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HOME        LONGEVITY LIBRARY CATALOG

Renal disease - diet; Kidney disease - diet, pre-dialysis diet, chronic renal failure diet

Definition   

A diet used in the people with abnormal kidney renal function to prevent progression of renal disease. It is usually low in protein and may be low-sodium, and low-potassium. It may also involve fluid restriction. In diabetic patients with renal disease a low carbohydrate diet may also be used.

Food sources   

This diet controls the amount of protein, sodium, and potassium. The controlled amounts of each of these nutrients are based on the person’s blood levels of potassium, sodium, and urea, as well as the fluid balance, creatinine clearance, and blood pressure. If the blood levels indicate the need to adjust the intake of calcium and phosphorus, then the amounts allowed in the diet are changed. Fluid is only restricted in patients who accumulate excessive volume.

Functions   

The purpose of a diet that restricts protein is to decrease the protein load on the kidney and slow down progression of renal disease. Sodium may be restricted to improve blood pressure control and to avoid fluid accumulation. Potassium is restricted because if it is not excreted effectively it can accumulate and result in dangerous heart rhythms.

Recommendations   

The amount of protein allowed in the diet is determined by checking the amount of protein (and protein waste byproducts) in the person’s blood. The suggested amount of protein in a low protein diet is 0.6g/kg/day. In patients who are losing large amounts of protein in their urine in diseases such as nephrotic syndrome, the kidney specialist will recommend a moderate protein restriction of 0.8g/kg/day.

Laboratory tests may include chem-20, creatinine, albumin, and blood urea nitrogen. Low-protein diets may prevent or slow the progress of some kinds of kidney disease. The amount of protein the person can eat is based on how well the kidneys are functioning and the amount of protein needed to maintain good health

Sodium content in the diet is also controlled. This helps maintain avoid fluid retention. Reduced amounts of sodium in the diet also helps control high blood pressure and congestive heart failure.

The daily intake of potassium is also a concern. Controlling it helps prevent hypokalemia (a low level of potassium, rarely a problem for people with renal disease) as well as hyperkalemia (a high level of potassium, a common problem for people with renal disease).

The mineral phosphorus is often controlled as well. When the amount of phosphorus is decreased by the reduced intake of dairy products and other foods high in phosphorus, there is a need to provide calcium supplements to prevent bone disease. The amount of phosphorus in the diet is controlled by the use of phosphorus binders (medications that bind the phosphorus in the food and make them unavailable to the body). Vitamin D supplements may also be provided to help control the calcium and phosphorus balance in the body.

During renal failure, the amount of urine the body produces may be decreased. The recommended daily amount of fluid is based on the amount of urine produced in a 24-hour period. Other considerations are the amount of fluid retention present, the level of dietary sodium, the use of diuretics, and the presence or absence of congestive heart failure.

People with renal disease are more prone to cardiovascular (heart) disease, so a diet with most of the calories from complex carbohydrates is recommended. Calories from fats should be from monounsaturated and polyunsaturated fats. The daily calorie intake needs to be adequate to maintain the person’s nutritional status at an optimal level and to prevent the breakdown of body tissue. The person’s weight and protein status should be monitored regularly, even daily.

Vitamin supplementation is very individualized. It is dependent on the various dietary restrictions, the extent of renal failure. The requirements for the fat-soluble vitamins (A, D, E, and K) are usually met by the diet. Vitamin D may need to be supplemented; this is an individual medical decision. The intake of water-soluble vitamins is usually adequate until a patient begins dialysis.

The minerals that are also monitored include calcium, iron and magnesium. The recommended supplementation of daily calcium is 1,000 to 1,500 milligrams per day. Iron supplementation is based on the person’s need. Magnesium supplementation is not recommended, as it can cause an increase in the magnesium levels in a person with renal disease. Iron is usually supplemented as most patients with advanced renal failure also have severe anemia.

Note: not all people with kidney disease need dietary supplements.

Side effects   

A low-protein diet can be deficient in some of the essential amino acids, the vitaminsniacin, thiamine, and riboflavin, and the minerals phosphorus, calcium, and iron. In advanced renal failure it can lead to malnutrition and should only be implemented under the guidance of a kidney specialist.

Benefits of implementation:

This special diet is very helpful as a decreased protein load decreases the stress on the kidney. Nonadherence can increase progression of chronic kidney disease.

  According to Dr. Avner, some recent studies on the effects of a soy protein diet on the progression of kidney disease in animal models of PKD are very interesting and deserve attention. Canadian reserchers at the labs of Drs. Holub and Ogborn are conducting this soy protein research
  In One study, The soy protein diet clearly decreased renal cyst volume and improved kidney function in one very well studied animal model. In a second study, Dr. Avner said, this soy protein diet "dramatically decreased cyst volume, decreased the amount of inflammation and fibrosis, and normalized kidney function in one of the very well established models of ADPKD (PKD1)."
  "Although the mechanisms are still a little bit unclear, these recently published data are very striking and deserve serious consideration," Dr. Avner said. "This is the kind of information that is very important," and he predicted that a number of laboratories will be looking at the mechanistic and other issues of this therapy.

  One of the most important ideas coming out of the accelerating PKD research is that there may be a multiprotein complex, key to a normal cellular process, that is disrupted in polycystic kidney disease. The involvemnet of multiple proteins would provide an explantion for why inherited defects in different proteins (polycystin 1 or polycystin 2, for instance) can cause diseases that are virtually indistinguishable at the clinical level.
  Based on various studies, scientists now beleive that the very large PKD1 protein sits in the cell membrane with part of the protein on the outside capable of receiving external signals, and an internal portion that can communicate with the interior of the cell and relay signals. The smaller PKD2 protein may also sit on the cell membrane.
  The PKD1 protein looks a lot like other proteins that are known to play key roles in the communication between cells, communication that is particualrly important during development. The PKD2 protein looks like proteins that normally control the inflow and outflow of salts (calcium and sodium ions) and are often involved in secretory activity and/or signaling.
  In very exciting findings, it has been shown in the test tube that the ends of the PKD1 and PKD2 proteins physically interact with each other, suggesting that they may interact with each other in the cell membrane. The implacation is that perhaps PKD1 and PKD2 are part of a multiprotein complex that can be disrupted by damage to either protein. This would account for the fact that very similar diseases can result from damages to either gene.
  Furthermore, evidence from Dr. Avner’s group, in collaboration with Dr. Richard Woychik’s group, has shown that a gene responsible for ARPKD in a mouse model codes for a protein (Tg 737) that looks a lot like other proteins known to be involved in cell cycle control. The Tg737 protein has been shown to interact physically with the PKD1 protein, as well as with molecules crucial to cell polarity, protein stability, and differentaion.
  The suggestion advanced by Dr. Avner is that "a number of different proteins (PKD1,PKD2, Tg737, etc.) may interact in a complex that, when disrupted by mutations in any PKD gene, may lead to altered epithelial proliferative activity, secretion, and cellular differentaion seen in cystic epithelia (membranous cellular tissue) through abnormal signaling pathways."
  Dr. Avner said the existence of such a multiprotein complex might help explain why "infants with ARPKD and infants with ADPKD can be indistinguishable in the newborn period in that they have big kidneys and similar clinical findings."
  "We may have a key to understanding why all of these diseases may have similar clinical features and the reason might be that we have a big protein complex, where an abnormality in one of the proteins may cause an imbalance in all of the others and trigger very similar processes in cells and then in the development of cystic disease.

THE POLYCYSTIC KIDNEY RESEARCH FOUNDATION’S NEWSLETTER ON LOW PROTEIN AND SOY PROTEIN IN THE DIET.

The news letter for the Polycystic Kidney Research Foundation (Vol.13, issue 1, Special Issue 1998) states that The Nutrition Research Group for the Retardation of Polycystic Kidney Disease studies have shown the restriction of dietary protein early in the course of PKD (before the manifestation of clinical symptoms) can significantly slow disease progression. The rate of enlargement of kidney cysts, including total kidney size, is significantly reduced. In addition, the amount of time for progression to kidney failure is delayed considerably. Also, We have demonstrated that soy protein isolate (an ingredient manufactured from soybeans and used in various food products), when substituted for animal protein (in the form of milk casein), was found to retard the progression of PKD. The progression of PKD in Japanese patients is significantly slower than that for corresponding North Americans. The slower rate of progression of PKD in Japan has previously been attributed to genetic factors. We are pursuing the likely possibility , based on our animal experiments, that the slower progression of PKD in Japan may partly reflect the differences in the Japanese diet. The Japanese diet has lower levels of protein (including higher intakes of low-protein, carbohydrate-rich, rice-based foods) and much higher levels of soy-based products and associated micronutrients.

WHAT IS A LOW PROTEIN DIET ?

It is a diet that limits protein to the minimum you need to be in good health. There are two versions of low protein diets used for kidney disease. One is a moderately restricted low protein diet where you get all your protein from food and the amount of protein is limited to only the amount necessary for good nutrition. This is the diet the Polycystic Kidney Research Foundation’s newsletter mentioned.
There is also the severe protein restiction diet where you are limited to a small amount of protein (under 25 gms. usually) with keto acid or amino acid supplements supplying the rest of the protein intake. In some studies, this diet has shown better results in preserving kidney function than the moderate restricted low protein diet but this also included other types of kidney disease. It is also harder to comply with. This is a rather strict vegetarian diet with meat of any kind, eggs, milk or cheese forbidden or rarely allowed. It requires a nephrologist’s monitoring and mineral and vitamin supplementation (especially vitamin B-12 which is found almost exclusively in animal products). Calcium and potassium supplements may also be needed. If you are interested in trying this diet, you should read "The Kidney Patient’s Book New Treatment, New Hope" by Timothy P. Ahlstrom which I will be quoting from like crazy in the next few questions.

WHAT ARE KETO ACID SUPPLEMENTS ?

Protein is made up of amino acids. There are about 20 different amino acids in protein of which 9 can not be made by the body and are called the essential amino acids. The other amino acids are called non-essential amino acids because the body can convert other amino acids into the ones it needs.
Keto acid supplements are a chemically different form of amino acids, created in the laboratory. The body transforms them into the essential amino acids it needs. Both supplements—amino acid and keto acids—provide the essential amino acids the body needs, but in a pure form that does not overload the diseased kidneys with the needs to process the phosphorus or nitrogen that would come from foods. (The Kidney Patient’s Book New Treatment, New Hope by Timothy P. Ahlstrom)
For those of you interested in amino acid supplements, here’s information about where you can get them. This is from an e-mail which Dr. Mackenzie (who is involved in research on low protein diets on kidney disease) was kind enough to send me.
"The amino acid preparations sold in food stores are useless. The only preparation consisting exclusively of essential amino acids, sold in US, is Aminess, marketed by Nestle (800 776 5446)."
I do want to add a warning here that I don’t think it’s a good idea to try the extreme low protein diet with supplements without a nephrologist who’s had some experience with this. This isn’t the easiest diet in the world and I think it’s too easy to get confused doing it by yourself. That said, you’re perfectly free to ignore me if you like.

HOW MUCH PROTEIN DOES MY BODY NEED ?

Most Americans eat much more protein than they need to stay healthy, by some estimates 2 or 3 times as much protein than needed. Your kidneys then have to break down all this extra protein and get rid of it. This makes your kidneys have to work harder and wear out faster than if they only broke down the amount of protein your body actually needed. Your body on average requires .6 gms. of protein / per kg. of bodyweight / per day. This can vary from a low of .45 gms. to a high of .8 gms. of protein (Polycystic Research Foundation Newsletter). Factors such as a higher percentage of muscle mass can require a higher intake of protein. I think this means wimps like me are on the lower end.

SO HOW EXACTLY DO I FIGURE THIS OUT ?

Part 1. First convert your weight to kilograms (kgs.) by dividing your weight in pounds (lbs.) by 2.2. If you’re not from the U.S, you probably already know your weight in kgs. and can skip this part.

Ex. My weight is usually around 120 lbs.

120 lbs divided by 2.2 is 54.55 kgs.

Part 2. Next you multiply your weight in kgs. by .6 (.45 for wimps or .8 for you weight lifters). Personally, I suggest sticking with the .6 and adjusting your protein up if you feel tired or down a little if you think you’ll feel ok.

Ex. 54.55 kgs multiplied by .6 is 32.73 gms. of protein I can eat.

Also make sure to tell your doctor that you’re trying a low protein diet and want to be tested after a few months to make sure you aren’t cutting it too close and getting a protein defeciency.


WHAT FOODS ARE LOW IN PROTEIN?

Fruits and most vegetables have little or no protein. There are some exceptions to this like peas, beans (both can be rather high) and some starchy vegetables (like potatoes and corn which are in the medium range). Listed below are some examples. The amount of protein can vary depending on serving size, if the food is fresh, dried (usually higher in protein) or frozen, and other factors so check the nutrition label for a more accurate measurement of protein when it’s available. These are only averages.

Author: Zoltan Rona, MD, MSc, Publication: Alive - Canadian Journal of Health and Nutrition, Dated: 4/1/1998

VitaGuide.com™ Review: Dr. Rona reports that, in addition to the natural approaches to dealing with a kidney cyst, such as vegetarian diet, avoiding sugar and refined carbohydrates, there are specific antioxidant supplements he recommends including "beta-carotene, Vitamin A, Vitamin B-complex, Vitamin C, Vitamin E, zinc, copper, selenium and bioflavonoids." He also recommends that a herb combination of "burdock, slippery elm, Turkish rhubarb and sheep sorrel . . . Has an immune system-boosting and anti-tumor effect."

Cystitis - Agrimony, Bistort, Burdock, Corn Silk, Dandelion Leaf, Goldenrod, Gravel, Irish Moss, Juniper, Marshmallow, Thuja, Usnea, Yerba Manza
Cystitis, acute catarrhal - Shepherd’s Purse
Cystitis with acidic urine, mucus, and pain - Uva Ursi
Cystitis with blood - Horsetail, Plantain
Cystitis, chronic - Buchu
Cystitis, painful - Kava Kava
Cysts, sebaceous - Calendula, Corn Silk