. Relapses in MS are caused by inflammation in the CNS, damaging the myelin of nerve fibers. Due to the varying lengths, severity, and nature of relapses, treatment is not always needed. (Hedley, 2012) Treatment is recommended for severe relapses when distress is experienced or when there is increased limitation of activities. Corticosteroids are the treatment of choice when there is demyelination. Methylprednisolone is a synthetic glucocorticoid that is a strong anti-inflammatory. (Hedley, 2012)  It is unclear what it does exactly with MS, but it is thought to aid by immunosuppression or to reduce the accumulation of fluid around nerve damage. Studies have shown that steroids are effective in speeding up recovery from relapse, however there are no benefits to the long-term progression of disease. (Hedley, 2012) There are short-term and long-term treatments available, however long-term treatment should be avoided due to the side effects. Side effects of long-term treatment include weight gain, acne, cataracts, osteoporosis, deterioration of the head of the thigh bone, and diabetes. The side effects of short-term treatment are minor. (Hillman, 2014)
-**Maintaining Symptoms**
-Treatment for complications that are associated with MS are also available. Common symptoms of MS are fatigue, bladder and bowel problems, weakness, spasticity, and swallowing difficulties.
-__Fatigue__
->Up to 95% of MS patients experience fatigue, and more than half describe it as one of the most troubling symptoms of MS. (Amato & Portaccio, 2012) The pathophysiology of fatigue in MS is not well understood. There are both pharmacological and non-pharmacological therapeutic approaches to MS. The most studied pharmaceuticals are amantadine, modafinil, and aminopyridines. There are several non-pharmacological interventions. One is neuro-rehabilitation, which improves compensation, adaptation and reconditioning. Another is exercise, which has very promising results such as reduced fatigue, improve in mood and quality of life. (Amato & Portaccio, 2012) Finally there is behavioural therapy, which strives to educate patients and caregivers about how to make small behavioural changes to reduce fatigue. This may include education on planning rest, relaxation techniques, adapting daily living activities, making everyday tasks more energy efficient, and controlling external temperature. (Amato & Portaccio, 2012)
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-**Figure 8**: Body weight assisted treadmill training. There is physical assistance for each
-leg due to impaired walking ability. (Source: http://agelessphysio.com)
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-__Bladder__
-> Another symptom of MS is an overactive bladder. To manage an overactive bladder, MS patients can reduce fluid intake and caffeine to reduce symptoms of urgency and frequency. However, a daily intake of 1-2 litres of water is recommended. (Fowler et al., 2009) Pharmacological interventions such as antimuscarinic medication is also available to reduce incontinence, frequency, and urgency in MS. (Fowler et al., 2009) Some physical interventions would include pelvic floor exercises to strengthen the pelvic floor and treat stress incontinence. This is effective in patients whose neural pathways to their pelvic floor muscles are intact. (Fowler et al., 2009) In MS patients with neurogenic bladder dysfunction, clean intermittent self-catheterization is used. (Fowler et al., 2009)
-__Walking Ability__
-> A common symptom of MS is impaired walking ability. Dalfampridine (Fampyra or Ampyra) can be used to improve walking ability. Dalfampridine is a potassium channel blocker that enhances conduction along demyelinated nerve fibres. (Hillman, 2014) In phase 3 clinical trials, walking speed was increased by about 25% within weeks in MS patients. (Hedley, 2012) There are, however, side effects such as a greater risk of seizures, anxiety, insomnia, dizziness, and tremor. (Hedley, 2012) In terms of physical therapy, exercise through treadmill training has been shown to improve walking endurance and velocity. (Amato & Portaccio, 2012) (See Figure 8)
-__Depression__
-> Depression can be a psychological symptom of MS or from interferon beta therapy. For MS patients with severe depression, interferon is avoided. (Hillman, 2014)
-**Complementary Therapies**
-Finally, there are therapies available that can be used alongside MS treatment that may help with the general sense of wellbeing in MS patients and help them to feel and cope better with the disease and the treatment. Some complementary therapies include reflexology, massage, tai chi, magnetic field therapy, neural therapy, and fish oils. (Hedley, 2012) Also linoleic acid, found in sunflower, corn, soya, and safflower oils, may reduce the progression of MS. (Hedley, 2012)
-**Current Research**
-The majority of research being done on MS primarily involves targeting new medications which better combat relapsing-remitting MS, as well as improving symptomatic treatments. However there is current research being done which aims to promote myelin repair, thus acting as a protective agent against MS.  A study done by de la Fuente et al. in 2015, looked at vitamin D as an agent to promote remyelination, which is the process which drives specialized cells to fix damaged myelin found in the CNS nerve fibres. This process happen naturally in a healthy individual, however those afflicted with MS experience a decrease in the function over time due to the continuous damage being done to their myelin (de la Fuente et al. 2015). Cells termed oligodendrocyte progenitor cells (OPC) are responsible for creating oligodendrocytes which manufacture the myelin sheath (de la Fuente et al. 2015). Vitamin D is important because it binds to a specific protein, retinoid X receptor-y (RXR-y), which aids in swiftly maturing OPC into oligodendrocytes. Thus increasing the rate at which the myelin repairing oligodendrocytes, this would be greatly beneficial in battling MS. The study looked at a MS like disease in rats, more specifically focusing on the vitamin D receptors. They found that the RXR-y protein interacts with the vitamin D receptor, which stays active during the remyelination stage. This led to improved remyelination. Furthermore when the vitamin D receptors were prevented from binding and functioning correctly, the OPCs did not develop properly into oligodendrocytes, therefore leading to malfunctioning remyelination in the rats. This type of study investigating the remyelination enhancement possibility from vitamin D is the trend in current research.
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 ====== Conclusion ======
-Multiple Sclerosis is an inflammatory, autoimmune disease which disrupts the neurons’ ability to trigger action potentials. As of today, the pathophysiology of this disease is not fully understood, however, considerable advances have been made in understanding the factors behind this disease. It is evident that further research needs to be conducted to figure out the precise mechanism of the demyelination and remyelination process. The findings of this research will lead to more efficient treatment mechanisms and may even lead to a cure for Multiple Sclerosis.
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+There is significant evidence presented in many scientific studies that recognizes high protein diets alter renal function in humans. However, there are inconsistencies between the results of short-term and long-term studies. Short term studies demonstrate an accompanied increase of GFR with high protein diets, whereas long-term studies lack statistical significance for a change in GFR, suggesting adapting renal physiology during chronic high protein intake. Additionally, source of protein and health status are important confounding variables that must be considered when evaluating the effects of kidney function of such diets. Despite the controversy surrounding the safety of high protein diets, there is no conclusive evidence supporting a direct causation between such diets and renal damage.
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 ====== References ======
-Amato, M. P. & Portaccio, E. (2012). Management options in multiple sclerosis-associated fatigue. Expert Opinion on Pharmacotherapy, 13(2), 207-216
+Aukema, H. M., Gauthier, J., Roy, M., Jia, Y., Li, H., & Aluko, R. E. (2011). Distinctive effects of plant protein sources on renal disease progression and associated cardiac hypertrophy in experimental kidney disease. Molecular nutrition & food research, 55(7), 1044-1051.
-Ascherio A, Munger KL (April 2007). "Environmental risk factors for multiple sclerosis. Part I: the role of infection". Annals of Neurology. 61 (4): 288–99.
-Brosnan, C. F., & Raine, C. S. (1996). Mechanisms of immune injury in multiple sclerosis. Brain Pathology, 6(3), 243-257.
-Compston A, Coles A (October 2008). "Multiple sclerosis". Lancet. 372 (9648): 1502–17
-de la Fuente AG et al. Vitamin D receptor-retinoid X receptor heterodimer signaling regulates oligodendrocyte progenitor cell differentiation. J Cell Biol. 2015; 211(5):975-85.
-Multiple Sclerosis Clinical Presentation. (2016). Retrieved September 18, 2016, from http://emedicine.medscape.com/article/1146199-clinical
-Dyment DA, Ebers GC, Sadovnick AD (February 2004). "Genetics of multiple sclerosis".Lancet Neurol. 3 (92): 104–10
-Fowler, C. J., Panicker, J. N., Drake, N., Harris, C., Harrison, S. C. W., Kirby, M., Lucas, M., Macleod, N., Mangnall, J., North, A., et al. (2009). A UK consensus on the management of the bladder in multiple sclerosis. Postgraduate Medical Journal. 85, 552-559.
-Gilden DH (March 2005). "Infectious causes of multiple sclerosis". The Lancet Neurology. 4 (3): 195–202
-Hedley, L. (2012). Multiple sclerosis treatment options. The Pharmaceutical Journal. 288, 247-250.
-Hillman, A. & Khorassani, F. (2014). Multiple sclerosis management. Pharmacy Times. Retrieved from http://www.pharmacytimes.com/publications/health-system-edition/2014/march2014/multiple-sclerosis-management
+Feiten, S. F., Draibe, S. A., Watanabe, R., Duenhas, M. R., Baxmann, A. C., Nerbass, F. B., & Cuppari, L. (2005). Short-term effects of a very-low-protein diet supplemented with ketoacids in nondialyzed chronic kidney disease patients. European journal of clinical nutrition, 59(1), 129-136.
-Löscher, W., & Potschka, H. (2005). Blood-brain barrier active efflux transporters: ATP-binding cassette gene family. NeuroRx, 2(1), 86-98.
+Frank, H., Graf, J., Amann-Gassner, U., Bratke, R., Daniel, H., Heemann, U., & Hauner, H. (2009). Effect of short-term high-protein compared with normal-protein diets on renal hemodynamics and associated variables in healthy young men. The American journal of clinical nutrition, 90(6), 1509-1516.
-Multiple Sclerosis Clinical Presentation. (2016). Retrieved September 18, 2016, from http://emedicine.medscape.com/article/1146199-clinical
+Friedman, A. N., Ogden, L. G., Foster, G. D., Klein, S., Stein, R., Miller, B., ... & Wyatt, H. R. (2012). Comparative effects of low-carbohydrate high-protein versus low-fat diets on the kidney. Clinical Journal of the American Society of Nephrology, 7(7), 1103-1111.
-Multiple Sclerosis Society of Canada. (2016). Retrieved September 18, 2016, from https://mssociety.ca/about-ms/what-is-ms
+Halbesma, N., Bakker, S. J., Jansen, D. F., Stolk, R. P., De Zeeuw, D., De Jong, P. E., & Gansevoort, R. T. (2009). High protein intake associates with cardiovascular events but not with loss of renal function. Journal of the American Society of Nephrology, 20(8), 1797-1804.
-Rolak, L. A. (2003). Multiple Sclerosis: It's Not The Disease You Thought It Was.Clinical Medicine & Research, 1(1), 57-60. doi:10.3121/cmr.1.1.57
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