Section Six: Nutrition and Renal Disease
The kidneys’ job is to keep the body’s fluids, electrolytes, and organic solutes in a healthy balance. Their functional units are the million or so nephrons in the renal cortex which filter most constituents of the blood other than red blood cells and protein, reabsorb needed substances, secrete hydrogen ions to maintain acid-base balance, and secrete wastes.1
Urine formation consists of three basic processes: glomerular filtration, tubular secretion, and tubular reabsorption. Several disease conditions can interfere with these functions. Inflammatory and degenerative diseases can involve the small blood vessels and membranes in the nephrons. Urinary tract infections and kidney stones can interfere with normal drainage, causing further infection and tissue damage. Circulatory disorders, such as hypertension, can damage the small renal arteries. Other diseases, such as diabetes, gout, and urinary tract abnormalities can lead to impaired function, infection, or obstruction. Toxic agents such as insecticides, solvents, and certain drugs may also harm renal tissue.
In nephrotic syndrome, an injury to the glomerular basement membrane causes an increased glomerular permeability, resulting in the loss of albumin and other plasma proteins in the urine. Urinary protein losses greater than 3-3.5 grams per day usually indicate nephrotic syndrome.
Although albumin synthesis in the liver is increased in nephrotic syndrome, it is not enough to compensate for losses in the urine. The loss of albumin leads to edema.
Low albumin levels also trigger cholesterol and lipoprotein synthesis in the liver, resulting in hyperlipidemia. At the same time, hepatic catabolism of serum lipoproteins is reduced and urinary excretion of HDL is increased. These lipid abnormalities can be exacerbated by medications often used to treat nephrotic syndrome, such as steroids, diuretics, and anti-hypertensive agents.
Diet for Nephrotic Syndrome
A well-planned diet can replace lost protein and ensure efficient utilization of ingested proteins through provision of adequate calories. Dietary changes can also help control hypertension, edema, and hyperlipidemia, and slow the progression of renal disease.
Protein: High-protein diets are not recommended as they may encourage damage to the nephrons, leading to a progression of renal insufficiency. Since albumin losses in nephrotic patients are due to increased catabolism, rather than a reduction in protein synthesis, low-protein diets, which decrease catabolism, may be more beneficial.2
The optimal amount of dietary protein necessary to prevent protein catabolism and progression of renal disease has not been established. A common recommendation is 0.6 grams of protein per kilogram of ideal body weight, adjusted depending on the glomerular filtration rate and nutritional status, plus gram-for-gram replacement of urinary protein losses.
A vegetarian diet, often used for lipid-lowering, also offers a convenient way to provide adequate, but not excessive, protein. In a 1992 study, a group of 20 nephrotic syndrome patients were put on a vegetarian diet for eight weeks. Protein intake averaged 0.7 grams per kilogram per day, which was more appropriate to their needs than the 1.15 grams per kilogram provided in their usual diet.3
Sodium and Fluid: A limit on sodium of 1-3 grams per day is usually recommended to control edema and hypertension. Diuretics may also be used. A fluid restriction is not warranted unless renal failure occurs.
Lipids: A diet low in saturated fat and cholesterol, combined with loss of excess weight, is recommended to reduce the risk of cardiovascular disease. Many clinicians recommend limiting cholesterol to less than 300 milligrams per day and fat intake to 30 percent of calories. However, research has shown that such recommendations lead to only minimal lipid lowering. As noted in detail in Section 1, low-fat vegetarian diets are much more effective for lipid control and usually lead to the reversal of atherosclerotic disease. Cholesterol-lowering drugs can be used adjunctively if needed.
An eight-week trial in 13 men and 7 women with hyperlipidemia and nephrotic syndrome showed that a vegetarian diet significantly reduced cholesterol, triglycerides, and phosphorus.3
Energy: Calorie intake should be adequate to achieve and maintain ideal body weight and maintain protein stores. Foods rich in complex carbohydrates should provide the majority of calories.
Supplements: Patients with nephrotic syndrome are often low in B vitamins and zinc, and can benefit from supplements. In addition, since a significant portion of serum calcium is protein-bound, it tends to be low when serum proteins are reduced. No modification is routinely needed for potassium, but potassium losses due to secondary hyperaldosteronism may require replacement.4
The following clinical values should be monitored:4
- Serum albumin and total protein
- Urinary protein
- Glomerular filtration rate
- Dietary protein, fat, and cholesterol
- Daily weights
- Serum lipids
Acute Renal Failure
Acute renal failure, manifested by oliguria or anuria, usually occurs suddenly and is often reversible. It is marked by a reduction in the glomerular filtration rate and a modification in the kidneys ability to excrete metabolic wastes.
Its causes can be prerenal, intrinsic, and postrenal. Prerenal causes include severe dehydration and circulatory collapse. Causes intrinsic to the kidney include acute tubular necrosis, nephrotoxicity, vascular disorders, and acute glomerulonephritis. Obstructive (postrenal) causes include benign prostatic hypertrophy and bladder or prostate cancer.1
The most common form of intrinsic renal disease is acute tubular necrosis, accounting for about 75 percent of cases. Acute tubular necrosis may be due to posttraumatic or surgical shock or to the toxic effects of drugs, metals, or organic compounds.
Nutrition strategies in acute tubular necrosis vary depending on its stage. During phase one, oliguria, less than 400 milliliters of urine is produced per day. This phase usually lasts one to three weeks. Signs and symptoms include nausea, vomiting, fluid overload, and elevation of BUN, creatinine, phosphorus, and potassium levels. Dialysis may be needed during this stage to reduce acidosis, control hyperkalemia, and correct uremia.
The diuretic phase of acute tubular necrosis lasts one to two weeks, and is characterized by increased urine output and a return of the ability to eliminate wastes. Fluid and electrolyte balance should be monitored and replacements made as necessary. The convalescent phase occurs over the next two to six months.1,2
Diet in Acute Renal Failure
Diet plays a critical role in the care of patients with acute renal failure. Clinicians should plan diets with an eye toward the possibility of uremia, metabolic acidosis, fluid and electrolyte imbalances, infection, and tissue destruction. Nutritional support of dialysis will be discussed below in the section on chronic renal failure.
Protein: A low-protein diet (0.5-0.6 grams per kilogram) is recommended initially. Protein may be increased in the diet as the glomerular filtration rate increases to normal. If dialysis is initiated, the protein level may be increased to 1.0-1.5 grams per kilogram per day if necessary to compensate for protein losses in the dialysate.
Calories: Calorie needs are generally elevated (35-50 kilocalories per kilogram) in order to provide positive nitrogen balance under stressful conditions. As protein is usually quite restricted, calorie needs may be met by providing greater amounts of carbohydrate and fat in the diet.
Sodium and Fluid: Sodium is restricted depending on urinary excretion, edema, serum sodium levels, and dialysis needs. During the oliguric phase, sodium may be restricted to 500-1000 milligrams per day, and fluid requirements are based on replacing losses via urine, vomitus, and diarrhea, plus approximately 500 milliliters per day.
Potassium: Potassium requirements vary depending on hemodynamic status and the degree of hypermetabolism due to stress, infection, or fever. High potassium levels are treated by dialysis or with kayexalate, an exchange resin which substitutes sodium for potassium in the gastrointestinal tract. During the oliguric phase, potassium may be restricted to 1,000 milligrams per day.3
Chronic Renal Failure
Approximately 90 percent of cases of end-stage renal disease are attributable to diabetes mellitus, glomerulonephritis, or hypertension. Kidney failure results in fluid and electrolyte imbalances, the build up of nitrogenous wastes, and reduced ability to produce renal hormones. The two treatment options are transplantation or dialysis.1
Mild renal insufficiency is defined as 40-80 percent of renal function. Moderate insufficiency is defined as 15-40 percent, and severe renal insufficiency is below these figures.2
Diet in Chronic Renal Failure
Low-protein diets may slow the progression of mild and moderate renal insufficiency. Therapeutic diets using plant sources of protein are more effective in delaying the progression of renal insufficiency, compared to those using animal proteins.5
Vegan (pure vegetarian) diets have been shown to provide adequate protein. A study of 22 patients with mild renal failure compared a vegan diet to a conventional low-protein diet. All patients were followed for at least six months. There was no sign of protein insufficiency and inorganic phosphorus levels remained normal.6
Dialysis changes dietary needs. Patients undergoing typical hemodialysis, involving about three treatments per week, follow diets that are restricted in protein, sodium, potassium, phosphorus, and fluid. Patients on continuous ambulatory peritoneal dialysis, involving several dialysate exchanges per day, can be more liberal in protein, sodium, potassium, and fluid intake.
Sodium: Sodium intake must be modified to prevent hypertension, congestive heart failure, and pulmonary edema. Limiting intake will help avoid thirst and maintain acceptable fluid balance. Restrictions range from 1,000-3,000 milligrams per day with hemodialysis and 2,000-4,000 milligrams per day for peritoneal dialysis. Major salt sources are described below.
Fluid: Fluid consumption should be controlled to avoid congestive heart failure, pulmonary edema, hypertension, and swelling of the legs and feet. Fluid allowances are 1,000-1,5000 milliliters per day and are based on urine output and type of dialysis.
Protein: Protein requirements range from 1.1-1.5 grams per kilogram, depending on the type of dialysis used and the patient’s nutritional status. It is important to ensure sufficient protein to maintain visceral protein stores, but to avoid excesses that could lead the accumulation of nitrogenous waste products in the blood (uremia).
Phosphorus: Kidney failure causes high levels of phosphorus to build up in the blood and disrupts calcium/phosphorus balance. Elevated phosphorus levels can lead to metastatic calcification (soft tissue calcification), secondary hyperparathyroidism, and renal osteodystrophy. Recommended intakes usually range from 800-1,000 milligrams per day with hemodialysis and less than 1,200 milligrams per day with periotoneal dialysis.
Potassium: Potassium restrictions depend on serum potassium levels, the type of dialysis, medications, and residual renal function. Patients on hemodialysis are usually restricted to 2,000-3,000 milligrams per day to prevent hyperkalemia between treatments. Patients on peritoneal dialysis may follow a more liberal dietary potassium intake, as potassium is lost in the dialysate solution during daily exchanges. Some high- and low-potassium foods are listed in Table 1, Section 5.
About 12 percent of Americans develop a kidney stone at some point in their lives. Stones usually result from the crystallization of calcium (which originally came in foods or supplements) and oxalate, a part of many plant foods. Some people have a tendency to lose excessive amounts of calcium or oxalate through their kidneys, and they have a greater likelihood of a stone.7-10 Kidney stones can also form from uric acid, which is a breakdown product of protein, or from struvite (ammoniomagnesium phosphate) or cystine.
The prevalence of kidney stones is three times higher in men than women, and is higher among Caucasians than Asians or African Americans, for reasons that are not clear. They are especially likely to strike between the ages of 40 and 60.
Nutritional steps are important in preventing stones and can also help prevent recurrences, which is important given that 30-50 percent of people diagnosed with a renal stone have a recurrence within five years.
Preventing stones is like keeping a salt crystal from forming in a glass of salty water. You can either reduce the concentration of salt or add more water. Epidemiologic studies have shown that certain parts of the diet help reduce the amount of calcium that filters into the urine. It is a simple matter to put these factors to work clinically.
WHAT’S IN A STONE? 7
|Ammoniomagnesium phosphate (struvite)
Certain parts of the diet clearly help reduce the risk. The first is no surprise.
Water. Water dilutes the urine and keeps calcium, oxalates, and uric acid in solution. In research studies, those subjects whose total fluid intake (from all sources) over 24 hours was roughly 2.5 liters, the risk of a stone was about one-third less than that of subjects drinking only half that much.7 (They do not need to drink 2.5 liters of water per day; rather this is the total fluid consumption, including juices, soups, etc.) Patients need to understand that their thirst sense can lag behind their hydration status, and they may need to develop a routine for extra water consumption.
High-Potassium Foods. A study of 46,000 men conducted by Harvard University researchers found that a high potassium intake can cut the risk of kidney stones in half. Potassium helps the kidneys retain calcium, rather than sending it out into the urine. Potassium supplements are not generally necessary. Rather, a diet including regular servings of fruits, vegetables, and beans supplies plenty of potassium.
Calcium. Although most stones contain calcium, the calcium in foods does not necessarily contribute to stones. Calcium supplements taken between meals may increase the risk of stones, because about 8 percent of any extra dietary calcium passes into the urine.9,11 On the other hand, calcium consumed with meals has the opposite effect, reducing the risk of stones. The reason, apparently, is that calcium binds to oxalates in foods and holds them in the digestive tract, rather than allowing them to be absorbed.
Caffeine. Caffeinated beverages reduce the risk of stones. Caffeine’s diuretic effect causes the loss of both water and calcium, but the water loss is apparently the predominant effect. Similarly, alcoholic beverages are associated with a reduced risk of kidney stones, again presumably due to a diuretic effect. This is not a compelling reason to drink either coffee or alcohol, but their diuretic actions do present this advantage.
Animal Protein. Animal proteins cause calcium to be leached from the bones and excreted in the urine where it can form stones. Diets rich in animal proteins also increase uric acid excretion. In a controlled research study, published in the American Journal of Clinical Nutrition, research subjects on a diet eliminating animal protein had less than half the calcium loss that they had on their baseline diet.12
The Harvard study mentioned earlier found that even a modest increase in animal protein, from less than 50 grams to 77 grams per day, was associated with a 33 percent increased risk of stones in men.7 The same is true for women. The Nurses’ Health Study, a long-term study of health factors in a large group of women, revealed an even greater risk of stones from animal protein than was found in previous studies in men.9
The association between animal proteins and stones probably relates both to the amount of protein they contain and to their content of the sulfur-containing amino acids. In particular, the sulfur in cystine and methionine is converted to sulfate, which tends to acidify the blood. As a part of the process of neutralizing this acid, bone is dissolved, and bone calcium ends up in the urine. Meats and eggs contain two to five times more of these sulfur-containing amino acids than are found in grains and beans.11,13
Between 1958 and the late 1960s, there was a sharp increase in the incidence of kidney stones in Great Britain. During that period, there was no substantial change in the amount of calcium or oxalate-containing foods consumed. However, the consumption of vegetables decreased, and the use of poultry, fish, and red meat increased. Statistical analyses showed a strong relationship between the incidence of stones and animal protein consumption.14
Sodium. Sodium increases the passage of calcium through the kidney and increases the risk of stones.9 When people cut their salt (sodium chloride) intake in half, they reduce their daily need for calcium by about 160 milligrams.15
Plants of any kind—grains, vegetables, legumes, and fruits—contain almost no sodium at all unless it is added during canning or other processing. Dairy products and meats contain more salt than plant products, and table salt, frozen meals, and canned and snack foods are the highest-sodium food products. For more information, see the sodium/potassium chart in Section 5.
Sugar. Sugar accelerates calcium losses through the kidney.16 In the Nurses’ Health Study, those who consumed, on average, 60 grams or more of sugar (sucrose) per day had a 50 percent higher risk of stones than those who consumed only about 20 grams.9
SUGAR IN COMMON FOODS (grams)
|Candy bar (2 ounces)
|Corn flakes (1 cup, 28 grams)
|Frosted corn flakes (1 cup, 41 grams)
|Fruit cocktail (1/2 cup, 124 grams)
|Grape jam (1 tablespoon)
|Ice cream (1/2 cup, 106 grams)
Soda (12 ounces)
|White bread (2 slices)
Source: package information
Climate. Kidney stones are also more common in warm climates, presumably because perspiration leads to dehydration and a more concentrated urine, and because sunlight increases the production of vitamin D in the skin which, in turn, increases calcium absorption from the digestive tract.17
Surprisingly, oxalate-rich foods, such as chocolate, nuts, tea, and spinach, are not associated with a higher risk of renal stones,7 nor is vitamin C, even though it can be converted to oxalate. A large study of men taking vitamin C supplements found that they had no more kidney stones than men who do not take them.8
Helping Patients Avoid Kidney Stones
Here are simple steps to help your patients avoid kidney stones.
- Encourage patients to drink plenty of water or other fluids, staying ahead of their thirst.
- Diets including generous amounts of vegetables, fruits, and beans are rich in potassium and very low in sodium.
- If you prescribe calcium supplements, encourage patients to take them with meals, rather than between meals.
- Encourage patients to avoid animal products. Their proteins and sodium content increase the risk of stones.
- Patients should keep salt and sugar use modest.
Cranberry Juice: An Old Remedy Is Clinically Tested
Cranberry juice has long been used as a folk remedy for urinary infections. A 1994 report in the Journal of the American Medical Association showed that it does indeed have at least a preventive effect. In a test involving 153 elderly women in Boston, half the subjects drank 300 milliliters (about one and one-quarter cups) of cranberry juice cocktail each day, using the same bottled beverage that is commonly sold in grocery stores.18 The other subjects consumed a drink that looked and tasted like cranberry juice, but had no real juice in it.
Over the next six months, urine samples were collected and tested for signs of bacteria. The women consuming cranberry juice had only 42 percent as many urinary infections as the control group. The number of cases that had to be treated by antibiotics was also only about half, which is a real advantage, since antibiotics can sometimes lead to yeast infections and other problems. It takes about four to eight weeks for the preventive effect to be seen.
The explanation for the effect of cranberry juice is probably not an acidification of the urine, because the placebo drink also reduced urinary pH. Rather, cranberries contain a substance that stops bacteria from being able to attach to cells, and this is probably true whether the cranberry juice reaches the bacteria in the digestive tract or the urinary tract. Substances that interfere with bacterial adhesion have also been found in blueberry juice, but not in orange, grapefruit, pineapple, mango, or guava juice.
Nutrition and Renal Disease Study Questions
- What are some of the main problems of nephrotic syndrome?
- Why are high protein diets not recommended with nephrotic syndrome? What are the alternatives?
- What type of dietary restrictions are used in acute renal failure?
- What are the treatment options for chronic renal failure? How do dietary regimens differ between hemodialysis and peritoneal dialysis?
- What steps can be taken to prevent kidney stones?
1. Mahan LK, Arlin M. Krause’s Food, Nutrition, and Diet Therapy. W.B. Saunders, Philadelphia, 1992.
2. The American Dietetic Association. Handbook of Clinical Dietetics, second edition. Yale University Press, 1992.
3. D’Amico G, Gentile MG, Manna G, et al. Effect of vegetarian soy diet on hyperlipidemia in nephrotic syndrome. Lancet 1992;339:1131-4.
4. The American Dietetic Association. Manual of Clinical Dietetics, fifth edition. American Dietetic Association, Chicago, 1996.
5. Gretz N, Meisinger M, Strauch M. Does a low protein diet really slow down the rate of progression of chronic renal failure? Blood Purif 1989;7:33:33-8.
6. Barsotti G, Morelli E, Cupisti A, Meola M, Dani L, Giovannetti S. A low-nitrogen, low-phosphorus vegan diet for patients with chronic renal failure. Nephron 1996;74:390-4.
7. Curhan GC, Willett WC, Rimm EB, Stampfer MJ. A prospective study of dietary calcium and other nutrients and the risk of symptomatic kidney stones. N Engl J Med 1993;328:833-8.
8. Curhan GC, Willett WC, Rimm EB, Spiegelman D, Stampfer MJ. Prospective study of beverage use and the risk of kidney stones. Am J Epidemiol 1996;143:240-7.
9. Curhan GC, Willett WC, Speizer FE, Spiegelman D, Stampfer MJ. Comparison of dietary calcium with supplemental calcium and other nutrients as factors affecting the risk for kidney stones in women. Ann Int Med 1997;126:497-504.
10. Soucie JM, Thun MJ, Coates RJ, McClellan W, Austin H. Demographic and geographic variability of kidney stones in the United States. Kidney Int 1994;46:893-9.
11. Lemann J. Composition of the diet and calcium kidney stones. N Engl J Med 1993;328:880-2.
12. Remer T, Manz F. Estimation of the renal net acid excretion by adults consuming diets containing variable amounts of protein. Am J Clin Nutr 1994;59:1356-61.
13. Breslau NA, Brinkley L, Hill KD, Pak CYC. Relationship of animal protein-rich diet to kidney stone formation and calcium metabolism. J Clin Endocrinol 1988;66:140-6.
14. Robertson WG, Peacock M, Hodgkinson A. Dietary changes and the incidence of urinary calculi in the U.K. between 1958 and 1976. J Chron Dis 1979;32:469-76.
15. Nordin BEC, Need AG, Morris HA, Horowitz M. The nature and significance of the relationship between urinary sodium and urinary calcium in women. J Nutr 1993;123:1615-22.
16. Lemann J Jr, Adams ND, Gray RW. Urinary calcium excretion in human beings. N Engl J Med 1979;301:535-41.
17. Soucie JM, Coates RJ, McClellan W, Austin H, Thun MJ. Relation between geographic variability in kidney stones prevalence and risk factors for stones. Am J Epidemiol 1996;143:487-95.
18. Avorn J, Monane M, Gurwitz JH, Glynn RJ, Choodnovskiy I, Lipsitz LA. Reduction of bacteriuria and pyuria after ingestion of cranberry juice. JAMA 1994;271:751-4.