Kidney Disease-4

Vitamin C. Vitamin C is an antioxidant that helps keep many different types of tissues healthy. Vitamin C helps wounds and bruises heal faster and may aid in preventing infection (2001e).

Vitamin D. Additional vitamin D, which promotes the absorption of calcium, along with calcium supplements, may also be recommended. Some physicians prescribe vitamin D in a pill form called vitamin D3 (National Kidney Foundation 2001e).

Vitamin E. Supplementation with vitamin E may protect the kidneys from free-radical damage, a major factor in renal health. In experiments in rats, Sadava et al. (1996) found that a dietary deficiency of vitamin E caused progressive and pronounced renal damage. Vitamin E has been shown to restore tubular flow to rats with severe kidney disease by suppressing the free radicals that cause tubulointerstitial damage (Hahn 1998).

Calcium. Calcium along with vitamin D helps keep your bones healthy. Calcium is also used to bind to phosphorus from dietary food. Your physician will advise you about taking calcium (National Kidney Foundation 2001e).

Phosphorus. The proper amount of phosphorus is needed for healthy bones. As noted earlier, when the kidneys do not work properly, blood levels of phosphorus can get too high, causing calcium to be taken from the bones. Calcium taken from the bones will make them weak. It is important to keep phosphorus and calcium balanced to maintain strong bones (National Kidney Foundation 2001c).

Potassium. Another function of the kidneys is to maintain the right amount of potassium. Potassium plays an essential role in keeping your heartbeat regular and your other muscles working properly, but high blood levels of potassium are to be avoided. You can help control your potassium level by avoiding foods that are high in potassium (National Kidney Foundation 2001d).

Iron. A low level of red blood cells is known as anemia. Because red blood cells carry oxygen to all the tissues and organs throughout the body, low levels of oxygen may result in reduced performance of vital organs including the kidneys. Anemia is common in people who have kidney disease. Healthy kidneys produce a hormone called erythropoietin (EPO). EPO stimulates the bone marrow to produce red blood cells. However, diseased kidneys often do not make enough EPO and therefore the bone marrow makes fewer red blood cells. Other common causes of anemia are from loss of blood during hemodialysis and low levels of iron and folic acid. Anemia often starts in the early stages of kidney disease and tends to worsen as the disease progresses. According to the NIDDK (2001a), nearly everyone with end-stage kidney failure has anemia.

A CBC (complete blood count) determines the hematocrit (Hct) or the percentage of the blood that consists of red blood cells. It also measures the amount of hemoglobin (Hgb) in the blood. If at least half of normal kidney function (serum creatinine is greater than 2 mg/dL) has been lost and Hct is low, the most likely cause of anemia is decreased EPO production. The National Kidney Foundation's Dialysis Outcomes Quality Initiative (DOQI) recommends that a detailed evaluation of anemia in men and postmenopausal women on dialysis should begin when the Hct value falls below 37%. For women of childbearing age, evaluation should begin when the Hct falls below 33%.

If no other cause for EPO deficiency is found, the deficiency can be treated with a genetically engineered form of the hormone (usually injected under the skin 2 or 3 times a week). Hemodialysis patients who cannot tolerate EPO injections in their skin can receive EPO intravenously during dialysis treatment. However, intravenous dosing requires a larger, more expensive dose and it may not be as effective.

Many people who need EPO treatment also need iron supplementation because EPO alone will not relieve the effects of anemia if iron levels are too low. Sometimes iron can be taken in a pill form, but according to the NIDDK, iron pills often do not work as well in people with kidney failure as iron given intravenously. Iron supplements should only be taken if prescribed by a physician based on blood analysis (National Kidney Foundation 2001e).

In addition to EPO and iron, some people also need vitamin B12 and folic acid supplements. Supplementation with EPO, iron, and appropriate B vitamins helps raise hemoglobin levels and most patients with kidney disease feel better, have more energy, and live longer (NIDDK 2001a).

L-Carnitine. For patients who are in a predialysis stage, are undergoing dialysis, or are post-transplant, nutritional supplementation with L-carnitine that has been lost during dialysis may reduce the side effects of common renal problems, such as cardiomyopathy and blood platelet aggregation, and may also help improve the patient's perception of their overall quality of life. L-carnitine is an amino acid that has shown effectiveness in providing cellular energy in both healthy individuals and those with chronic diseases.

General muscle weakness is a common complaint among patients undergoing hemodialysis. One study that measured the serum amount of L-carnitine found that hemodialysis lowered L-carnitine levels and posed new problems for patients (Wanic-Kossowska et al. 1998). This study measured muscle atrophy via nerve conduction and velocity testing and found indications of "neurogenic atrophy of the muscles." This well-known type of muscle weakness was further studied by doctors in Japan who reported that low dosages of L-carnitine (500 mg daily) showed improvement in two-thirds of 30 patients who were studied for 12 weeks. The patients reported less muscle weakness, general fatigue, and cramps and aches. This study concluded that low doses of L-carnitine could improve muscle weakness and should be considered as a prolonged adjuvant therapy for dialysis patients (Sakurauchi et al. 1998).

ESRD affects every aspect of a patient's life. Therefore, improved quality of life is very important for dialysis patients, potentially affecting compliance with medical, nursing, and nutritional prescriptions. In one study, patients were given the Medical Outcomes Study Short Form to assess quality of life from their perspective before taking L-carnitine and at 1.5-month intervals for the duration of the study (Sloan et al. 1998). This double-blind study was conducted on 101 patients who received L-carnitine or placebo just before and immediately after dialysis. After 3 months of supplementation (1 gram of L-carnitine before and after every hemodialysis treatment), patients reported an "improved vitality and general health." It was noted that serum albumin concentration was directly correlated with the patients' feelings of well being.

A study of L-carnitine therapy on erythropoiesis and blood platelet aggregation was conducted in patients with chronic renal failure, and it was found that L-carnitine caused a "significant rise in collagen-induced platelet aggregation." The 22-month study divided the patients into three groups. Group I received erythropoietin; Group II received erythropoietin and L-carnitine; and Group III received L-carnitine. Iron concentration and platelet count measured in urea concentration were relatively unchanged. The rise of collagen was observed after only 2 months of L-carnitine therapy (Kalinowski et al. 1999).

Curcumin. A potent antioxidant extract from the spice turmeric (Curcuma longa), curcumin has a wide range of health benefits: antiviral, anti-inflammatory, anticancer, and cholesterol-lowering. An interesting study in rats investigated the effect of curcumin on nephrosis caused by adriamycin. Adriamycin is a drug commonly used in chemotherapy (Venkatesan et al. 2000). The results indicated that curcumin "remarkably" prevented kidney injury caused by adriamycin. Venkatesan et al. (2000) stated that their data demonstrated that curcumin offered protection "by suppressing oxidative stress and increasing kidney glutathione content and glutathione peroxidase activity." They suggest that administration of curcumin offers promise in the treatment of nephrosis that is caused by adriamycin.

Another group (Suresh Babu et al. 1998) studied the effect of curcumin on streptozotocin-induced diabetes. Streptozotocin is also a commonly used chemotherapy drug. According to Suresh et al. (1998), their data "suggested that dietary curcumin brought about significant beneficial modulation of the progression of renal lesion in diabetes." This benefit of dietary curcumin on diabetic nephropathy may be mediated by its ability to lower blood cholesterol levels.

Ginkgo Biloba. Already known for its antioxidant effects, ginkgo biloba may also protect small blood vessels against loss of tone, prevent capillary fragility, inhibit atherosclerosis, and treat diabetic vascular disease. Naidu et al. (2000) studied gentamicin-induced nephrotoxicity in rats. Gentamicin is an antibiotic used to treat serious infections. Unfortunately, it has the undesirable side effects of causing kidney damage and irreversible hearing loss. Naidu et al. (2000) found that gentamicin treatment increased levels of blood urea and serum creatinine. However, they also found that ginkgo biloba extract (GBE) protected the rats from gentamicin-induced nephrotoxicity by preventing changes in blood urea, serum creatine, and creatine clearance.

Also in a study in rats, Umegaki et al. (2000) examined the effects of GBE extract on the development of hypertension, platelet activation, and renal dysfunction in deoxycorticosterone acetate-salt hypertensive rats. After 20 days, the rats fed a 2% GBE diet had attenuated development of hypertension.

In another interesting study in rats by Fukaya et al. (1999), encouraging results of co-administration of cisplatin and GBE were reported. Cisplatin is an effective antineoplastic agent (cancer killing) used for treating solid tumors. However, cisplatin also has the undesirable side effects of causing hearing loss and nephrotoxicity. Fukaya et al. (1999) concluded that co-administration of cisplatin with GBE was beneficial to ameliorate cisplatin-induced toxicity without attenuating the antitumor activity of cisplatin.

Grape Seed Extract. Known for its powerful antioxidant qualities, grape seed extract also acts as a smooth muscle relaxant in blood vessels to combat hypertension. Ray et al. (2000) studied the protective effects of grape seed extract against biological, pharmacological, and toxicological effects of certain drugs to the kidneys, lungs, and heart in mice (acetaminophen, amiodarone, and doxorubicin). Ray et al. (2000) found that "grape seed extract preexposure prior to acetaminophen, amiodarone, and doxorubicin provided near complete protection in terms of serum chemistry changes and significantly reduced DNA fragmentation." Moderate to massive tissue damage occurred by all three drugs in the absence of grape seed extract. Bagchi et al. (2000) also found that grape seed extract "demonstrated excellent protection against acetaminophen overdose-induced liver and kidney damage."

Green Tea. Yokozawa et al. (1999) studied the effects of green tea tannin to ameliorate cisplatin-induced renal injury in rats. They found that green tea tannin suppressed the cytotoxicity of cisplatin, "the suppressive effect increasing with the dose of green tea tannin." Additional testing showed rats given green tea tannin had decreased blood levels of urea nitrogen and creatinine and decreased urinary levels of protein and glucose, indicating less kidney damage. Yokozawa et al. (1999) concluded that "based on the evidence available, it appeared that green tea tannin eliminated oxidative stress and was beneficial to renal function." Earlier, researchers (Wardle 1999; Yokozawa et al. 1996) reported that green tea tannin was found to be beneficial for the kidney under oxidative stress. In 1991, Mukoyama et al. found that green tea had antiviral activity, inhibiting rotaviruses and enteroviruses in rhesus monkeys.

Soy. There is evidence that dietary phytoestrogens have a beneficial role in chronic renal disease (Velasquez et al. 2001; Ranich et al. 2001). Nutritional intervention studies demonstrated that consuming soy-based protein and flaxseed reduced proteinuria and attenuated renal functional or structural damage in both animals and humans. To date the studies have been of relatively short durations and involved small numbers of subjects. However, the results are encouraging and further investigations are needed. Three groups of researchers (Tomobe et al. 1998; Aukema et al. 1999; Ogborn et al. 2000) investigated the effects of a soy protein diet on polycystic kidney disease. Although the studies were conducted in rats and mice, the research teams suggested that dietary soy protein-based diets had beneficial effects in polycystic kidney disease: soy diet prevented significant elevation in serum creatinine in diseased vs. normal animals (Ogborn et al. 2000); soy protein is effective in retarding cyst development and this beneficial effect may be unrelated to genistein (an isoflavonoid present in soy protein) content (Tomobe et al. 1998); dietary protein level and source significantly affect polycystic kidney disease, with the effects being most pronounced in female animals fed low protein diets and soy protein-based diets (Aukema et al. 1999).

Taurine. Taurine is abundant in the brain, heart, gallbladder, and kidneys and plays an important role in health and disease in these organs. Taurine is an amino acid that has been shown to protect against experimentally induced lipid peroxidation of the renal glomerular and tubular cells and may alleviate tubular disorders such as glomerular impairment (Trachtman et al. 1996). It is also thought to lower blood pressure by balancing the ratio of sodium to potassium in the blood. Taurine may also regulate the increased nervous system activity that can contribute to high blood pressure. According to Franconi et al. (1995), some people with Type I diabetes appear to be deficient in the amino acid taurine.

Trimethylglycine (Betaine). Trimethylglycine (TMG) plays a role in the manufacture of carnitine and serves to protect the kidneys from damage (Chambers 1995). TMG has been reported to play a role in reducing blood levels of homocysteine, a toxic breakdown product of amino acid metabolism that is believed to promote atherosclerosis. The main nutrients involved in controlling homocysteine levels are folic acid, vitamin B6 and vitamin B12, but TMG has been reported to be helpful in some individuals whose elevated homocysteine levels did not improve with these other nutrients. TMG has also shown to be helpful in certain rare genetic disorders involving cysteine metabolism (Wilken et al. 1983; Wendel et al. 1984; Gahl et al. 1988; Barak et al. 1996; Selhub 1999; van Guldener et al. 1999). Its primary use as a nutritional supplement is in supporting proper liver function and possibly reducing the risk of urinary tract infections.


SUMMARY

The kidneys are remarkably resilient organs and can sometimes recover normal function from acute trauma as a result of injury, overdose of drugs, or poisoning, with prompt medical attention. However, there are forms of kidney disease that include conditions that can rapidly reduce kidney function or slowly reduce kidney function over several years, producing few or no symptoms. Damage from these conditions is not reversible. When kidney function is reduced to less than 10-15%, dialysis is required. When dialysis is no longer able to support kidney function, kidney transplantation is the only recourse.

If you have healthy kidneys, protect them. Start with a healthy diet; drink lots of water; give careful attention to the over-the-counter medicines you take, particularly when combined with prescription medicines or other over-the-counter products; consume alcohol responsibly (remember, over-the-counter or prescription drugs can be very damaging to the kidneys when combined with alcohol); protect your kidneys from injury if you engage in sporting activities; and consider taking protective supplements and nutrients to support overall kidney health.

As part of an annual physical checkup, request tests for blood levels of creatinine and blood urea nitrogen and urine levels of protein. Small elevations of creatinine can be an early sign of kidney disease. Early detection leads to early treatment which can occur at a stage when there is treatment to help prevent kidney disease from advancing to a more serious stage.

Because diabetes is the leading cause of chronic kidney disease, followed by hypertension, see your physician regularly and follow prescribed dietary and drug treatment to control blood sugar levels and hypertension (National Kidney Foundation 2001a) (refer to the Life Extension protocols on Diabetes and Hypertension for additional information).

Prevent damage to the kidneys from kidney stones by increasing water intake to 12 full glasses of water every day; limiting coffee, tea, and colas because caffeine increases fluid loss; increasing calcium intake using dietary factors; and including appropriate calcium/magnesium supplementation (taken only with food).

Research into gene therapy holds great hope for genetic kidney diseases. Of particular interest is research on the PKD1 gene, which is responsible for 85% or more of all ADPKD disease. ADKPD often progresses to kidney failure in young adulthood or middle age and accounts for the need for kidney transplantation for many persons.

If you have early stage kidney disease or chronic kidney disease, follow the dietary recommendations of your physician or a renal dietitian. For example, a diet low in sodium, potassium, and phosphorus, three substances regulated by the kidneys, is essential in managing kidney disease. Other dietary restrictions, such as reducing protein, may be required depending on the cause of kidney failure and the type of treatment being used (e.g., such as dialysis). Patients with chronic kidney failure may also need to limit their fluid intake.