DIETARY RECOMMENDATIONS FOR GN

DYAD THREE (3)
Byron Webb A. Romero
Von Deneb H. Vitto
Raymond C. Ursal

According to Martin, Armstrong, and Rodriguez, 2005) diet recommendation for patients with glomerulonephritis is basically the same as those with other kidney problems. They recommend patients to be on a low protein diet as protein would increase glomerular pressure and hyperfiltration. The increase in glomerular pressure may lead to renal injury and cause other chronic kidney diseases. A diet of only 0.6-0.8g/kg/day of protein may be beneficial for the patient of there is protenuria of 3g/day and serum creatinine of more than 1.5mg/dL per day according to Glassok (1999). A low protein diet for GN patients was noted as significantly reducing the risk of renal failure (Goldfarb and Heinrich, 1998). If the patient is already manifesting signs of edema, fluids may be restricted and sodium intake may also be kept to a minimum (Papanagnou, 2008). Restriction of sodium is done especially during the oliguric phase of acute GN. A study by Clanclaruso, et.al in 1996 noted that normal sodium balance is achieved during the 4th or 5th day of low salt diet therapy for those who have renal diseases such as chronic GN.
This study only accounted for 21 patients and randomization was not done, although it is textbook knowledge that sodium may be restricted in patients with renal problems, this study may not be very significant in terms of reliability.

References:
Cianciaruso, B., Bellizzi V., Minutolo R., Colucci G., Bisesti V., Russo D., Conte, G. and Nicola, L., (1996).Renal adaptation to dietary sodium restriction in moderate renal failure resulting from chronic glomerular disease, Journal of the American Society of Nephrology. 7:306-313.

Goldfarb S.,and Henrich, W., (1998). Update in Nephrology, Annals of Internal Medicine, January, 1998.

Glassock, R., (1999). The treatment of IgA nephropathy: status at the end of the millennium. Journal pf Nephrology 1999. 12:288-296, 1999

Martin, W., Armstrong, L., and Rodriguez, N., (2005). Dietary protein intake and renal function. Nutrient Metabolism (London). Sept. 2005; 2: 25.

Papanagnou, D. (2008). Acute Glomerulonephritis. Retrieved on June 18, 2009, from
http://emedicine.medscape.com/article/777272-overview

Dyad 6 guomanman and chenya

Diet and Kidney Health

Diet Therapy

In his milestone treatise in 1946, Thomas Addis argued from personal clinical experience that reduction in renal "work" by judicious dietary protein restriction was effective in minimizing further loss of kidney function in patients with chronic kidney insufficiency from a variety of causes.2,3 Thus, for the past sixty years doctors and patients should have known that the primary focus of attention for the preservation of the kidneys should be diet. The kidneys filter and eliminate most of the nutrients that we do not use, as well as many nonnutrients. (The liver, skin and lungs are also organs that eliminate waste.) Dietary excesses, protein being the primary one, can easily become a burden. (You can actually observe the effects of eating excess protein with the formation of frothy bubbles in the toilet bowl after urinating following a single high protein meal. You (or at least some people) can also smell asparagine, an amino acid, found in high concentration in the protein of the vegetable asparagus when you urinate.) The human body needs no more than 5% of the calories consumed to be from protein in order to build all cell structures, enzymes and hormones; once these needs are met then the excess must be excreted from the body. The typical Western diet, focused as it is on meat, poultry, eggs, and dairy products, is loaded with protein; as a result, many people consume a diet with 30% or more of the calories from protein. In the process of eliminating the protein excesses, the blood flow and filtration rates of the kidney tissues (nephrons) increase, which in turn, causes a condition known as “intra-glomerular hypertension.”
4 Sustained hypertension in the glomeruli leads to progressive damage. This damage is most important and apparent when people have pre-existing kidney loss from conditions such as donation of a kidney, physical injury, diabetes, atherosclerosis, hypertension, and polycystic kidneys. The excess protein accelerates the loss of kidney tissue to the point of end stage kidney disease all too soon in these people. Even under “normal” conditions, the burden of excess protein from the typical Western diet “overworks” the kidneys, causing the loss of kidney tissue.4 In an otherwise healthy person, 25-50% of his functional kidney capacity will be destroyed after seven to eight decades of eating typical foods.4
-6 Even so, we have so much reserve tissue that with only 30% of kidney function remaining all of the wastes are still removed; and the damaged and failing kidneys go unnoticed.

Two common forms of kidney disease deserve a little more attention. Approximately 40% of people with diabetes severe enough to require insulin will eventually develop kidney damage.25 In patients with diabetic
kidney disease there is a 40-fold difference in the rate of progression of disease.1 The important and controllable difference is due to the patient’s diet. Once kidney disease begins there is a relentless decline in kidney function and a decline in overall health. The median survival time once kidney disease is established (as seen by the presence of persistent proteinuria) is only 5 to 10 years.25 These grim statistics can all be changed with a healthy diet and lifestyle.1,25-28 Chronic glomerulonephritis, also called nephritis, is a disease of the kidneys in which the glomeruli, the tiny filters in the kidneys, become inflamed or damaged. This chronic inflammation will slowly destroy the kidneys unless the cause is removed. An allergic-type of reaction to animal proteins is the most common correctable cause of nephritis. Many children and adults with glomerulonephritis have been cured by changing to a diet of low-allergy vegetable foods.

reference

1) Maroni BJ, Mitch WE. Role of nutrition in prevention of the progression of renal disease. Annu Rev Nutr. 1997;17:435-55.
2) Remuzzi G, Benigni A, Remuzzi A. Mechanisms of progression and regression of renal lesions of chronic nephropathies and diabetes. J Clin Invest. 2006 Feb;116(2):288-96.
3) Addis T. Glomerular nephritis: diagnosis and treatment. New York: Macmillan, 1948.
4) Brenner B. Dietary protein intake and the progressive nature of kidney disease: The role of hemodynamically mediated glomerular injury in the pathogenesis of progressive glomerular sclerosis in aging, renal ablation and intrinsic renal disease. N Engl J Med 307:652, 1982.
5) Kennedy G. Effects of old age and over-nutrition on the kidney. Br Med Bull 13:67, 1957.

A person with acute glomerulonephritis may need to avoid some foods and limit the amount of others. Waste products that failing kidneys cannot handle include protein, sodium, potassium, and phosphorus.
Calories：They are an essential part of any diet. The number of calories you eat affects your ability to gain and lose weight. An inadequate number of calories will burn protein derived not only from the protein that you eat, but also from the body's own muscle stores. A healthy diet must give your body both the required amount of protein for tissue growth and repair, as well as enough calories for your energy needs. Excess calories and protein will put an unnecessary strain on a diseased kidney.
Fluids：Fluid overload can contribute to shortness of breath, hypertension, and swelling of the hands, legs, and feet. This condition can lead to congestive heart failure and excess build up of fluid in the lungs.
Sodium： Excessive amounts of salt in the diet result in the retention of too much water. This may cause a sudden increase in weight, swelling of the tissues and joints, high blood pressure, shortness of breath, and congestive heart failure. High sodium foods include processed and smoked meats, foods with salt toppings such as chips or nuts, sauces, and prepared and canned foods. Many kidney disease patients must limit their sodium intake to 2 grams per day or less.

Potassium：The mineral potassium plays a key role in the normal functioning of the muscles and nerves as well as in regulating the pumping action of the heart. Muscle weakness and cardiac arrhythmias may be the result of high levels of potassium in the blood. Since the heart is a muscle, a buildup of potassium may lead to sudden death (cardiac arrest). Potassium is found in almost all foods and in salt substitutes. Your potassium level should be monitored closely. A dangerously high blood potassium level in a patient with end-stage kidney disease is a criterion for emergent kidney dialysis.

Protein： When kidney function is impaired, the end product of protein metabolism, urea, accumulates in the bloodstream. The best kind of protein to eat is the kind that is used most efficiently by the body. Doing this leaves the least amount of protein waste behind. These proteins are referred to as complete or high quality proteins that contain all the essential amino acids. High quality proteins include eggs, meat, fish, fowl, and some dairy products. Low quality proteins are found in foods such as vegetables, fruits, breads, cereals, and starches.

Calcium and Phosphorus：The balance of calcium and phosphorus in the body is crucial to the maintenance of healthy bones, muscles, and nerves. Too much phosphorus may cause the bones to become brittle and break easily. This results from the body's removal of calcium in the bones to balance the excess phosphorus. Foods high in phosphorus are usually also high in potassium (another mineral that must be restricted). Phosphorus rich foods are dairy products, meats, shellfish, bran, whole grain products, beans, nuts, and chocolate. Calcium is found in most dairy products, but will need to be supplemented (OS-CAL) in most cases.

Vitamins and Minerals：Vitamin and mineral supplements such as (OS-CAL) are frequently needed since dietary restrictions may prevent a renal patient from receiving all the needed nutrients necessary for a healthy and balanced diet. Kidney dialysis can also remove vitamins from the bloodstream. Vitamin supplements should only be prescribed by a physician in patients with kidney disease.

Reference: http://www.freemd.com/acute-glomerulonephritis/home-care-kidney-diet.htm

Response: Diet
By: D2- Gil Legarda and Joanalyn Balino

Title: Short-term effects of a very-low-protein diet supplemented with ketoacids in nondialyzed chronic kidney disease patients.
Feiten, S., Draibe, S., Watanabe, R., Duenhas, M., Baxmann, A., Nerbass, F., and Cuppari, L.

Feiten, S.P.. et al. made a prospective, randomized, controlled clinical study that aimed to assess the effects of very-low-protein diet (VLPD) supplemented with ketoacids on the nutritional and metabolic parameters. And also, to compare it with a conventional low-protein diet (LPD) in patients with advanced CKD. A total of 24 Chronic Kidney Disease (CKD) patients participated in the study. The inclusion criteria were: (1) creatinine clearance 25 ml/min/1.73 m2; (2) age should be older than 18 years old; (3) absence of catabolic illnesses, auto-immune disease, diabetes mellitus, and malignant hypertension. Patients that participated in the study were instructed to eat a low protein diet (0.6 g/kg ideal body weight/day) for a period of at least 1 month. After the period of at least 1 month, the patients were randomly assigned to either a very-low-protein diet( prescribed a 0.3 g/kg/day of vegetal origin protein) supplemented with a mixture of ketoacids and amino acids this is the VLPD+KA group. And the remaining were prescribed low protein diet consisted of 0.6 g/kg/day of protein (50% of high biological value) and called LPD group. These patients were studied for a 4-month period. For both groups, energy prescription was 126–146 kJ/kg ideal body weight/day (30–35 kcal/kg ideal body weight/d). Nutritional assessment were; (1) Dietary assessment (Energy and nutrient intake were estimated from a 3-day food diary (3 week days); (2)Anthropometric data and body composition (body weight, height, midarm circumference and triceps skinfold thickness (TSF), and the body mass index (BMI)). (3)Biochemical data; serum and urinary urea and phosphorus, serum creatinine, ionized calcium, and bicarbonate. A 24-hour urine collection was obtained to measure protein excretion and to estimate glomerular filtration rate using standard creatinine clearance corrected for the body surface area (1.73 m2).

Baseline BMI data for both group is between 18.5 and 24.9 kg/m2 and 50% of them were overweight (BMI >25 kg/m2) and there were no change in follow-up. Percentage of body fat of the female at baseline was 34.0 9.6% and for male patients was 17.6 3.1% in the VLPD+KA group. It was 40.2 4.6 and 18.4 5.3% for the LPD group. Biochemical data: VLPD+KA group has decreased Serum urea nitrogen but not significantly in the LPD group. Serum urea nitrogen decreased in 11 patients (92%) in the VLPD+KA group and in only 6 patients (50%) in the LPD group (P<0.07). All patients in the VLPD+KA had decreased Urinary phosphorus while only five (45%) in the LPD group (P=0.01). Serum calcium increased in six patients (54%) in the VLPD+KA group in contrast with only 2 patients (17%) in the LPD group (P=0.89). During the 4-month study period in the VLPD+KA group, PTH concentration did not change but it was increased significantly in the LPD group. 10 patients (83%) in the LPD group had increased PTH concentration in contrast to only 3 patients (30%) in the VLPD+KA group (P<0.03). PTH concentration decreased in seven patients (70%) in the VLPD+KA group and 2 patients (17%) in the LPD group (P<0.03). The change in PTH concentration was negatively correlated with changes of ionized calcium concentration in the LPD group (r=-0.75, P=0.02). It was positively correlated with changes in serum phosphorus (r=0.71, P=0.03). Similar correlations in VLPD+KA group were not observed.

It is safe to maintain the nutritional status of CKD patients using a VLPD+KA at least during a 4-month period like the convectional low protein diet. The VLPD+KA group’ significant reduction in phosphorus intake with a consequent decrease in urinary phosphorus may have contributed to the tendency of a reduction in serum phosphorus. Furthermore, the calcium salts of the ketoacids may have acted as intestinal phosphate binder. An advantage in calcium and phosphorus metabolism and serum urea nitrogen reduction in the VLPD+ ketoacid group over LPD group was also established. So with this study, LPD+KA might be another therapeutic alternative in the treatment of patients with chronic kidney disease.

Feiten, S., Draibe, S., Watanabe, R., Duenhas, M., Baxmann, A., Nerbass, F., and Cuppari, L. (2004). Short-term effects of a very-low-protein diet supplementedwith ketoacids in nondialyzed chronic kidney disease patients. European Journal of Clinical Nutrition 59, 129–136. Retrieved June 29, 2009 from http://www.nature.com/ejcn/journal/v59/n1/full/1602050a.html

Dyad 1 : Nancelle Dumlao / Rodel Perez

DIET NEPHROTIC SYNDROME and GLOMERULONEPHRITIS

The kidneys are susceptible to structural damages due to the various blood components being filtered on a daily basis. One cause of damage is the circulating immune complexes (CIC) which may increase when large protein food molecules are released into the blood through the digestive tract. Since the cause of the problem is the food that we take in, then this problem may also be resolved by controlling the kind of food that we eat. Through the years, there are numerous studies conducted to understand what foods may have damaging effects on the kidneys (Ferri, et al, 1993; Jackson, et al, 1992; Coppo, et al, 1991; Rostoker, et al, 1991). It has been proven that food-source of circulating immune complexes (CICs) contribute to some kidney problems. Glomerulonephritis, a serious kidney inflammation, is one disease which may sometimes be triggered by CICs which has food protein antigens. It has been suggested that recurring triad of signs and symptoms which are flank pain, blood or protein in urine are caused by “food allergy” until proven otherwise. Hence, diet which exclude antigenic material should be implemented (i.e. Alpha ENF which is a diet program offered to supplement those nutrients such as amino acids, Vit B, D, B12 and minerals such as calcium, magnesium, potassium, and zinc). . It is advisable that patients with kidney disease should eat low protein foods to decrease demands on deteriorating kidney function.
It is believed that proteins in general are high-risk food components in kidney disease and hydrolyzed proteins may have harmful effects. High protein foods that are excluded in the Alpha ENF list include gluten, the proteins in wheat, rye, barley and oats. Other high-protein foods are albumin from eggs and milk, muscle proteins from meat, globulin and casein from milk, and soy proteins. However, proteins from vegetables are better tolerated and maybe included in kidney diet. Alpha ENF provides pure amino acids which replaces protein from the regular diet.
Likewise, nephrotic syndrome, which involves increased glomerular excretion of protein should also be advised to modify diet containing low-protein foods. In a case study (Gabordi, et al), a 6 yr old girl with nephritic syndrome, celiac disease and dermatitis herpetiforms was cured when gluten grains was removed from her diet. In another case by Sandberg et al, 6 patients had remission from nephrotic syndrome when milk was removed from their diet and had exacerbation when it was reintroduced. Also, 6 out of 17 children with steroid resistant nephrotic syndrome had remission of proteinuria in 3-8 days when milk removed from their diet. Using dietetic therapy to prevent further deterioration of kidney function is further reinforced by a study done by Ferri, et al (1993) on dietary macromolecular antigens which can be associated in the pathogenesis of IgA nephropathy (IgAN). The study was about the effect of a low-antigen-content diet of 21 patients with active IgAN. It was discovered that heavy proteinuria in 12 cases was decreased or has disappeared in 11 patients after the diet therapy.

These studies just prove that what appears to be very difficult to cure complex kidney diseases may be controlled or health of the patient may be improved by just adhering to a simple diet program specifically tailored to a particular kidney disease (ex. glomerulonephritis and nephritic syndrome). These studies reinforce the fact that following a low protein diet and avoiding food-source of circulating immune complexes (CICs) may greatly control and enhance the function of the kidneys. For patients with kidney problems, it is vital that they are referred to kidney dietician in order to have a diet program that is tailored to their current health condition in order to reduce workload of their damaged kidneys.
Although most of these studies were undertaken prior to 2003, I used them since they are relevant in the management of kidney diseases which could lead to ESRD which is increasing in prevalence worldwide. They also support current studies on the advantages of low-protein diet for CKD/ESRD patients.

References:
Ferri C; Puccini R; Longombardo G; Paleologo G; Migliorini P; Moriconi L; Pasero G; Cioni L. Low-antigen-content diet in the treatment of patients with IgA nephropathy. Nephrol Dial Transplant, 1993, 8:11, 1193-8.
Jackson S; Moldoveanu Z; Kirk KA; Julian BA; Patterson TF; Mullins AL; Jilling T; Mestecky J; Galla JH. IgA-containing immune complexes after challenge with food antigens in patients with IgA nephropathy. Clin Exp Immunol, 1992 Aug, 89:2, 315-20


[b]

DYAD 4
BALAJADIA, BOND
ZANO, ALEXIS

Salt restriction in kidney disease—a missed therapeutic opportunity?

The importance of salt restriction in the treatment of patients with renal disease has remained highly controversial. In the following we marshal the current evidence that salt plays a definite role in the genesis of hypertension and target organ damage, point to practical problems of salt restriction, and report on novel pathomechanisms of how salt affects blood pressure and causes target organ damage.

Currently there is an animated discussion as to whether reduction of salt intake might have negative consequences. It goes without saying that radical salt restriction causes hypovolemia, with the attendant adverse effects, e.g. reduced resistance against circulatory shock and possibly also predisposition to acute renal failure. Extremely low salt intake also causes more long-term adverse effects, such as acceleration of atherosclerosis, as shown in a genetic model of atherosclerosis, the apoE−/−mouse: a low-salt diet stimulated the renin–angiotensin system and increased the size of atherosclerotic plaques in the aorta. It is also of interest that, in pregnant rats, an extremely low salt intake (0.03%) causes intrauterine growth restriction and adult hypertension in the offspring.
The explanation of why both too high and too low a salt intake cause adverse effects is the fact that high salt intake induces inhibitors of the Na+K+ pump (cardiotonic steroids) on the one hand, whilst low salt intake up-regulates the activity of the renin–angiotensin system, increases angiotensin II, and up-regulates NADPH oxidase, thus generating reactive oxidant species. A sound balance between these two extremes is struck by current guidelines, which recommend for adults a reduction in the usual daily sodium intake to 80–100 mmol, corresponding to an intake of 4.7–5.8 g salt.

There is strong evidence that salt intake plays an important role in the genesis of hypertension and target organ damage. Both high and low sodium intake cause adverse effects. The average salt intake of healthy children and adults exceeds, by far, the recommendations of current guidelines. The sodium content of most commercially available food items is too high, and this accounts for nearly three-quarters of salt intake. The most important aspect of strategies to reduce salt intake is an effort to make the food industry reduce nutrient salt content. Especially in renal patients, diuretics are usually needed in addition to reduction of dietary salt intake. The fascinating insights into novel pathomechanisms underlying salt-induced target organ damage, e.g. cardiotonic steroids, may ultimately yield new therapeutic interventions.

Reference: Ritz, E et. al. Salt restriction in kidney disease—a missed therapeutic opportunity?. PMC. April 2008