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CKD and Nutritional Interventions

Food & Nutrients in Disease Management
Throughout time, food has been used in healing. In recent decades food and medicine have taken divergent paths. Food has become bereft of nutrients, and modern medicine has sought to heal with technical advances that initially seem dazzlingly more powerful than food. Consequently, the healing potential of food is underutilized in modern medicine. Editor

by Allan E. Sosin, M.D.
Dr. Sosin is an expert in the use of natural approaches to replace drugs and surgery. He has over forty-five years of clinical experience in treating patients with traditional therapies and thirty years of using alternative methods in combination with conventional medicine.

I. INTRODUCTION

Chronic kidney disease is underdiagnosed and underappreciated as a cause of illness and mortality. Fundamental changes in lifestyle predispose people in Western societies to compromised renal integrity and progressive deterioration of renal function. It is important to include the proper evaluation of renal status in overall health assessment. Prompt diagnosis provides an opportunity to implement the strategies presented in this chapter and improve the current statistics.

II. EPIDEMIOLOGY

At present 350,000 people are on dialysis therapy in the United States, and that number is increasing at the rate of 7% yearly. Hemodialysis, peritoneal dialysis, and renal transplantation are the methods of treatment for chronic renal failure. Although they permit survival in an otherwise uniformly fatal condition, they are difficult and costly procedures, and impact quality of life.

The major causes of end-stage renal disease (ESRD) are diabetes mellitus, accounting for 45% of cases, and hypertension, accounting for 27%. Since the majority of cases of diabetes and hypertension are preventable, and nearly all can be mitigated, optimal clinical management would greatly reduce the prevalence of end-stage renal disease.

There are five stages of kidney disease, comprising a total of nearly 20 million affected individuals:

  • Stage 1: Chronic kidney disease with normal or increased glomerular fi ltration rate (GFR >90)
  • Stage 2: Mild loss of kidney function (GFR 60–89)
  • Stage 3: Moderate loss of kidney function (GFR 30–59)
  • Stage 4: Severe loss of kidney function (GFR 15–29)
  • Stage 5: Kidney failure (GFR <15 or on dialysis)

One-third of patients with stage 4 disease will develop ESRD within 3 years. The median age of patients beginning dialysis in the United States is 65 years. The mortality rate of dialysis is high, 24% per year, primarily due to heart disease and stroke, approaching that of lung cancer.

III. PATIENT EVALUATION

Two measurements of kidney function should be made: glomerular filtration rate (GFR) and the degree of albuminuria. A routine chemistry panel provides the level of creatinine, a protein metabolite.

Utilizing this number along with age, weight, and sex in the Cockroft-Gault equation, GFR can be calculated Click Here

GFR (cc/min) = (140−age) × (weight in kg) × (0.85 for women or 1.0 for men) / 72 × creatinine

Serum creatinine alone is not sufficient to estimate GFR. Creatinine production reflects muscle mass, which is less in older people, thinner people, those who are inactive, and women. Thus, a creatinine of 1.0 indicates normal kidney function in a 300-pound football lineman, but signifies substantial renal compromise in an 85-pound, 80-year-old woman. This distinction becomes especially important when administering drugs to older people, whose serum creatinine level does not reflect the degree of renal disease, and whose prescription selections and dosages should be modified.

Albuminuria, or protein loss through the kidneys, is a marker for the degree of renal damage.

Protein loss, especially in diabetics, occurs prior to the rise of serum creatinine. This is most easily assessed by measuring the ratio of albumin to creatinine, preferably in the fi rst morning urine.

Monitoring albuminuria offers information on the rate of loss of renal function, since the rate of loss of GFR increases with the rate of protein loss. Additionally, the degree of albuminuria correlates with the risk of cardiovascular complications, including myocardial infarction, stroke, and congestive heart failure. Albuminuria can be reduced, and this reduction is accompanied by a lessening of cardiovascular events. In diabetics, suppression of albuminuria helps to preserve kidney function.

As we will discuss, this can be achieved with medication, dietary protein restriction, and specific nutrient supplementation.

Urinary albumin losses greater than 3 g/day are accompanied by edema and hyperlipidemia, defining the nephrotic syndrome. Albumin itself may be toxic to renal tissue, and accelerate renal disease. Other compounds may be lost, including 1,25-dihydroxyvitamin D, and clotting factors IX, XI, and XII, leading to coagulation defects. Loss of antithrombin III may cause increased thrombosis. A quarter of patients with nephrotic syndrome will have clotting disorders.

IV. PATHOPHYSIOLOGY REVIEW OF RENAL PHYSIOLOGY

The kidneys have multiple functions, the loss of which impacts other system operations:

1. Waste product excretion—renal impairment leads to metabolic acidosis, anorexia, nausea, loss of muscle protein and general depletion, neurologic dysfunction due to accumulated toxins, and soft tissue deposition of oxalates and phosphates.
2. Exquisite regulation of electrolyte concentrations and fl uid volumes—impairment leads to hyponatremia, hyperkalemia, hypocalcemia, hyperphosphatemia, hypermagnesemia, and intolerance to electrolyte or mineral loading.
3. Blood pressure regulation—impairment leads to hypertension and cardiovascular disease, and accelerates the progression of renal disease.
4. Endocrine mediators:

a. Erythropoietin—defi ciency leads to anemia.
b. Renin system activation—leads to hypertension and damage to arterial walls.
c. 1,25-dihydroxyvitamin D production—decline leads to osteoporosis and immune dysfunction.
d. Secondary hyperparathyroidism due to hyperphosphatemia and hypocalcemia, leading to metabolic bone disease and disseminated soft tissue calcification.
e. Prolonged half-lives of peptide hormones due to reduced degradation, including insulin, glucagon, growth hormone, parathyroid hormone, prolactin, gastrin, and folliclestimulating hormone.

PATHOPHYSIOLOGIC MECHANISMS

Symptoms and signs of renal impairment often do not occur until disease is advanced. It is therefore important to detect abnormalities prior to the onset of clinical manifestations. The progression of renal disease can be modified, but in most cases it is not possible to restore renal function once lost. Exceptions include auto-immune disease such as lupus erythematosus or idiopathic nephrotic syndrome, and acute renal failure.

The following factors contribute to the progression and initiation of renal disease:

1. Uncontrolled diabetes mellitus
2. Hypertension
3. Nephrotoxic medicines
4. High protein diet
5. High phosphorus diet
6. Proteinuria
7. Acidemia
8. Inflammatory renal response, with release of cytokines
9. Calcium oxalate or calcium phosphate deposition in the kidney
10. Lead and cadmium toxicity
11. Hyperuricemia
12. Platelet aggregation in the kidney

V. PHARMACOLOGIC CONSIDERATIONS IN NEPHROTOXICITY

Prescription and nonprescription drugs frequently damage renal function. Acute interstitial nephritis is largely a consequence of pharmaceuticals, including antibiotics (penicillins, rifampin, sulfa drugs, vancomycin, ciprofl oxacin, cephalosporins, erythromycin, acyclovir), diuretics (furosemide, thiazides, triamterene), and nonsteroidal anti-infl ammatory drugs (NSAIDs). NSAIDs cause both acute and chronic interstitial nephritis, and should be avoided, along with acetaminophen and aspirin, in patients with renal impairment. Despite having reduced kidney function, it is common for patients to employ NSAIDs or acetaminophen, without receiving cautionary advice from their physicians.

Osteoarthritis is ubiquitous in older people, and NSAIDs, acetaminophen, and aspirin are often prescribed or purchased over the counter. It is crucial that individuals with impaired renal function be told the risk of taking these drugs, kept on minimal required doses for the briefest period, and monitored for a rise in serum creatinine. Combinations of nephrotoxic drugs should be avoided.

Other drugs known to provoke toxic kidney effects include the anti-seizure drugs phenytoin, phenobarbital, sodium valproate, and carbamazepine. Lithium, allopurinol, ranitidine, omeprazole, interferon, cyclosporin, methotrexate, and cisplatin are other medications frequently causing kidney damage.

It was recently discovered that the magnetic resonance imaging contrast injectable gadolinium
may cause a severe systemic reaction in people with preexisting renal disease. Called nephrogenic systemic fibrosis, the disease involves induration and hyperpigmentation of the skin, with fibrosis of
skeletal muscles, heart, lungs, liver, and central nervous system. The condition is progressive and
usually irreversible, and no treatment is effective. It is crucial to measure serum creatinine prior to injecting gadolinium in any patient. Gadolinium should be withheld from any patient with GFR less than 30, if possible.

Aristolochia, a Chinese herb used primarily for weight loss, may cause chronic interstitial nephritis. It also causes urologic malignancies, and was responsible for the deaths of over 60 people in China, and several cases of renal failure in Belgium, England, and other European countries.

The use of statin drugs (HMG-CoA reductase inhibitors) is controversial in kidney disease.

Statins may cause rhabdomyolysis with heme pigment tubular toxicity.5 Nevertheless, because renal disease is a cardiac equivalent, statins are often prescribed to those with renal failure. Recent studies, however, reveal no significant reduction of cardiovascular events in dialysis patients receiving statins, despite the lowering of cholesterol.

Radiologic contrast dyes are a frequent cause of renal toxicity. Contrast-induced nephropathy, defined as an increase of creatinine greater than 0.5 mg/dL within 3 days of contrast administration without alternative cause, is the third most common cause of acute renal failure in hospitalized patients. Nephropathy occurs in up to 10% of patients with normal renal function, but in up to 25% of those with preexisting kidney disease or other risk factors such as diabetes, congestive heart failure, older age, and concomitant use of nephrotoxic drugs. Although the kidneys may eventually recover, permanent damage requiring chronic dialysis therapy may occur.

Prevention of contrast-induced nephropathy includes adequate hydration with intravenous saline before and after the procedure, a dose of 100 cc/hour for a total of 6 to 12 hours. N-acetylcysteine is also provided, 600 to 1200 mg orally, the day before and the day after the procedure. N-acetylcysteine is an inexpensive nutritional supplement with virtually no side effects, and should likely be provided to all patients receiving intravenous contrast dyes.

The profusion of pharmaceutical agents, along with rampant prescribing of multiple drugs by some physicians, sets the stage for undesirable drug interactions and adverse patient reactions. Doctors should assess their patients’ vulnerabilities prior to offering drug therapy, caution patients about risks, monitor the metabolic effects of these agents, and rapidly terminate drug use when organ deterioration appears. Renal effects may be progressive and irreversible, and when the patient enters stage 4 or 5 kidney disease, dialysis may be inevitable. Safe nutritional alternatives to drugs exist for the treatment of diabetes and hypertension, the two major causes of renal failure, and these should be employed in combination with, or in preference to, drugs whenever possible.

VI. COMORBIDITIES

HYPERTENSION

Hypertension is not only a major cause of kidney disease, but also determines the rate of progression and the risk of kidney failure. Blood pressure of less than 130/80 is the recommended target blood pressure for individuals with chronic kidney disease.

Patients with greater proteinuria derived more benefit from tighter blood pressure control in the National Institutes of Health–funded study, Modification of Diet in Renal Disease. Nutritional and lifestyle modifications included restrictions in dietary sodium and alcohol intake, along with exercise and weight loss. In 840 adults with chronic kidney disease of various origins, the usual blood pressure goal was a mean arterial pressure of <107 mm Hg, while the low blood pressure goal was a mean arterial pressure of <92 mm Hg. After 10 years, the incidence of kidney failure in the low blood pressure group was only 0.68 the incidence in the usual blood pressure group. The low blood pressure group also had a reduced risk of all-cause mortality. The type of medication used to lower blood pressure did not influence the results. In general, angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) are used preferentially for blood pressure control in patients with renal impairment because of their superior effects on proteinuria. Patients taking these medications must be monitored for hyperkalemia.

Protein intake also influences blood pressure. The International Study of Macronutrients and Blood Pressure confi rmed that more vegetable protein, but not animal protein, was associated with lower blood pressure.

The Dietary Approaches to Stop Hypertension (DASH) Study revealed that salt restriction and an increase in protein intake from 14% to 18% of calories reduced systolic and diastolic blood pressure in both hypertensive and nonhypertensive patients. In another study, Chinese adults with prehypertension or mild hypertension were given a diet high in soy protein. Both systolic and diastolic blood pressures fell significantly. Soy protein may reduce blood pressure by increasing insulin sensitivity, or by increasing nitric oxide production from arginine.

High blood pressure affects one-third of adults in industrialized societies. Excess sodium intake is a notorious contributor to hypertension. Primary and age-related hypertension are almost unknown in populations with sodium chloride intake of less than 50 mmol (about 3g) per day. The median urinary sodium excretion in a study involving 32 countries and 10,000 participants was 170 mmol/day, representing a salt intake of 10g.

Processed foods are high in sodium and low in potassium. A cup of canned chicken noodle soup contains 48 mmol of sodium and 1.4 mmol of potassium, while an orange contains no sodium and 6.0 mmol of potassium. Primitive populations eating unprocessed foods have an intake of potassium greater than 150 mmol/day, a sodium intake of 20 to 40 mmol/day, and a ratio of dietary potassium to sodium of 3–10/1. By contrast, people in industrialized societies ingest foods with a potassium to sodium ratio less than 0.4

Low potassium aggravates the hypertensive effect of high sodium. Increasing potassium intake in rats has lowered blood pressure and reduced stroke and renal damage. Potassium supplementation reduces the requirement for antihypertensive medication. In one study, increasing potassium intake reduced the dose of antihypertensive medication by over half in 81% of patients, and allowed for termination of medication in 38%.

The kidneys eliminate 90% of potassium, the rest exiting by the fecal route. The kidneys are not well adapted to handle a high-sodium diet. A low-potassium diet results in greater sodium retention.

High sodium intake increases renal losses of potassium. The long-term effect of potassium  depletion is to further promote sodium retention. Thus, our aberrated modern diet of high sodium and low potassium promotes a vicious cycle of physiologic impairment leading to hypertension, arterial wall thickening and rigidity, and arterial thrombosis and atherosclerosis.

Potassium intake should be at least 5 g/day, twice our current intake. The forms of potassium not containing chloride, such as those found in fruits and vegetables, allow more effective cellular exchange of sodium for potassium, and a better antihypertensive effect.

In our practice, nutrients used for blood pressure control include:

1. Fish oils, 1500 to 3000 mg/day of combined EPA/DHA.
2. Magnesium chelate or citrate containing 400 to 800 mg of elemental magnesium (monitor blood levels in renal disease).
3. Potassium citrate containing 400 to 800 mg/day of elemental potassium (monitor blood levels in renal disease).
4. Calcium chelate, malate, or aspartate, containing 400 to 1000 mg/day of elemental calcium.
5. L-arginine, 2000 to 4000 mg/day. L-arginine promotes formation of nitric oxide, a vasodilator.

METABOLIC SYNDROME

The metabolic syndrome is defined as three or more of the following factors:

1. Elevated blood sugar
2. Low HDL cholesterol
3. High triglycerides
4. Elevated blood pressure
5. Abdominal obesity

The metabolic syndrome has long been recognized to be a significant risk factor for heart disease, stroke, and diabetes. A recent study has identified metabolic syndrome as a risk factor for the development of chronic renal disease as well. In Chen et al. the odds ratio of chronic kidney disease (GFR less than 60) was 2.6 in persons with metabolic syndrome compared to normals. The odds ratio of kidney disease for individuals with four components of the metabolic syndrome was 4.2, and for those with five components it was 5.8. The risk for microalbuminuria (urinary albumin-creatinine ratio of 30 to 300 mg/gm) increased in a similar fashion.

Individually and collectively, low HDL and high triglycerides, obesity, high blood pressure, and elevated blood sugar in the pre-diabetic range, correlate strongly with the development of renal disease. In fact, it is uncommon to find renal disease in people without any element of the metabolic syndrome.

Thus, lifestyle measures employed for the management of obesity, hypertension, diabetes, and
cardiovascular disease will be effective for the prevention and slowing of renal disease. In our practice we recommend a Mediterranean-style diet, low in salt, high in fiber, with protein predominantly vegetable in origin. Compared with a low-fat diet, the Mediterranean diet has superior effects on systolic blood pressure, glucose levels, and cholesterol/HDL ratio. A Mediterranean diet also tends to be an alkalinizing diet.

There is controversy regarding the implementation of soy products in nutritional programs, related to the fact that most soy products in the United States are derived from genetically modified seeds, and possible connections between soy and thyroid disease and bladder cancer. Soy protein, however, has demonstrated benefits in rat studies of aging nephropathy and polycystic kidney disease. Soy modified all components of renal remodeling, proliferation, inflammation, and fibrosis.

These favorable changes may result from reduced arachidonic acid synthesis in favor of the anti-inflammatory prostaglandins.

Nutrients used for blood sugar control in our practice include:

1. Chromium—up to 1000 μg/day. Facilitates glucose uptake into cells.
2. Vanadium—50 mg/day. Enhances insulin action. No evidence of toxicity at this dose.
3. Alpha-lipoic acid—300 to 1800 mg/day. Improves insulin sensitivity, also effective in treating diabetic neuropathy. It is a strong anti-oxidant and detoxifier, regenerates vitamins C and E, and glutathione.
4. Biotin — 3000 μg/day. Improves both insulin sensitivity and diabetic neuropathy.
5. Gymnema sylvestre — 400 mg/day, which may act to increase insulin release. Gymnema sylvestre is an herbal product. There have been numerous reports of problems found in various herbal preparations, including contamination with heavy metals and pesticides, lower dosage than stated, or even the wrong ingredient. It is best to obtain these products from a reputable source, and to verify the absence of contaminants and correct identification of the product.
6. Cinnamon as a spice and in supplemental doses of cinnaminic acid supplements, Cinnulin™, 150 mg/day.

The medical literature indicates that over 50% of diabetes type 2 is preventable using lifestyle changes in individuals with impaired glucose tolerance.

VII. TREATMENT INTERVENTIONS

  • CHELATION AND RENAL DISEASE

Chelation therapy with EDTA has been offered as a treatment for cardiovascular disease with the proviso that chelation therapy should not be employed in the presence of elevated creatinine. Recent evidence indicates that chelation therapy may actually delay the progression of renal disease.

Investigators in Taiwan studied patients with chronic renal insufficiency (creatinine 1.5 to 3.9 mg/dL). One gram of calcium disodium ethylenediaminetetraacetic acid (EDTA) was infused over 2 hours, and urine lead was measured in a 72-hour collection. Patients with urinary lead excretion over 80 μg were assigned to either weekly chelation therapy or placebo. Chelation therapy was provided weekly for 24 months.

GFR increased by 11.9% in the chelation therapy group, while it declined in the control group.

The body lead burden prior to therapy was similar to that in the general population. Results suggested that chronic low-level environmental lead exposure may aggravate the progression of chronic renal disease, and that chelation therapy may delay progression in patients with chronic renal disease.

  • FISH OIL FOR GLOMERULAR DISEASE

IgA nephropathy is the most common type of glomerulonephritis, and leads to kidney failure in about 25% of patients. Disease recurs in transplanted kidneys, and causes graft failure in half of them.

Fish oil therapy reduces proteinuria and protects kidney function. In one case, proteinuria recurred 5 years after renal transplantation. In that patient, proteinuria was quantified at 3299 mg/day prior to therapy. Six capsules of fish oil were given twice daily, for a total dose of 4320 mg eicosapentaenoic acid (EPA) and 2880 mg docosahexaenoic acid (DHA). Proteinuria declined to 458 mg/day, and did not worsen over the next 5 years.

The action of fish oil is thought to be a reduction of vasoconstrictive and proinflammatory eicosanoids, and a decrease in cytokine release.

In another study, fish oils were given to 10 patients with focal sclerosis or membranous glomerulonephritis. The dosage was 10 g/day of combined EPA and DHA, as ethylesters. Platelet thromboxane declined 25%, triglycerides fell 30%, and bleeding time increased by 2 minutes. Proteinuria declined from 3.7 g/day to 2.6 g/day at week 6, when treatment was stopped. The decline in proteinuria persisted for another 12 weeks, and then returned to prior levels.

CHRONIC RENAL FAILURE

Dietary protein restriction is the mainstay of therapy in chronic renal failure. When animals with renal injury were fed a high-protein diet, renal failure ensued, while a low-protein diet slowed the progression. High-protein diets may aggravate renal disease by:

1. Stimulating nephron cell hypertrophy and proliferation, and glomerular scarring
2. Increasing reactive oxygen species
3. Creating an acid load, causing ammonium production and complement formation
4. Increasing urea formation, causing hypertrophy of renal tubules
5. Generating aldosterone and angiotensin II

Low-protein diets result in less uremic toxicity, so patients fed these diets may be able to avoid dialysis therapy at lower levels of renal function than patients on high-protein regimens. Soy protein, compared with casein, an animal protein, more effectively slowed progression of renal disease.

When glomerular filtration rate falls to between 25 and 70 mL/1.73m2/minute, recommended protein intake is 0.6 g/kg/day. With GFR below 25 mL/1.73m2/minute, it becomes increasingly important to pursue protein restriction. The low-protein diet generates fewer toxic nitrogenous byproducts, and has the additional benefit of lower potassium and phosphorus content. At this stage, renal excretion of potassium, magnesium, and phosphorus is usually impaired, and blood levels may rise excessively.

When GFR falls below 5 mL/1.73m2/minute, the risk of malnutrition and uremic toxicity is high, and renal replacement therapy through transplantation or dialysis should be pursued. Hemodialysis patients should receive 1.1 to 1.2 g of protein/kg/day. Peritoneal dialysis patients lose about 9 g of protein daily into the dialysate, as well as 2.5 to 4.0 g of amino acids. They should receive 1.2 to 1.3 g protein/kg/day.

In nephrotic syndrome, seen in glomerular diseases and common in diabetic renal disease, the heavy urinary protein loss is accompanied by the loss of protein-bound nutrients, including iron, copper, and vitamin D. Heavy proteinuria potentiates renal failure, perhaps through the irritative effect of proteins on glomerular tissue.

Renal failure causes weakness, nausea, and vomiting, weight loss, anemia, itching, muscle cramps, tremors, neuropathy, irritability, and cognitive dysfunction, eventuating in coma. Potassium, magnesium, and phosphorus levels rise, calcium declines due to hyperphosphatemia, and bicarbonate falls due to retained acids. Aluminum, mercury, and other toxic metals may accumulate due to the loss of usual renal excretion. Deficiencies of vitamin B6, vitamin C, and folic acid occur. 1,25-dihydroxyvitamin D production by the kidneys is greatly impaired.

Amino acid metabolism changes. Taurine levels are low, and l-carnitine levels are depressed in dialysis patients, impairing the metabolism of long-chain fatty acids in mitochondria and perhaps affecting energy production. L-carnitine supplementation is often provided either intravenously or orally, mainly to patients with muscle weakness, cramps, cardiomyopathy, anemia, and hypotension. The oral dose is 0.5 g/day.

Uremia is invariably fatal without intervention in the form of renal transplantation or dialysis, either hemo- or peritoneal dialysis. The success rate of transplantation has greatly improved, now 90% at 1 year, but there is a shortage of donor kidneys. The majority of patients are treated with dialysis, but long-term survival is limited, and dialysis itself is sometimes poorly tolerated. Daily dialysis therapy offers an improved quality of life.

Cardiovascular mortality in dialysis patients is extremely high, 25% per year, somewhat related to preexisting disease. Homocysteine levels are markedly elevated. Treatment with high doses of folic acid, vitamin B12, and vitamin B6, while reducing homocysteine levels, has not affected cardiovascular complications signifi cantly.34 Cholesterol levels are also often elevated in dialysis patients, but treatment with statin drugs has not improved survival.35 The results suggest a different pathophysiology of cardiovascular disease in dialysis patients, perhaps related to the dialysis process itself.

Phosphorus levels rise in chronic renal failure, lowering serum calcium and leading to hyperparathyroidism. This causes increased morbidity and mortality. Reduced phosphorus intake, a concomitant of the low-protein diet, slows the advance of chronic renal failure. Phosphorus levels should be kept between 2.7 to 4.6 mg/dL. Aluminum-containing phosphate binders, once commonly employed, should be avoided, because aluminum may induce a syndrome of osteomalacia, anemia, weakness, and dementia. Instead, calcium carbonate, citrate, or acetate can effectively lower phosphorus levels.

Calcium requirements increase in renal failure because of impaired renal production of 1,25-dihydroxyvitamin D and resistance to vitamin D actions. Further, the low-protein and low- phosphorus diet is also low in calcium. Most renal failure patients on low-protein diets require supplemental calcium of 1000 to 1400 mg/day. If the 25-hydroxyvitamin D level is less than 30 ng/mL, replacement should be provided with vitamin D2 (ergocalciferol). In addition, for patients with high parathyroid hormone levels (over 300 pg/mL of the intact hormone), the hyperparathyroidism can be suppressed using 1,25-dihydroxyvitamin D (calcitriol) or a related compound such as alpha-calcidol or paricalcitol.

Table: Recommended nutrient intakes in chronic renal failure and dialysis patients.

Table 22.1

Patients with advanced renal disease or on dialysis may be depleted of water-soluble vitamins and certain
minerals. Anorexia, poor food intake, and the protein-limited diet cause these deficiencies, along with altered metabolism, prescribed medications, and the dialysis process itself. Vitamin B6, vitamin C, and folic acid are most often deficient. Vitamin B12 is stored in the body, is protein-bound and not lost in dialysis, so that deficiency is uncommon. Vitamin C should not be given in doses higher than 60 mg/day. Ascorbic acid may be converted to oxalate, which is highly insoluble and may be deposited in tissues, thus aggravating renal insufficiency. A 31-year-old renal failure patient had been taking 2 g of vitamin C daily for 3 years while on dialysis. Her kidney transplant initially functioned well but later failed, and she had widespread deposition of calcium oxalate crystals in the transplanted kidney.

Vitamin A levels are elevated in uremia, and vitamin A should not be supplemented. Doses above 7500 IU/day may cause bone toxicity.

Nutritional modifications in renal failure are so substantial and difficult to implement that patients should not be confronted with all requirements at once. Of primary importance is restriction of dietary protein, phosphorus, potassium, and magnesium, and supplementation of calcium. Fluid and sodium control, increased dietary fi ber, and reduced saturated fat and refi ned carbohydrate intake are of secondary importance.

VIII. SUMMARY

Kidney disease is largely a consequence of hypertension, obesity, diabetes, metabolic syndrome, and drug and environmental toxicities. The same factors are underlying causes of many chronic degenerative diseases. Correction and prevention of these conditions will yield a reduced incidence of renal failure.

Medical professionals should pay greater attention to the signs of altered renal function. These are:
• Increasing serum creatinine, even within the normal range.
• Proteinuria—measure urine microalbumin in all patients with hypertension, diabetes, and prediabetes. Repeat this test at regular intervals. The level of proteinuria correlates with the presence and the advance of kidney disease.
• Increasing hypertension.
• Possible drug toxicities—patients taking one or more drugs known to cause kidney damage, especially NSAIDS and antibiotics.

Kidney disease is often not discovered until it is advanced, and the opportunity to reverse the damage has become remote. If renal impairment is detected early, and corrective measures are implemented, it need not progress.

Proteinuria can be reversed, with concomitant preservation of renal function, by using fish oils in high dosage, and preferentially using ACE inhibitors and ARBs for the management of hypertension and proteinuria.

A low-protein diet, consisting mainly of vegetable protein, slows the progression of kidney disease. The diet should also be alkalinizing.

The additive effect of reno-toxic medications, given in consort, should be considered when prescribing medications. Doses should be lower when there is evidence of renal compromise. Renal status should be monitored during the course of therapy, and drugs should be stopped if renal impairment intervenes.

Reno-protective measures should be followed under all circumstances, and not reserved only for those with known kidney impairment. Adequate hydration and N-acetylcysteine prevent contrastinduced nephropathy, have no risks, and should be routinely provided.

Perhaps the most effective means of protecting renal integrity is yet the most difficult to implement — lowering blood pressure by reversing the sodium/potassium ratio in the Western diet.

Potassium content is high in plant-based, whole-foods diets, while sodium content is low. Refined foods and packaged products contain sodium in excess. Doctors should instruct their patients on ways to establish potassium dominance in meal planning.

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