WHEN BLOOD POTASSIUM is too HIGH (Hyperkalemia), chapter XIII

by Charles Weber, MS

This article explores some possible strategies for those whose blood potassium is high (hyperkalemia). Do not rely solely on this discussion of nutrients and strategies, but seek other consultation from medical doctors and nutritionists as well.

CONTENTS of other chapters: Back to INTRODUCTION chapter -- II. Arthritis Research -- III. Arthritis and Potassium -- IV. Roles of Potassium in the Body -- V. Electrolyte regulation (sodium and potassium) -- VI. Purpose of cortisol -- VII. Copper nutrition and physiology -- VIII. Nutritional Requirements -- IX. Potassium in Foods -- X,cont. Losses in the kitchen -- XI. Supplementation -- Side Effects and Heart Disease -- XIV Potassium and thiamin in heart disease -- Strategies for CFS and fibromyalgia

POTASSIUM NUTRITION (a book by Charles Weber) Potassium losses from perspiration, in urine, during diarrhea, from stress, poisons, and disease states are discussed in the book available here, as well as methods to supplement potassium safely, especially as involved in heart disease, gout, high blood pressure, and rheumatoid arthritis, and indirectly in diabetes. It is published by iUniverse publishing company and it is a very comprehensive book about potassium, probably much more so than any other. You may see the table of contents with chapter summaries and the introductory chapter by clicking here.

We comply with the HONcode standard for trustworthy health
verify here.


Some people are afflicted with high potassium in their blood (hyperkalemia). Even a fairly small consistent rise in serum or plasma potassium of 0.5 milliequivalents (meq) or so over the norm, which is 4.8 [Scribner], is cause for some concern, because a healthy body is capable of a rather precise regulation of potassium, and a considerable portion of the kidney (renal) function must be gone before symptoms start to show. In my opinion the potassium must rise 1.0 meq/liter or so before one would start to use the word alarm. The electrocardiogram changes at 6.5 meq [Seekles]. I believe the dangerous symptoms of metabolic shock start to materialize after about 7.0 meq. I believe death is possible in the vicinity of 8.0 meq at which point the first clinical symptoms of heart failure appear [Seekles] and that life is impossible beyond 10.0 meq or so. Very high potassium that gives very noticeable symptoms is a MEDICAL EMERGENCY AND A HOSPITAL SHOULD BE SOUGHT. Only 2 or 3 decades ago potassium was not even listed in the index of books devoted to discussing metabolic shock, even though metabolic shock IS high blood potassium. It was another manifestation of the cavalier attitude of most medical professionals toward potassium then and to a considerable extent now. Potassium supplements were referred to by such euphemisms as “pharmaceuticals”, “salt substitutes”, “polarizing solutions”, “GIK”, and “ORT salts”. It is so even today to some extent.

Before assuming that your potassium is too high be sure that the analysis of blood is of plasma and not of serum since serum can give inaccurately high readings. Analysis of serum within one half hour would prevent the disparity [Bellevue]. This inaccuracy results when blood stands at low temperatures and potassium can leak from the cells and also there can be cell losses if the blood is handled roughly. Even without poor technique serum potassium will be higher than plasma by 0.2 meq/liter in normal subjects [Ifudu]. ]. Even with careful determination plasma potassium can be anonymously high because of potassium losses from platelets during rheumatoid arthritis. A difference of 0.4 mEq/liter can occur when platelets release potassium. [Ifudu]. If there is an inappropriate high reading there can be a degrading of health from the treatment itself as well as sometimes high, unnecessary expense. Electrocardiogram readings (ECG) can act as a check on serum analysis in the case of readings above 5.5 or so and affects on the heart are the most important manifestations anyway. As levels increase, the first ECG change is tall peaked T waves. The QT interval is normal or diminished. As potassium levels continue to rise, the PR interval becomes prolonged, then the P wave amplitude decreases. The QRS complex widens into a sine wave pattern, with subsequent cardiac arrest.


There are things one can do to ameliorate high blood potassium temporarily at home, and I will propose some possible strategies. However, high blood potassium is a symptom of a rather serious underlying problem and you should contact a medical professional and make a great effort to find out what the problem is and correct it if at all possible. You may see mention of the symptoms of too high a blood potassium [Recheigl] in Chapter XI, on supplements and Chapter XII, on side effects which also has many of the references for statements in this article. Some symptoms are said to be irregular or fast heartbeat, paralysis of limbs, drop in blood pressure, convulsions, coma, cardiac arrest, black or bloody stool, diarrhea, confusion, breathing difficulty, vomiting, extreme fatigue, irregular heart beat, nausea, numbness, tingling hands and feet, and breathing difficult. The two most likely causes of a chronic situation are damaged kidneys or a hormone disruption. People tend to get despondent at such times, and not completely without reason. However, if the underlying cause is removed, and you then eat, drink (such as fluoride), or breath (translate; smoke) no poison and receive all the nutrients originally in your food including most of a small amount of protein from high quality sources such as meat, eggs, and milk and no overwhelming amounts of any (say sodium, chloride, zinc, vitamin B-1, or phosphate of soft drinks) and get plenty of exercise (one contraindication to the value of excessive exercise is probably chronic fatigue syndrome or CFS (CFIDS)), it is my belief that there is a good chance that adequate healing will usually take place if the damage has not been overwhelming. The body has considerable power to repair itself for most tissue, although I am not certain of the kidney’s ability to do so. If there has been extensive damage to the kidneys it probably will not be possible to return completely back to normal especially in people past 15 years of age or so, but this need not be cause for despair because a healthy pair of kidneys has much more capacity than they need to just maintain normal life. They are said to be able to unload 26,000 mg of potassium in a day if necessary [Peterson]. So losing some capacity is not necessarily ruinous. I could be mistaken in this, but if it were me, I would not give up trying, even if I was on a dialysis machine. Keep in mind that people beyond 50 or 60 usually heal up slowly though, and much more than a year may be necessary if it is possible. In the rare cases when a genetic defect is involved the underlying problem may be intractable. However some reasonable changes in lifestyle may nevertheless ameliorate the situation.

It is instructive to know what the possible causes of high blood potassium are. Most of them are probably renal (kidney) failure. Diabetes causes over 30% of kidney failure for unknown reasons. Forty percent of persons with Type I diabetes and 30-40% of persons with Type II diabetes develop the renal microvascular complication of diabetes known as diabetic nephropathy. Once this develops the disease inevitably progresses to renal failure making diabetes the most common cause of end stage renal disease in the United States. In kidney failure during diabetes, potassium elevates after eating 100 grams of glucose, unlike normal people who show a slight decline [Knochel p447]. The slight decline in normal people is no doubt related to the fact that insulin along with adrenaline stimulates the cell’s potassium pump in muscles. I suspect that this in order to furnish potassium to form glycogen. About 30% are related to hypertension, which itself is at least several syndromes. Black people have 18 times more hypertensive kidney failure than white people which Tobian believes is due to a much lower potassium intake. Potassium protects against lesions of the kidney tubules, arteries, and glomeruli [Tobian]. As many as 15% of cases are thought to result from atherosclerotic renovascular disease from plaque build up on the kidney arteries, which in turn, along with glomerular derangement, may often be from a copper deficiency combined with a high salt intake [Moore]. Osteoarthritis itself probably does not cause kidney damage, but too much acetaminophen (Tylenol, Anacin-3, Liquiprin, Panadol. and Tempra) taken for it probably will. Tylenol also damages the liver. Since pain-killing drugs usually do not cure a disease, it is usually better to tolerate the pain if at all possible. An additional reason is that painkillers have been implicated as a risk factor in acquiring chronic fatigue syndrome (CFS). I do not know which ones are implicated yet. One exception to adverse affects of pain medicines may be Methylsulfonylmethane (MSM). It is said to be fairly effective and virtually free of side affects. Pain, itself, can cause increased losses of potassium but I do not know if it can cause increased retention. I suspect not. People at risk, such as diabetics, should have regular urine and blood tests so that if small changes show up from the baseline they can be alerted to a much more serious underlying problem since kidney capacity is normally much more than we need and obvious problems are late in showing up. Systemic lupus erythmatosis (SLE or lupus) has caused such extensive damage to kidney tubules that the patients had chronic high plasma potassium which was not responsive to aldosterone [De Pronzo]. Since Lupus patients have been shown to have visibly damaged tubule in 66% of patients examined, the investigators believe that this hyperkalemia is more common than realized. Since Lupus is listed as one of the arthritic diseases and has some similar symptoms, there may be a temptation to use potassium supplements to heal it. Not only should this probably not be attempted, but also even foods high in potassium may be undesirable in the light of this report. Maybe with some lupus victims potassium intake must have a narrow safe range. Research to cast light on this would be highly desirable. Several circumstances have been found to act oppositely in rheumatoid arthritis from lupus such as pregnancy, estrogen, and schizophrenia [Mawson].

Other causes of hyperkalemia are crush injury, severe burns, hemolysis (red blood cell destruction), hyperkalemic periodic paralysis (during paralysis episodes), acute tumor destruction after chemotherapy, transfusion of hemolyzed (aged) blood, Addison’s disease (rare), hypoaldosteronism (very rare), severe dehydration, and respiratory acidosis. The last is a failure of the lungs to remove carbon dioxide leaving behind carbonic acid. Since acid (hydrogen and ammonium ion) interferes with potassium excretion, potassium can build up. Respiratory acidosis can result from failure of the lung to remove carbon dioxide because of bronchitis, asthma or airway obstruction. In this case, the hyperkalemia can be mild or severe. People who have weak kidneys probably should sleep at night with the window open. In my opinion excessive dreaming is an indication of high carbon dioxide in the air. It is also conceivable that there is rarely such a thing as a 16alpha,18dihydroxydeoxycorticosterone tumor analogous to aldosterone tumors rarely. It would presumably cause potassium to be retained. If such a tumor exists, I have not heard of it being reported.

There are several poisons which can cause high blood potassium (hyperkalemia) for a short time after actual use. Angiotensin-converting enzyme (ACE) inhibitors {Captopril, Enalapril, Fosinopril}, non-steroid anti-inflammatory drugs (NSAIDs) {Indomethacin, Ibuprofen, Ketorolac}, and potassium sparing diuretics {spironolactone, triamterene, amiloride} prevent excretion. The combined use of nonsteroidal anti-inflammatory drugs (NSAIDs) and beta-adrenergic blockers may increase the risk of life-threatening hyperkalemia [Kaufman p83] through their suppressive effect on the renin-aldosterone system, whereas the simultaneous administration of Lobenzaret (CCA) with NSAIDs through impairment of the renal tubular function [Ichinohe]. Cox-2 medicines for rheumatoid arthritis have a damaging affect on kidney function. I do not know what the affect on potassium excretion is. Angiotensin receptor blockers {Losartan, Valsartan, Irbesartan, Candesartan} and antiinfective agents {Trimethoprim-sulfamethoxazole, pentamidine} are said to be involved by a mechanism unknown to me. Digitalis glycosides, digoxin, and oleander (nerium oleander fluoride) inhibits the sodium/potassium cell wall pumps. Arginine (nuts and chocolate are very high in arginine), hypertonic solutions, and salts cause cell leakage. The inclusion of fluoride above would seem to cast some doubt on use of fluorinated water for those with hyperkalemia or old people (and certainly everybody) especially since fluoride has been proposed to inhibit the thyroid and damage the kidneys. The National Kidney Foundation has issued a warning against use of fluoridated water in dialysis. Researchers have demonstrated the existence of an unusually strong hydrogen bond between the fluoride ion and amides (RCONHR') which they suggest may be involved in how fluoride interferes with normal biological functioning. Whereas the fluoride ion is comparatively stable in aqueous solution and not very reactive in normal covalent bond-forming and bond-breaking reactions, "its strong hydrogen bonding potential toward the NH group of amides and related biomolecules," provides”, in the words of Emsley, et al., "an explanation of how this reputedly inert ion could disrupt key sites in biological systems." (scroll down)Fluoride has also been linked to bone cancer in boys. Richmond says that fluorinating water has no perceptible affect on kidneys in children, but that fluoride in water for dialysis should be controlled [Richmond p133, 134]. For old people who are forced to drink a lot of water (or imagine they are) fluoridation seems a very dubious strategy to me though. Drinking it may not be the only problem. It has been proposed that we get even more fluoride from taking showers, etc. than by drinking. Autopsy results showed serious kidney abnormalities in animals that drank water containing both sodium fluoride and aluminum fluoride. The Varner team said that “Striking parallels were seen between aluminum-induced alterations” in cerebral blood vessels that are associated with Alzheimer’s disease and other forms of pre-senile dementia. They concluded that the alterations of the blood vessels may be a primary event triggering neuro-degenerative diseases [Varner]. Aluminum has been found to be significantly higher in chronic fatgue syndrome than in normal people [Van Rensburg]. Aluminum in baking powder and pots and pans should be not used at all. Aluminum in vaccines have been significantly linked to a chronic fatigue syndrome like disease [Gherardi]. Aluminum has been linked to bone degeneration in horses. Aluminum has also been proposed to act synergistically with fluoride to produce Alzheimer's disease. You may see a blog devoted to persuading officials to discontinue fluoride here.

You may see a very extensive discussion by Thomas Petrie on the awful side effects of fluoride in http://tompetrie.net/id6.html .

The anticoagulant Heparin, alpha-adrenoreceptor stimulants, succinylcholine, and beta-adrenergic nerve blocking agents also produce high blood potassium.

The kidneys are said to be a critical target organ for cadmium and this is especially ominous because the half-life of cadmium in the body is 17 years [World Health Organization p64]. I do not know if the damage affects potassium. In my opinion cadmium should not be used for plating screws or cathodic protection, and carpenters should not hold plated screws in the mouth.

Poisoning rarely causes severe high blood potassium directly unless the kidneys have been damaged or muscles destroyed as well. This is probably because of the high capacity of healthy kidneys.

I believe that damage to the kidneys is the most common chronic problem. Ironically the kidneys can be damaged by a potassium deficiency with lesions of the distal portions of kidney and collecting ducts, which cause depression of renal concentrating ability [Epstein, p272] especially if high blood pressure is also involved [Tobian]. A deficiency state is very common in our society. Rubini believes that even a modest deficiency can cause irreversible kidney lesions [Rubini] in the collecting tubules, which is where the potassium is excreted. Some people with end stage kidney disease can have a total body cell deficit even though plasma potassium is normal [Knochel p450]. This is because when the cell potassium is low the body attempts to make the plasma potassium low also, in order that nerve impulses can continue to fire. . So even though the plasma potassium seems normal, it is higher than the body would like it to be for nerve transmission. Excess calcium can also damage the distal tubules of the kidneys with results the same as potassium deficiency [Epstein, p272]. It is possible that this is caused by an interference with magnesium absorption, which deficiency in turn prevents the potassium pumps from operating. It is said that excessive magnesium can damage the kidneys, especially for those who have poor kidney function to begin with [from a dead site]. I do not know if any of those damages can directly cause damage of such a nature that potassium can not be excreted properly. However I would be greatly surprised if it did not at least contribute to making poison or other damage somewhat more severe since the effect of a potassium deficiency is very generalized and any decrease in the effective size of the kidneys makes any other situations more difficult as well. Besides, in chronic kidney failure aldosterone secretion is often high and more potassium is excreted per unit of decreased glomerular filtration [Knochel p446], probably partly because of increase of pumps on the cell wall [Schon]. This is no doubt a considerable part of the reason why a large loss of kidney function must take place before adverse symptoms show up. Persistent high blood pressure can damage the glomerulus, which is where the fluids are initially filtered into the kidney tubules. The most common glomerulus degeneration in the world is called Immunoglobulin A (IgA) nephropathy (IgAN) [Donadio]. Its progress can be muted by increasing ingestion of omega 3 oil in food [Donadio]. The ratio of omega 6 to omega 3 should be one, but it is usually much higher in our society [Simopoulos]. I am not certain of what that kind of damage does to the potassium equilibrium. Probably it is not an important part of it by itself. Albumins in the urine are an indication of such damage. Early problems can only be detected by routine special tests on microalbinuria. People with insulin dependent diabetes should have such tests.

There are medications which can damage the kidney tubules. Among the prescription and over the counter medications that predispose patients to such damage are acetaminophen (Tylenol, Anacin-3, Liquiprin, Panadol, and Tempra) but not aspirin [Perneger] (There is a link to aspirin [Fored] but predisposing conditions could not be ruled out), the following antiinfective medicines; pentamidine (NebuPent, Pentam), cephalosporins, and amphotericin B or Fungizone (80% affected by this drug), foscarnet, cidovir, vancomycin (Vancocin) , and the aminoglycosides, [Schwartz] which include gentamicin or Garamycin (20% of patients on gentamicin develop renal insufficiency), amikacin (Amikin), tobramycin (TOBI, Nebcin), neomycin (Mycifradin), and aminoglycoside gentamycin (Garamycin). Cox-2 inhibitors are suspected to cause kidney damage. It has been proposed that acetaminophen damages the liver by degrading the detoxifier, glutathione peptide so it is possible that that is the mechanism for the kidneys also. If so, anyone who must take that drug should possibly increase cysteine (perhaps by means of whey), glutamate, and glycine in the diet, since those amino acids make up glutathione, and take as little as possible of the drug. Immune stimulation by cytokine treatment (mainly interferon-alpha) involves several kinds of autoimmune renal diseases like acute interstitial nephritis or glomerulonephritis as well as interstitial and vascular rejection of renal transplants. [Schwarz] Aristolochic acid found in certain plants and botanicals is toxic to the kidneys and is a potential carcinogen. This chemical can cause serious kidney damage and the use of products that contain aristolochic acid has been associated with several occurrences of kidney failure. The use of aristolochic acid-containing product has also been linked to increased risk of kidney cancer in people who have consumed it. Bluelight, Inc., Ithaca, N.Y. has initiated a recall of these products sold under the “Treasures of the East” label with “MFG #200008” (2000=year, 08=month) and earlier production dates. Products with “MFG # 200009” and later production dates are not affected. The American Food and Drug Administration has a program called MEDWATCH for people to report adverse reactions to untested substances, such as herbal remedies and vitamins call 800-332-1088.

Never permit a radiological (x-ray) dye into your blood stream out of mere curiosity, but only if it is desperately important. A high percentage of people have kidney damage from such drugs, especially people with mild to moderate kidney impairment [Black] and over half of diabetics [Thompson]. In my opinion it is highly probable that healthy people have some hidden damage also, even in the absence of symptoms, from all the above substances. It is therefore not a good idea to use these drugs for trivial problems like pain, discomfort, reduction of a low fever (which should not be done anyway since fever is one of the body’s defenses against infection), or for problems which can be solved in time with nutritious, non poisoned foods and healthy living or emotional support.

I do not know if diuretics can damage the kidneys. However there is a study which indicates that patients with kidney failure who are on diuretics had a higher death rate but also a higher rate of subsequent chronic kidney failure requiring dialysis. This may have been due to a potassium deficiency produced by the diuretics. The death rate was especially high in patients who failed to quickly respond to the diuretics with an increased flow of urine [from a dead URL].

Other toxic agents that can damage kidneys include heavy metals like lead, arsenic (arsenic is given to chickens for worm control and gives young poultry meat 0.39 parts per million [Laskey] ), and mercury (side effects of tooth amalgams), carbon tetrachloride (used in the dry cleaning industry), pesticides, and fungicides. Hydrocarbons are said to cause damage to the kidneys [Ravnskov]. I do not know which of these last poisons causes damage which prevents excretion and which prevents retention.

Lead probably prevents retention [in my opinion] and is the main cause of gout [Batuman]. Lin has statistical evidence linking gout to lead poisoning [Lin 2002]. The lead poisoning makes the aldosterone system insensitive to potassium concentration and increases the potassium content of the blood plasma [Gonzalex]. The blood lead content is no indicator of toxicity and the status must be obtained with an EDTA mobilization test [Batuman]. Ethylenediaminetetraacetic acid chelator of lead has successfully increased uric acid excretion [Lin 2001]. Other poisons may move one a little closer to gout also, such as timalol [Blocadran] combined with hydrochlorothiazide and amiloride (Moduretic) [Laren]. I have no information in the medical literature on any direct link between gout and a potassium deficiency. I have a strong suspicion that there is a link however. I have heard of a doctor who gave his patients potassium losing diuretics and thus triggered an attack of gout. By adding a potassium supplement he was able to remove the gout. William Ellis has used potassium supplements for years for gout [private communication]. Gout can be triggered by the same agents that cause potassium losses such as fasting, surgery, and potassium losing diuretics [Rodman]. A potassium deficiency can increase urate levels in the blood [Davis][Halla] so there is a circumstantial connection. Urate kidney stones form during gout in a fifth of the cases. Making the urine less acid with potassium citrate or sodium bicarbonate is a current treatment for urate stones [Shekarriz]. Potassium citrate has been successfully used to eliminate urate stones.I suspect that potassium bicarbonate would be much more preferable than sodium bicarbonate, but I have no evidence. This assumes, of course, that hyperkalemia is not involved. The initiating factor for gout is probably usually lead poisoning though [Wright]. Personal experience leads me to believe that toluene in automobile enamel reducers is also a poison which can trigger gout and Echinacea herb may be involved. There is an association in peoples minds between gout and rich foods and lifestyle, probably because people with gout have trouble excreting nitrogen, which is high in meat, in a soluble form and perhaps also because wine bottles and plumbing used to contain lead. Until such time as the matter is elucidated it would be a good idea to stop eating lead, eat less proteins, and not allow any potassium to be lost from one’s food, providing one’s kidneys are not retaining potassium to cause high blood potassium. There is a discussion of current alternate treatment for gout online, which include black cherries. One would think that people with kidney failure that causes potassium retention would not have gout, but I know of no evidence for such a correlation. Orotic acid has been recommended for gout since it decreases uric acid. A dosage of 4,000 mg (possibly too high) of Orotic Acid has been recommended (Pyrimidinecarboxylic acid, also known as orotic acid or vitamin B13, Animal Galactose Factor, Oro, Orodin, Oropur, Orotonin, Oroturic, Orotyl, or whey factor. But it is not really recognized as a vitamin. It is manufactured in the body by intestinal flora.) is normally used for a maximum of six days in Gout patients. Orotic acid is not necessarily always good in excess since it is said to bind zinc to a non-biologically active state and can damage the liver, but I would think that the 50 to 100 milligrams that has been recommended for normal supplementation should be safe. Sources of oratate are whey, yogurt, beetroot, carrots, and jerusalem artichoke. It looks as if people with high blood potassium should avoid such supplements and maybe foods.

If there is a partial blockage of the urinary tract it can interfere with excreting potassium. Blockage would be most common in men because of the problem of swelling of the prostate tissue being common. I suspect that this prostate swelling is most often caused by a deficiency of the vitamins linoleic or linolenic acids (omega 6 and omega 3 oils) produced by the foolish custom of hydrogenating vegetable oils. I also suspect that it is sometimes caused by a zinc deficiency which in turn can be created by excessive intake of copper. Anyone having trouble with high potassium should have a urologist rule out prostate blockage as a source or contributor to the problem early on. It is also possible to check the matter oneself by inserting a catheter after urinating. If a significant amount of urine continues to come out there is an obstruction in the prostate or bladder opening. You have to be very careful and use good sterilization of both the catheter and as much of the organ as possible or bacteria can be introduced into the bladder and may be anyway. Bladder infections are difficult to get rid of although they are not usually dangerous. If there is an obstruction from swollen prostate it can usually be corrected surgically without the necessity of an abdominal incision. There are also hormone therapies which are said to be fairly effective for lesser prostate swellings.

Blockage is presumably possible from kidney stones. I do not know what affect this has on potassium. I do have some information on some of the causes. If calcium intake is normal but phosphorus is too low, calcium citrate stones can form [Sager]. On the other hand if phosphorus is much too high, say from drinking soft drinks especially colas [Hall], calcium phosphate stones should form [I have no reference for this and am not sure it happens from soft drinks]. Stones are said to have an incidence as follows; calcium oxalate (65% - 75%), calcium phosphate (5%), uric acid (7%), cystine (2%), and ammonium phosphate (2%) stones [from a dead site]. Uric acid stones are less probable when potassium was adequate in the diet in healthy people.

Medications which can cause too high a blood potassium are cyclosporine, lithium, heparin, enalapril, triampterene, amiloride, spironolactone, and trimethoprim. They imply other malfunctions to make the increase possible. Indomethecin by inhibiting prostaglandin stimulation of renin and captopril by prevention of angiotensin II can also produce hyperkalemia [Kaufman].

There has also been proposed a rare, unknown genetic malfunction as a cause of hyperkalemia [Stewart]


There are some procedures available in a hospital that can provide some short term relief from a dangerous surge in blood potassium. Intravenous calcium, intravenous glucose and insulin [Schwartz 1978] will work for an hour or so. The calcium is probably effective because calcium inside kidney cells stimulate potassium excretion across collecting tubule membranes. Intravenous aldosterone will help the kidneys get rid of excess potassium. Both in a hospital and at home, sodium bicarbonate will help considerably short term [Schwartz 1978] if there is any kidney function left, especially if the hyperkalemia is caused by acidosis (low blood alkalinity or pH), but is said to be dangerous if used for prolonged periods.

It has been found that early or late administration of N-acetylcysteine (NAC) attenuates the progression of chronic renal failure in rats [Massola].

Drinking salt (sodium chloride) water as a vehicle for the bicarbonate is helpful. Increased urine flow increases potassium loss, so part of the effect of the salt solution may be from this phenomenon [Giebisch]. While sodium is a good antidote for high serum potassium, kidneys which have been conditioned by a prior low sodium intake can excrete an additionally larger amount of potassium from the collecting ducts than kidneys which have had a prior large intake. Furthermore, a low sodium intake causes higher potassium losses than an excessive sodium intake [Peterson 1977]. So it seems to me that a very low sodium intake normally would be the best way to go to avoid hyperkalemia. However I am not certain of this and in any case it may be the chloride that is involved.

Drinking extra water should be helpful, and indeed essential if dehydrated. However, drinking huge amounts of water (say a gallon) if severely dehydrated without sodium chloride is very dangerous and can kill you from hyponatremia (low sodium). Such dehydrated states should be relieved slowly and combined with some sodium chloride salt, as well as some potassium chloride in the case of normal people with adequate kidney function. Oral rehydration therapy, or ORT salts, is in order for people with adequate kidney function. Of course it is best not to become dehydrated in the first place. Too yellow a urine has been proposed as a symptom of dehydration. However this cue can not be used if you have been taking iboflavin (vitamin B-2) supplements, since that vitamin turns the urine a bright yellow.

You may see a discussion of drugs to correct hyperkalemia (but aldosterone is not discussed) along with doses, contraindications, symptoms, tests, and ECG charts at this site. Also flurocortisone acetate; FCA, has been found to increase potassium excretion without many other changes [Furuya]. If this is happening by release of potassium from the cells, it is a dangerous procedure. If drinking extra water is prescribed and you gag on pure water, adding extra water to your soup and using two thirds of fruit juice as water (although I do not recommend fruit juice routinely during kidney failure because of a high potassium content relative to its other nutrition) should help. You would immediately think that reducing the amount of potassium which you eat was in order long term and this is, indeed, usually prescribed. The main problem is that potassium tends to be correlated with other essential nutrients. However an immediate gain can be achieved by cutting out foods unusually high in potassium per calorie such as celery. It would seem to be in order to cut out foods moderate in potassium per calorie which are rather low in other nutrients such as apple juice. Increasing intake of foods unusually high in other nutrients such as wheat germ and liver (liver if uric acid is normal) would no doubt solve part of the above problem. You may see a table which expresses potassium in food as weight per calorie at; this site. A table like that is unobtainable elsewhere in that format. This same table may be viewed in descending potassium concentration here. You may see the table from which the previous two tables are computed in the USDA handbook #8 site. It is an unusually good site and even gives amino acids. You must press “enter” to search and then divide a value of any nutrient obtained by the kCal number in order to et useful comparisons. It is available in a PDF printable form for potassium only also. with links to PDF caloric contents and other nutrients. There are also links in it to PDF types of printouts from the table for individual nutrients available here Just scroll down and click on the “A” or “W” button for the nutrient you desire. A site is available which shows foods that are high in one nutrient and low in another nutrient (including calories). This last site should be especially convenient for people with high blood potassium. It would be extremely valuable for someone with high blood potassium who suffers from a genetically caused deficiency or extra need for another nutrient.

Chitosan has been found to have a profoundly advantageous affect on people with kidney failure by an unknown mechanism, but these researchers do not give information on potassium in their abstract [Jing].

It is entirely possible that it would be necessary to take vitamin and mineral supplements as well. If so, be sure they are complete and balanced as a rule, excepting if you know you are low in one or two. Dangerous imbalances are possible otherwise. In particular, unless you get copper at about one-seventh the amount of zinc, you could suffer from a severe copper deficiency with hemorrhoids, slipped or herniated discs, and aneurysms (which cause strokes in the brain) some of the most dangerous symptoms. The reverse is also true for copper’s affect on zinc with other adverse symptoms, such as swollen prostate, although they are somewhat less immediately dangerous symptoms. You should keep in mind that no vitamin capsules have adequate amounts of the macro nutrients such as potassium, calcium, magnesium, sodium, chloride, phosphate, and amino acids, so imbalances are possible even if the tablet is balanced with what micro nutrients it does contain.

If animal experiments are an indication, vitamin B-1 (thiamin) is a potentially dangerous imbalance with respect to potassium. If vitamin B-1 is deficient when potassium is adequate, the wet heart disease of beriberi is possible [Folis] and the reverse. Presumably cell potassium IS adequate when blood potassium is high (although not necessarily always) so presumably this reverse of excessive vitamin B-1 would usually not apply in high blood potassium, although I know of no evidence. Even if you are eating foods adequate in vitamin B-1 you could still possibly have a problem from high or adequate potassium if you are also eating foods which have sulfites in them such as wine, vinegar, beer, bottled lemon juice, and some dried fruits, since sulfites degrade vitamin B-1 in the intestines [Amerine] [Fitzhugh], so such foods must surely be disadvantageous for people who have lost kidney function.

Wine can be obtained without sulfites but since it also has a poison in it which interferes with potassium excretion [McDonald], wine should not be used during high blood potassium in any case. I have no information as to whether this poison has been identified and ethanol is said to increase excretion [McDonald]. However by all means cut out wine and alcoholic beverages fermented with sulfur dioxide whether potassium is high or not and cut them out with or without sulfur dioxide during high blood potassium. I do not know how potent the affect is, but there is no point testing the matter on yourself. Wine has been proposed as good for the heart in normal people, but if the mechanism for this goodness is retardation of potassium excretion, I suggest that getting adequate potassium is a superior strategy for kidney intact people and not getting overwhelming amounts of vitamin B-1 from pills. There is no good substitute for nutritious, unprocessed food free of poison, for then you do not usually have to scratch your head over how to balance things.

When the protein in meat, eggs, and milk is burned for energy the nitrogen in it degrades to ammonium, uric acid, and urea. Damaged kidneys can have trouble excreting these wastes also. The trouble is direct for potassium excretion since ammonium is excreted by the same cells that excrete potassium. For this reason people with damaged kidneys are often urged not to eat excessive amounts of high protein foods. A trial suggests that 0.6 gram of protein per kilogram of body weight slows down progression of kidney disease [D’Amico]. This would be roughly less than 50 grams for a lean 150-pound person. There may be an additional reason so far as potassium is concerned. When the body suffers from a potassium deficiency the kidneys activate an enzyme which degrades glutamic acid. This seems to me to be an adaptation to conserve potassium by interfering with excretion at the excretion site. It may be that extra ammonium in the body may interfere somewhat as well, not something desirable when suffering from an excess of potassium. It is probable also that the ammonium can act as if it were potassium so far as nerve conduction is concerned because it has the same size and charge which would make the situation even worse than the potassium value itself would seem to indicate. I know of no experimental evidence which would cast light on ammonium in the blood in nerve conduction though. In any case it is fairly important in the long run not to remove meat, milk and eggs from the diet completely since these foods provide amino acids lysine and methionine, which plants are low in. I suspect that the equivalent of the weight of an egg at each meal would be adequate. They also provide vitamin B-12 although that is easy to provide with pills. An additional argument is often advanced against using meat, liver, and eggs because of the anti cholesterol fad. It is very unlikely that dietary cholesterol is an important part of the problem, but rather excessive synthesis within the body. Cholesterol has only gone up in the diet from 683 to 734 milligrams between 1909 and 1961 and the Masai tribe have low cholesterol [Brown p8] in spite of a high meat diet. If the problem is most often caused by low copper [Carr] as I suspect, warning against eating shellfish or liver is exaggerating the problem, not helping, because those foods are high in copper. So be sure to get a small amount of high quality protein at every meal, or at least within 2 hours of a meal. If your cholesterol is high, make sure the protein is not milk, which is low in copper or supplement copper. But do so moderately, especially if you have diabetes.

Glucosamine is currently being touted as advantageous for some of the arthritis diseases. I have a suspicion that part of its efficacy may be due to it furnishing glutamine for ammonium synthesis in the kidneys for ammonia production goes up and potassium excretion goes down when ingesting glutamine [Tannen p458]. If so, I suspect that taking this material should be counter productive and therefore contraindicated during high blood potassium, and perhaps food containing large amounts of it also.

Acids which can be absorbed but not burned (metabolized) will interfere with potassium excretion since hydrogen ion competes with potassium at the excretion site. Unfortunately I do not know which foods are involved. However, I do suspect vinegar (acetic acid) since vinegar has been suggested as being advantageous for rheumatoid arthritis which I am convinced is accentuated by a potassium deficiency. Acetic acid can be metabolized [Winegrad] but it could be that much of it is excreted before entering the cells or that well-fed people do not burn it all. Cherries and cranberries fall into this same suspicion also (however researchers have proposed antioxidants responsible for the affect of cherries on arthritis and gout), cranberries because I have heard they increase urine acidity (but no hard evidence). I am almost certain that the citric acid in citrus fruit is burnt in the body since citric acid is part of the Kreb’s cycle so I assume that citrus fruits are safe. It is possible that the low metabolism during the night could prevent citrate from being burnt, and thus make susceptible people more prone to headaches and potassium retention. It would be a good idea for researchers to perform experiments to determine this for sure or to make the information well known if it has already been done since a little fruit like citrus should be reasonable if a patient’s potassium overage is mild and the low nutrition value of fruit would not be a major problem in that case.

Of course potassium supplements, salt substitutes, ORT salts, some athletic drinks, and potassium-based baking powders must not be used at all if you have high blood potassium, except possibly during virulent diarrhea.

Since aldosterone suffers a drastic decline during dehydration it is important that you drink more water than just barely enough to satisfy thirst. Extra water probably makes it easier for the kidneys to unload potassium in addition. Perspiration should help considerably to remove excess potassium also, but only if it is not allowed to dehydrate the body, for perspiration contains potassium. I am not certain beyond a doubt that this is a wise way to augment kidney function, but it sounds at least reasonably safe. Sweat glands are not nearly as efficient at retaining vital materials as kidneys. Saunas should enable perspiration. You may see some theory about saunas here and how to construct various kinds of saunas in that same site. Enemas also cause large potassium losses [Dunning]. Leaving water in contact with the mucous membranes for a long time increases the losses. I do not know whether this is a desirable strategy routinely or not, but I should think it would be helpful in an emergency.

Licorice has a chemical, glycyrrhetinic acid, in it which interferes with degradation of aldosterone, so licorice (but not the licorice candy, which is said to be anise seed extract) should be a reasonably safe temporary palliative. I do not know if long term use is desirable or not. The fact that licorice also increases cortisol indicates that it probably is not. The same degradation is said to be true of grapefruit. I do not know what the status of other citrus fruits is. Aldosterone injection is excellent for increasing survival in metabolic shock, but amounts must be kept between 0.2 and 0.4 milligrams per kilogram of body weight in rats [Schumer]. This last would only be available in a hospital of course. It may be that deoxycorticosterone (DOC) would be better for people eating too much salt.

Since acid interferes with potassium excretion, it should not be surprising that bicarbonate of soda (baking powder) causes large potassium loss. This also should be a reasonably safe temporary palliative. Whether it is safe as a routine strategy or not, I do not know. Sodium bicarbonate is often used as baking powder, but this is not necessarily a good idea. It has recently been questioned as to being of any help in life threatening high blood potassium, but I find this hard to believe except maybe in almost complete loss of kidney function.

Hyperventilating (breathing rapidly) gets rid of carbon dioxide (carbonic acid) to an abnormal extent. This should be an advantageous procedure to know if you are in a taxicab on the way to a hospital to treat metabolic potassium shock. I have no knowledge of it being tried, but I would have thought it should help temporarily to avoid a lethal ending.

I do not know for sure what value potassium must attain before drastic remedial action should be taken. I suspect that over 6.0 meq per liter is necessary to start to threaten actual death. However attempting to alleviate the problem nutritionally until the underlying problem is discovered should be inherently fairly safe and without a doubt almost always a desirable additional strategy at least.

It is good sense to forego processed food, alcohol, and tobacco in order to stay as healthy as possible even when that garbage is not the direct cause of the disease you are trying to avoid. What little phony pleasure, financial advantage, or excitement that garbage gives you is much more than counter balanced by the pain and misery that garbage ultimately brings, in my opinion. It would be better to attempt to attain camaraderie or good jokes.

REFERENCES are below


Dr. Reza Rastmanesh from Iran has recently performed a large controlled clinical trial testing potassium supplements against rheumatoid arthritis with dramatic decreases in pain in all subjects and increases of cortisol [Rastmanesh]. He would now like to continue his clinical research testing potassium in conjunction with other nutrients, especially magnesium, in an English speaking country. His credentials are impressive. If you know of any nutrition or rheumatology department able to employ him, please contact me with email; isoptera at att.net .

The health of people in the USA is abysmal (numerous statistics), and a major part of it is poor nutrition. As the 12th century physician, trying to cure by diet before he administers drugs, said; “No illness that can be treated by diet should be treated by any other means” or as Hippocrates expressed it in 460 - 377BC; “If we could give every individual the right amount of nourishment and exercise, not too little and not too much, we would have found the safest way to health.” It would seem that a healthy life style has been known for a long time.

There is an article discussing cashew nuts to cure a tooth abscess, which will prove useful
There is also an article which proposes some speculation about diabetes.
See this site for how to cure hemorrhoids, aneurysms, one type of anemia, and slipped or herniated spinal discs with copper.
See this site for some links to health articles.

You may see the search section of a site which explores nutritional solutions by using existing research and logical thinking to explore possible environmental, especially nutritional, links in a variety of inherited connective tissue disorders (Marfan syndrome, Ehlers-Danlos syndrome, osteogenesis imperfecta, etc.) and related features such as scoliosis, pectus excavatum, mitral valve prolapse and TMJ.

See this site for some links to health articles.
For a procedure that discusses tetrathiomolybdate for removing copper and thus preventing further solid cancer growth and Hodgkin’s, see this site. This might buy some time until you can persuade a doctor to try tumor necrosis factor or interferon or an opioid antagonist drug called Naltrexone (Naltrexone in the large 50 mg size, originally manufactured by DuPont under the brand name ReVia, is now sold by Mallinckrodt as Depade and by Barr Laboratories under the generic name naltrexone) that blocks some endorphin receptors. Said blockage is thought to cause the body to temporarily secrete more endorphins, especially after midnight at night. These endorphins are thought to stimulate the immune system, and in particular to stimulate the TH-1 or type 1 antiviral response by decreased interleukin-4 and with increased gamma interferon and interleukin-2 and a simultaneous decrease of type 2 anti bacterial response [Sacerdote]. It appears to be especially effective for minimizing symptoms and retarding progression of multiple sclerosis (MS) There are drugs listed in this site that should not be taken with low dose Naltrexone, including cortisol. There is information in this site for mitigating side effects, including starting with one milligram doses. Advice how to proceed if you have been taking cortisol may be seen here. (also see these sites; this site and this site and this site and a trial) . A few doctors have had encouraging results in Crohn's Disease, and even to some extent in cancer. Low doses of Naltrexone (LDN), 1.5 to 4.5 milligrams, at bedtime is used (timing is important, and it is important not to buy slow release forms). It is said to have no known bad side effects at those doses other than insomnia the first week or two in some. There is also reports from an extensive survey in this site. and an extensive discussion at this site. I think some clinical studies on Naltrexone are in order, and it should not be a prescription drug (I have a petition to make Naltrexone an over the counter drug with the Center for Drug Evaluation and Research FDA Rockville MD 20857, Re; Docket No. 2006P-0508-CPI. Perhaps if enough people wrote supporting the petition it could be enacted). Though side effects appear unlikely, it is not proven over longer periods. There are suggestions on how to obtain Naltrexone without a prescription in this site. Naltrexone is currently being used by Dr. Enlander, a New York City doctor, but with limited success using 3 to 4.5 milligram doses for CFS or CFIDS. . It is also being explored for AIDS by Dr. Bernard Bihari, 29 W 15th St. New York, NY 10011, 212) 929-4196 who is still prescribing Naltrexone for HIV/AIDS. (and currently Executive Director of the Community Research Initiative). Dr. Gale Guyer of Advanced Medical Center located in Zionsville, Indiana also is using it for cancer. Dr. Bihari has shown promising results for a large percentage of his cancer patients.

Olive leaf extract has shown clinical evidence of effectiveness against a wide range of viruses, including AIDS [Bihari], herpes, and cold viruses. It sometimes produces a Herxheimer or pathogen die off symptoms (from effectiveness against bacteria?). There is evidence that it is synergistic (reinforce each other) with Naltrexone. There have been a few case histories of improvement in what were probably arthritis patients and CFIDS patients. The active ingredient is said to be oleuropein or enolate. There has been very little follow up research done on it.

See this site for evidence of a correlation between magnesium deficiency and cancer. The taurate is proposed as the best magnesium supplement. Taurine or 2-aminoethanesulfonic acid is an acidic chemical substance sulfonated rather than carboxylated found in high abundance in the tissues of many animals (metazoa), especially sea animals. Taurine is also found in plants, fungi, and some bacterial species, but in far less abundance. It is an amine with a sulfonic acid functional group, but it is not an amino acid in the biological sense, not being one of the twenty protein-forming compounds encoded by the universal genetic code. Small polypeptides have been identified as containing taurine, but to date there has been no report of a transfer RNA that is specifically charged with taurine [from Wikipedia]. It is essential to babies. It has been found that supplements of the amino acid, taurine, will restore the abnormal electrocardiogram present during a potassium deficiency by an unknown mechanism. This information has been used in several case histories by George Eby to control a long standing type of cardiac arrhythmia called pre atrial contractions (PACs), a benign but irritating and nerve racking heart problem, with 2.5 grams of taurine with each meal.

Taurine is said to be low in the diets of vegetarians. The 2.5 grams recommended by the American Heart Association causes diarrhea in some people and should probably be reduced in those people. Taurine has been used for high blood pressure, migraine headache, high cholesterol, epilepsy, macular degeneration, Alzheimer’s disease, liver disorders, alcoholism, and cystic fibrosis, and depression. Keep in mind that some people may have a genetic defect that limits the amount of taurine tolerated and that adequate molybdenum may desirable. I assume, though, that people whose kidneys can not excrete potassium well would not have a potassium deficiency.

Here is an article with anecdotal evidence for pressurized oxygen, zinc, vitamin B6, and vitamin C after head injuries. They also claim a fair percentage of prison inmates preserved from psychiatric disorders after head injuries.
See this site for evidence of a correlation between magnesium deficiency and cancer.

A site is available which shows. foods which are high in one nutrient and low in another (including calories). This last site should be especially useful for a quick list of foods to consider first, or for those who must restrict another nutrient because of a genetic difficulty with absorption or utilization

You may find useful for definitions and easy to use a search for abstracts of journal references, “Gateway”. For those which have abstracts available, click on “expand” or for definitions click on “term finder”. and also you can search in a similar way here or a list of medical search engines and also a site with several links to potassium nutrition articles and another site that has many links to nutrition sites around the world.

If you use medication, you may see technical evaluations and cautions of drugs at the bottom of this site.

The very extensive USDA Handbook #8 may be seen here. To access the information you must press “enter” to search, and then divide Kcal into milligrams of potassium. This last table is very comprehensive, is used in search mode, and even lists the amino acids.

There is a free browser called Firefox, which is said to be less susceptible to viruses or crashes, has many interesting features, imports information from Iexplore while leaving Iexplore intact. You can also install their emailer. A feature that lists all the URLs on a viewed site can be useful when working on your own site.

There is a tool bar by Google that enables you to search the internet from the page viewed, mark desired words, search the site, give page rank, etc., and links to a search journal articles (the Scholar program). There is a

free program available which tells on your site what web site accessed you, which search engine, statistics about which country, statistics of search engine access, keywords used and their frequency. It can be very useful.

The author has a degree in chemistry and a master of science degree in soil science. He has researched this subject for 40 years, primarily library research. He has cured his own early onset of arthritis. He has published articles on allied subjects in; The Journal of Theoretical Biology (1970, 1983), The Journal of Applied Nutrition (1974) which gained the best article of the year award, Clinical and Experimental Rheumatology (1983), and Medical Hypotheses (1984, 1999, 2007, 2008). This article is solely funded by the author and no advertisements have been knowingly included.

Send email to Charles Weber; ----- isoptera at att.net – or; phone = 828 692 5816

Confidentiality of data relating to individual patients and visitors to a medical/health Web site, including their identity, is respected by this Web site. The Web site owner undertakes to honor or exceed the legal requirements of medical/health information privacy that apply in the USA.


Amerine MA Ough CS 1972 Recent advances in enology. CRC Critical Reviews in Food Technology V2 issue 4407-526.

Batuman V Maesaka JK Landy E Haddad B Wedeen P Tepper E 1981 The role of lead in gout nephropathy. New England Journal of Medicine 304; 520-3

Bellevue R Dosik H Spergel G Gussof BD1975 Pseudohyperkalemia and extreme leukocytosis. Journal of Lab.Clin. Med. 85; 660-664

Bihari B 1995 Efficacy of low dose Naltrexone as an immune stabilizing agent for treatment of HIV/AIDS [letter] AIDS Patient Care 9; 3.

Black, R. M. (1996). Rose and Black’s clinical problems in nephrology. Boston: Little, Brown, & Co.

Brown J Bourke GJ Gearty CF Finnegan A Hill M Hefferman-Fox FC Fitzgerald DE Kennedy J Childers RWBishop WJE Trulson MF Latham MC Gronin S McCann WB Clancy RE Gore I Stoudt HW Hegsted DM Stare FJ 1970 Nutritional and epidemiological factors related to heart disease. World Rev. Nutr. Diet 32.

D’Amico G Gentile MG Fellin G Manna G Cofano F1994 Effect of dietary protein restriction on the progression of renal failure: A prospective randomized trial. Nephrology Dialysis Transplantation 11; 1590-1954.

Davis WH 1970 Does potassium deficiency hold a clue to metabolic disorders associated with liability to heart disease?. South African Med. Journal 44; 1297

Donadio JV. 2001The emerging role of omega-3 polyunsaturated fatty acids in the management of patients with IgA nephropathy. J Ren Nutr. 2001 Jul;11(3):122-8.

Epstein FH 1960 Calcium and the kidney. Journal of Chronic Diseases 11; 255-277.

Fitzhugh DG Knudsen L Nelson A 1946 The chronic toxicity of sulfites J. Pharm. Exptl. Therap. 86; 37-48

Flink EB 1983 Nutritional aspects of potassium metabolism p37-44. in; Whang R Aikawa JK eds. Potassium its Biologic Significance. CRC Press, Boca Ratyon, Fla.

Folis RH 1942 Myocardial necrosis in rats on a potassium low diet prevented by thiamine deficiency. Bull. Johns-Hopkins Hospital. 71; 235-241.

Fored C M et al 2001 N Engl J Med ;345:1801-1808.

Furuya R, Kumagai H, Sakao T, Maruyama Y, Hishida A. 2002 Potassium-lowering effect of mineralocorticoid therapy in patients undergoing hemodialysis. Nephron. 92(3):576-81.

Gherardi RK 2003 Lessons from macrophagic myofasciitis: towards definition of a vaccine adjuvant-related syndrome [Article in French]Journal: Rev Neurol (Paris) Feb;159(2):162-4.

Giebisch G 1979 Membrane Transport in Biology. p215-298 Giebisch G editor. Springer Verlag, Berlin, NY

HallJR Swaine RL 1972 Trends in the carbonated beverage industry. Critical Reviews in Food Technology, V2, issue 4; 517-536.

Hunter M et al 1985 Regulation of single potassium ion channels from apical membrane of rabbit collecting tubule. American Journal of Physiology – Renal Physiology 251; F725-731.

Ichinohe T, Kuwahara T, Yata K, Seo T, Suyama K, Onaka H, Ono T, Ueda S, Matsuo T 1991. Recurrent hyperkalemia in the course of rheumatoid arthritis—a case report Nippon Jinzo Gakkai Shi. Aug;33(8):811-6.

Ifudu O Markell MS Friedman EA 1992 Unrecognized pseudohyperkalemia as a cause of elevated potassium in patients with renal disease. American Journal of Nephrology 12; 102-104.

Jing SB et al 1997 Effect of chitosan on renal function in patients with chronic renal failure. Journal of Pharm. & Pharmacology 49; 721-723.

Kaufman CE Popper S 1983 Hyperkalemia. in; Whang R Aikawa JK eds. Potassium its Biologic Significance. CRC Press, Boca Raton Fl.

Knochel JP 1977 Role of glucoregulatory hormones in potassium homeostasis. Kidney International 11; 443-452

Lasky T, Sun W, Kadry A, Hoffman MK. 2004 Mean total arsenic concentrations in chicken 1989-2000 and estimated exposures for consumers of chicken. Environ Health Perspect. 2004 Jan;112(1):18-21.

Lin JL, Tan DT, Ho HH, Yu CC 2002 Environmental lead exposure and urate excretion in the general population. . Am J Med. 2002 Nov;113(7):563-8.

Massola Shimizu MH, Coimbra TM, et al, 2005 N-acetylcysteine attenuates the progression of chronic renal failure, Kidney Int., 68(5): 2208-17. (Address: Nephrology Department, University of Sao Paulo School of Medicine, Sao Paulo, Brazil).

McDonald JT Margen S 1979 Wine vs ethanol in human nutrition. Fluid sodium and potassium balance. American journal of Clinical Nutrition 32; 817-822

Moore RJ Hall CB Carlson EC Lukaski HC Klevay LM 1989 Acute renal failure and fluid retention and kidney damage in copper-deficient rats offered a high NaCl diet. Journal Lab. Clin Med. 113;516-524

Perneger TV, Whelton PK, Klag MJ. 1994 Risk of kidney failure associated with the use of acetaminophen, aspirin, and nonsteroidal antiinflammatory drugs. N Engl J Med. 1994 Dec 22;331(25):1675-9.

Peterson CG 1972 Perspectives in Surgery. Lea & Febiger, Philadelphia.

Peterson L & Wright FS 1977 Effect of sodium intake on renal potassium excretion. American Journal of Physiology 233; 225-234

Rastmanesh R 2008 A pilot study of potassium supplementation in treatment of hypokalemic patients with rheumatoid arthritis: a randomized, double-blinded, placebo controlled trial. The Journal of Pain 9; 722.

Ravnskov U. 2000 Hydrocarbon exposure may cause glomerulonephritis and worsen renal function. Evidence based on Hill´s criteria for causality. Quarterly Journal of Medicine; 93:551-556

Recheigl M, Jr, editor 1978 CRC Handbook Series in Nutrition and Food, Section E Nutritional Disorders, V. 1

Richmond VL 1985 Thirty years of fluoridation: a review. American Journal of Clinical Nutrition 41; 129-138.

Rubini Chojnacki . Am. J. Clin. Nutr. 25; 96-113.

Sager RH Spargo B 1955 The effects of low phosphorus ration on calcium metabolism in the rat with production of calcium citrate stones. Metabolism 4; 519

Schon DA Silva P Hays J. 1974 Mechanism of potassium excretion in renal insufficiency. Am. J. Physiol. 227; 1323-1330.

Schumer W & Nyhus LM, editors 1970 Corticosteroids in the treatment of shock. Univ. of Illinois Press, Urbana, Ill

Schwartz AB 1978 Potassium-related cardiac arrhythmias and their treatment. Angiology 29(3):194-205.

Schwarz A, Perez-Canto A. 1998 Nephrotoxicity of antiinfective drugs Int J Clin Pharmacol Ther. 36(3):164-7.

Scribner BH & Burnell JM 1956 . Metabolism 5; 468-479.

Seekles L 1960 Pathology of potassium in animals in; “Potassium in the Animal Organism”, which is Proceedings of the 6th Congress of the International Potash Institute, Amsterdam, printed by International Potash Institute, Berne, Switzerland.

Shekarriz B, Stoller ML 2002 Uric acid nephrolithiasis: current concepts and controversies. J Urol. 2002 Oct;168(4 Pt 1):1307-14.

Simopoulos AP. 2002 The importance of the ratio of omega-6/omega-3 essential fatty acids. Biomed Pharmacother. 2002 Oct;56(8):365-79.

Stewart GW Corrall RJ Fyffe JA Stockdill G Strong JA 1979 Familial pseudohyperkalemia, a new syndrome. Lancet 1979 ii/8135; 175-177

Tannen RL 1977 Relationship of renal ammonia production and potassium homostasis. Kidney International 11; 453-465.

Thompson, J., & Henrich, W. (1991). Nephrotoxic agents and their effects. In H. G. Jacobsen, G. Striker, & S. Klahr, The principles and practice of nephrology, (pp. 563 - 569). Philadelphia: B.C. Decker.

Tobian L MacNeil D Johnson MA Ganguli MC Iwai J 1984 Potassium protection against lesions of the renal tubules, arteries, and glomeruli and nephron loss in salt loaded hypertensive dahl S rats.

Van Rensburg, SJ., Potocnik, FC., Kiss, T., Hugo, F., van Zijl, P., Mansvelt, E., Carstens, ME., Theodorou, P., Hurly, PR., Emsley, RA and Taljaard JJ. 2001 Serum concentrations of some metals and steroids in patients with chronic fatigue syndrome with reference to neurological and cognitive abnormalities. Brain Research Bulletin, , 55, 2, 319-325.

Varner JA, et al., 1998 Chronic administration of aluminum-fluoride or sodium fluoride to rats in drinking water: Alterations in neuronal and cerebrovascular integrity. Brain Research, Feb. 16, 784 (1-2): 284-98.

Winegrad AT Reynold AE 1958 Effects of insulin on the metabolism of glucose, pyruvate, and acetate. Journal of Biol. Chem. 233; 267.

World Health Organization 2001 Health Effects. Evaluation of certain food additives and contaminents.WHO Technical Report Series. 55th Report of the Joint FAO/WHO Expert Committee on Food Additives. p63-66.

You may contact me by email using isoptera at att.net or phone 828 692 5816 . This article has been updated in Aug.2012.
This page has been visited times