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Kidney Health

Natural and Adjuvant Treatment

Dietary Management

In the early stages, careful dietary management may slow down the process of kidney disease. A diet low in sodium, potassium, and phosphorus, three substances regulated by the kidneys, is essential in managing kidney disease. Other dietary restrictions (eg, reducing protein) may also be required. Your physician might suggest you consult a renal dietitian with special training in diets for persons with kidney disease. Vegetarians have diets that are naturally high in potassium and phosphorus; therefore, need good nutritional advice. If required to limit phosphorus, sodium, or protein, remember the following:

  • Phosphorus is especially high in dairy products (eg, milk, cheese, ice cream), dried beans and peas, nuts and peanut butter, some salt substitutes, cocoa, beer, and cola soft drinks.
  • Sodium is especially high in table salt, canned soup, processed cheese, snack foods, prepared and "fast foods," pickles, olives, sauerkraut, and smoked and cured food (eg, ham, bacon, luncheon meat).
  • Protein is especially high in food from animal sources (eg, poultry, meat, seafood, eggs, and dairy products). Protein is found in smaller amounts in food from plant sources (eg, bread, cereal, grain, vegetables, and fruit).

However, a certain amount of phosphorus, sodium, and protein is necessary for good health. To keep yourself healthy, it is important to learn to read labels and make better choices. For example, non-dairy creamers and milk substitutes are a good way to lower dietary phosphorus.

Avoid losing too much weight. It is important to maintain a good calorie intake because calories give you energy. If limiting protein, get more calories from other food sources including (NKF 2002):

  • Unsaturated fats from oils (eg, canola or olive oil).
  • Simple carbohydrates (eg, honey, jam, and jelly)
  • Note: The recommendations for using sugar may not be appropriate for diabetics or overweight individuals. If you are diabetic, consult your physician or renal dietitian for alternative recommendations.

Dietary Supplements

Dietary supplements are often recommended by physicians and renal dietitians (National Kidney Foundation 2001e). Their recommendations are guided by regular blood testing utilized to monitor kidney function. Always speak with a physician or renal dietitian before using or adding any supplements or herbal products.

Multivitamins. In addition to a diet containing appropriate nutrients and protein, a comprehensive multivitamin is often required to replace vitamins lost during dialysis treatments (National Kidney Foundation 2001e).

B Vitamins. Vitamins B6, B12, and folate (folic acid) are members of the B vitamin group. The B vitamins are known for having many beneficial qualities, including promoting growth, improving heart function, lowering homocysteine, protecting against atherosclerosis caused by excess homocysteine, helping with the formation and regeneration of red blood cells (thus preventing anemia), and increasing energy as well as endurance (McGregor 2000).

The formation of advanced glycation end-products (AGEs) is a well-established factor in the onset and progression of kidney disease.

A formidable AGE antagonist is the vitamin B6 compound pyridoxamine. A plethora of research confirms its power to halt formation of AGEs (Voziyan 2005; Ahmed 2007; Williams 2006). Evidence has also emerged that pyridoxamine drastically limits formation of equally deadly advanced lipoxidation end products (ALEs)—another deadly catalyst for kidney disease (Alderson 2004; Metz 2003; Metz 2003).

A convincing body of research on pyridoxamine therapy in humans with CKD has also emerged in recent years. In 2007, researchers set out to determine optimal interventions to halt the progression of kidney disease in diabetics (Williams 2007). They conducted two 24-week multicenter placebo-controlled trials in patients with known diabetic nephropathy—treatment of which is known to delay the onset of ESRD in diabetics. Doses of pyridoxamine ranged from 50 to 250 mg twice daily.

Pyridoxamine significantly inhibited the waste product creatinine, one of the key biomarkers of kidney dysfunction and a predictor of kidney failure. Urinary levels of inflammatory cytokines were also significantly lower in the treated group compared to controls.

In 2009, the FDA classified pyridoxamine as a drug, putting it out of reach for many Americans suffering from this deadly condition. No one should be forced to bear the outrageous burden of costly pharmaceuticals and their toxic side effects when a perfectly safe alternative exists.

Fortunately, an equally safe option exists; that is, another form of vitamin B6 known as pyridoxal-5-phosphate (P5P) that also exerts potent anti-AGE effects. P5P has been shown to prevent the progression of diabetic kidney disease in pre-clinical models (Nakamura 2007). In fact, as far back as 1988, it was used by a German research group to reduce blood lipids in humans with CKD (Kirsten 1988).

Vitamin C. Vitamin C is an antioxidant that helps keep many different types of tissues healthy. Vitamin C, which helps wounds and bruises heal faster, 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 using rats, it was found that a dietary deficiency of vitamin E caused progressive and pronounced renal damage (Sadava 1996). 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 bones healthy. Calcium is also used to bind to dietary phosphorus. Speak to a physician about taking calcium (National Kidney Foundation 2001e).

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

Potassium. Another kidney function is to maintain the right amount of potassium. Potassium plays an essential role in keeping the heartbeat regular and other muscles working properly; however, high blood levels of potassium are to be avoided. In order to help control potassium levels, avoid foods high in potassium (National Kidney Foundation 2001d).

Iron. Because red blood cells carry oxygen to all tissues and organs throughout the body, low levels of oxygen may result in reduced performance of vital organs (including the kidneys). Anemia (ie, a low level of red blood cells) 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; therefore, bone marrow makes fewer red blood cells. Other common causes of anemia include 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. It has been shown that nearly everyone with end-stage kidney failure has anemia (NIDDK 2001a).

A CBC (complete blood count) measures the hematocrit (Hct) (ie, percentage of blood consisting of red blood cells) and amount of hemoglobin (Hgb) in the blood. If at least half of normal kidney function (ie, serum creatinine > 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 Hct falls below 37%. For women of childbearing potential, evaluation should begin when Hct falls below 33%.

If no other cause for EPO deficiency is found, it 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 that may not be as effective.

Because EPO alone will not relieve the effects of anemia if iron levels are too low, many people who require EPO treatment also need iron supplementation. Iron can be taken in a pill form; however, according to the NIDDK, iron pills often do not work as well in people with kidney failure as intravenous iron. Iron supplements should only be taken if prescribed by a physician based on blood results (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 help raise hemoglobin levels resulting in most kidney disease patients feeling better, having more energy, and living longer (NIDDK 2001a).

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

General muscle weakness is a common complaint among patients undergoing hemodialysis. One study that measured serum L-carnitine found that hemodialysis lowered L-carnitine levels and posed new problems for patients (Wanic-Kossowska 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 20 of 30 patients studied for 12 weeks. The patients reported less muscle weakness, general fatigue, 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 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 before taking L-carnitine and at 1.5-month intervals for the duration of the study (Sloan 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. The 22-month study divided the patients into 3 groups (group 1 received erythropoietin alone, group 2 received erythropoietin and L-carnitine, and group 3 received L-carnitine alone). Iron concentration and platelet count measured in urea concentration were relatively unchanged. However. it was noted that L-carnitine therapy caused a "significant rise in collagen-induced platelet aggregation" after 2 months Kalinowski 1999).

Coenzyme Q10. Because of tremendous blood flow and high concentration of metabolic toxins continuously circulating through the kidneys, they are the site of extraordinary oxidative stress, which is known to contribute to progressive kidney damage and its complications (eg, high LDL and increased cardiovascular disease risk) (Gazdikova 2000).

CoQ10 fortifies the body’s natural antioxidant capacity and reduces levels of oxygen free radicals, indicating its important defense against CKD. CoQ10 has been used experimentally to control hypertension and kidney disease in laboratory animals since the early 1970s (Igarashi 1974; Morotomi 1975).

Human studies have shown that CoQ10 levels substantially decline, while markers of oxidation (eg, malondialdehyde) are dramatically elevated in kidney disease patients with even mild renal dysfunction (Yao 2007). Decreased CoQ10 levels also make circulating lipoproteins (eg, LDL) more vulnerable to oxidative damage, which in turn increases risk for further cardiovascular damage, adding to renal burden and substantially increasing risk of kidney disease (Lippa 2000).

Kidney disease patients that undergo transplantation typically have marked disturbances in lipid profiles as a result of tremendous oxidative stress. The European group supplemented their patients with 30 mg of CoQ10 3 times daily for 4 weeks, and monitored levels of oxidation factors (such as malondialdehyde), natural antioxidant enzymes in the body, and lipid profiles (Dlugosz 2004).

Significant improvements were seen after 4 weeks, with a reduction in LDL, increase in beneficial HDL, and decrease in the presence of inflammatory cells. These results suggest a potentially dramatic improvement in both quality of life and survival rates for patients whose disease has progressed to the point of kidney failure (ie, requiring transplantation or dialysis). They also bode well for those with early-stage kidney disease.

Animal studies have also shown that CoQ10 can protect kidney tissue from numerous nephrotoxic drugs, including gentamicin, a powerful antibiotic with a notorious propensity for causing kidney damage (Farswan 2005; Upaganlawar 2006).

Silymarin. Silymarin is extracted from milk thistle (Silybum marianum), a plant rich in the flavonolignans silychristin, silydianin, silybin A, silybin B, isosilybin A and isosilybin B, which are collectively known as the silymarin complex.

This safe, natural compound has a long history as a traditional therapy for liver and kidney conditions (Post-White 2007; Wojcikowski 2007). It has been used in Western medicine for more than a quarter of a century as the treatment of choice for serious kidney injury resulting from severe mushroom poisoning, owing to its potent antioxidant and nephron-protective effects (Floersheim 1978). In fact, it was noted in 1979 that kidney injury by mushroom poisoning in animals pre-treated with silymarin can be almost entirely prevented (Vogel 1979). These effects make it a natural choice for protection against drug-induced kidney damage, since so many drugs can act like poisons, exerting extreme oxidant stress on kidney tissue.

Mushroom poisons (mycotoxins) are among the most deadly natural toxins known. Their kidney toxicity is surpassed only by some of the most aggressive chemotherapy agents. Physicians have therefore looked to silymarin as a potential “renoprotective” agent for patients undergoing chemotherapy.

Silymarin is also protective against several classes of nephrotoxic drugs, in particular cisplatin and Adriamycin®, two of the most potent chemotherapeutic drugs—but also two of the most damaging to the kidney owing to oxidative damage and severe inflammation (Launay-Vacher 2008; Machado 2008; Yao 2007). Researchers around the world have found that silymarin and its components reduce and often entirely prevent kidney damage caused by these drugs (Bokemeyer 1996; Gaedeke 1996; Karimi 2005; El-Shitany 2008).

Curcumin. Curcumin is a potent antioxidant extract from the spice turmeric (Curcuma longa). It has a wide range of health benefits: antiviral, anti-inflammatory, anticancer, and cholesterol-lowering. A study in rats investigated the effect of curcumin on nephrosis caused by Adriamycin (ie, a drug commonly used in chemotherapy) (Venkatesan 2000). Results indicated that curcumin "remarkably" prevented kidney injury caused by Adriamycin. The researchers in this study 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 caused by Adriamycin.

Another group studied the effect of curcumin on streptozotocin-induced diabetes. Streptozotocin is also a commonly used chemotherapy drug. 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 (Suresh Babu 1998).

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. Gentamicin-induced nephrotoxicity in rats was studied (Naidu 200). Gentamicin is an antibiotic used to treat serious infections. Unfortunately, it can cause kidney damage and irreversible hearing loss. This study 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 creatinine, and creatinine clearance.

In another study, the effects of GBE on the development of hypertension, platelet activation, and renal dysfunction in deoxycorticosterone acetate-salt hypertensive rats were examined. After 20 days, the rats fed a 2% GBE diet had attenuated development of hypertension (Umogaki 200).

In yet another study in rats, encouraging results of co-administration of cisplatin (ie, an effective antineoplastic [cancer killing] agent used for treating solid tumors) and GBE were reported (Fukaya 1999). However, cisplatin can also cause hearing loss and nephrotoxicity. This study concluded that co-administration of cisplatin with GBE was beneficial to ameliorate cisplatin-induced toxicity without attenuating the antitumor activity of cisplatin.

Resveratrol. The considerable advance in our understanding of the cyclical relationships between oxidative stress, endothelial dysfunction, inflammation, atherosclerosis, and chronic kidney disease points to resveratrol as an intervention in the chain of events that ultimately lead to renal failure (Caimi 2004).

Italian researchers are among the leaders in resveratrol research. One group published remarkable research demonstrating the impact of resveratrol on preserving kidney structure and function in rats exposed to ischemia/reperfusion injury (Bertelli 2002; Giovannini 2001).

Japanese and Indian urologists followed that up in 2005 and 2006 with reports detailing the mechanisms by which resveratrol combats oxidative damage following reperfusion, markedly reducing kidney dysfunction (Saito 2005; Chander 2005a,b; Chander 2006a,b). Overwhelming bacterial infections (sepsis) are a common cause of kidney failure in the intensive care unit and following surgery or trauma. Turkish physiologists demonstrated that resveratrol can reduce or prevent both kidney and lung injury in septic rats (Kolgazi 2006).

Resveratrol’s unmatched antioxidant and anti-inflammatory potential has been tapped in studies of its ability to prevent drug-induced kidney damage as well. Nephrotoxicity in rats exposed to the antibiotic gentamicin was significantly reduced and more rapid healing of injured kidney tissue was attained using resveratrol, with dramatic reduction in markers of oxidant injury (Silan 2007). A team of toxicologists in Brazil demonstrated its kidney protective power against cisplatin, the powerful chemotherapy agent responsible for drug-induced kidney damage (Do Amaral 2008). Finally, by pretreating the animals with resveratrol, Indian pharmacologists were successful in protecting animal kidneys from damage caused by cyclosporine A, another common chemotherapy and immune suppressant drug (Chander 2005b).

Since diabetes is the leading cause of kidney disease—and because the damage it inflicts is largely mediated by free radical production resulting from destructive alteration of proteins by glucose (glycation)—researchers have explored resveratrol as a preventive in diabetic kidney damage. Indian pharmacologists have shown that they could significantly attenuate kidney damage in rats with experimentally induced diabetes, even 4 weeks after the diabetes was induced (Sharma 2006).

Lipoic acid. Lipoic acid is a powerful antioxidant with few known side effects (Amudha 2006). Lipoic acid has been successfully employed in the laboratory to block oxidative damage caused by ischemia/reperfusion injury, thereby opening the door to another effective treatment for this common cause of acute kidney failure (Takaoka 2002). In 2008, researchers showed that they could reverse all adverse effects on renal function and lab abnormalities following experimental ischemia/reperfusion injury in animals (Sehirli 2008).

Lipoic acid has been comprehensively studied worldwide for its power to prevent or mitigate drug-induced kidney damage. Lipoic acid is an effective kidney-protective agent against damage inflicted by Adriamycin® (Malarkodi 2003a,b), the immunosuppressive drug cyclosporine A (Amudha 2006; Amudha 2007a,b), and even against acute toxic doses of the pain reliever acetaminophen. In studies of protection against cyclosporine toxicity, lipoic acid also helped to normalize blood lipid abnormalities (Abdel-Zaher 2008).

Nephrologists at Georgetown University are examining lipoic acid in the context of diabetic kidney disease. Their results show it can improve renal function in diabetes by lowering sugar levels (Bhatti 2005).

They have also recently demonstrated that lipoic acid lowers proteinuria (ie, protein loss in urine) and improves kidney structure and function in diabetic laboratory animals by reducing oxidative stress (Bhatti 2005).

Green Tea. The effects of green tea tannin to ameliorate cisplatin-induced renal injury in rats were studied (Yokozawa 1999). 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. This study concluded that "based on the evidence available, it appeared that green tea tannin eliminated oxidative stress and was beneficial to renal function." Earlier, researchers reported that green tea tannin was found to be beneficial for the kidney under oxidative stress (Wardle 1999; Yokozawa 1996). In 1991, it was found that green tea had antiviral activity, inhibiting rotaviruses and enteroviruses in rhesus monkeys (Mukoyama 1991).

Soy. There is evidence that dietary phytoestrogens have a beneficial role in CKD (Velasquez 2001; Ranich 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. Study results are encouraging and further investigations are needed. Three groups of researchers investigated the effects of a soy protein diet on polycystic kidney disease (Tomobe 1998; Aukema 1999; Ogborn 2000). Although the studies were conducted in rats and mice, research teams suggested that 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 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 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 1999).

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

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 believed to promote atherosclerosis. The main nutrients involved in controlling homocysteine levels are folic acid, vitamins B6 and B12; TMG, however, 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 (Wilcken 1983; Wendel 1984; Gahl 1988; Barak 1996; Selhub 1999; van Guldener 1999). Its primary use as a nutritional supplement is in supporting proper liver function and possibly reducing the risk of urinary tract infections.


Kidneys are remarkably resilient organs that with prompt medical attention can sometimes recover normal function from acute trauma as a result of injury, drug overdose, or poisoning. However, there are forms of kidney disease that include conditions that can either rapidly 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 can no longer support kidney function, kidney transplantation is required.

If you have healthy kidneys, protect them. Eat a healthy diet, drink a lot of water, pay careful attention to use of over-the-counter medication(s) (particularly when combined with prescription medication or other over-the-counter products), consume alcohol responsibly (over-the-counter or prescription drugs can be very damaging to the kidneys when combined with alcohol), protect kidneys from sports-related injury, and consider taking protective supplements and nutrients to support overall kidney health.

As part of an annual physical, request creatinine and blood urea nitrogen (BUN) be checked, along with urine protein levels. 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 treatment may help prevent kidney disease from advancing to a more serious stage.

Because diabetes is the leading cause of CKD, followed by hypertension, see your physician regularly and follow prescribed dietary and drug treatment to control blood sugar and blood pressure levels (National Kidney Foundation 2001a). Refer to the Life Extension’s Diabetes and High Blood Pressure protocols for additional information.

Prevent kidney stones by increasing water intake to 12 full glasses daily, limiting caffeine (eg, coffee, tea, and colas) because it increases fluid loss, increasing dietary calcium, 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 cases. ADKPD, often progressing to kidney failure in young adulthood or middle age, results in kidney transplantation for many individuals.

If you have early stage or CKD, follow the dietary recommendations of your physician or 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 (eg, reducing protein) may be required depending on the cause of kidney failure and type of treatment being used (eg, dialysis). Patients with chronic kidney failure may also need to limit their fluid intake.