Urinary - Kidney support


by Sharol Tilgner, N.D.

Medical Herbalism 10(3):1

Traditional herbalism offers plenty of information available regarding treatment of kidney infections and kidney stones. Until now, there has been almost no information available on methods to prevent or treat kidney failure. This article provides current methods to support normal kidney function, treat acute and chronic kidney failure, as well as support those on dialysis and the person with a kidney transplant. The herbs listed for treatment of complicating factors associated with renal failure, such as hypercholesterolemia, are currently thought to be safe to use in renal failure. There may be other efficacious and safe herbs which can be used. However, we have been conservative and have not listed them if we are unsure about their actions on kidney function. If dosage information is known it is listed for a 150 pound person. Most Western information on kidney support is taken from research on animals and some human clinical trials. More clinical results are necessary for specific clinical protocols to be created. Please share your clinical results with us. This will allow us to update practitioners on clinical protocol in the future.

1. Review of kidney function

2. Kidney failure

3. Identifying those at high risk and prevention of kidney failure

4. Supporting the person in chronic kidney failure

5. Supporting the person on dialysis

6. Supporting the person with a kidney transplant

7. Herbs used to support kidney function and how they are thought to work, as well as a list of herbs used to treat complications of kidney failure, dialysis, kidney transplantation or drug side effects

8. Research abstracts

9. Case histories

The contented Kidney

by Sharol Tilgner, N.D.

Medical Herbalism 10(3):2-3,5-13

Review of Kidney Function

The kidneys weigh about 100-160 grams each. Each kidney is about the size of a clenched fist. They are responsible for ridding the body of waste material and controlling the volume and composition of body fluids. Specific functions include:

Regulation of water and electrolyte balances: filter and reabsorb potassium, magnesium, chloride, sodium, etc.

Maintain blood pressure: maintain adequate water volume, filter and reabsorb sodium, synthesis of renin, kinin, prostaglandins

Filter and excrete metabolic waste products: BUN, urea, uric acid, creatinine (BUN and creatinine also secreted)

Filter and excrete foreign chemicals

Secrete hormones: erythropoietin (acts on the stem cells of the bone marrow to stimulate red blood cell production - 90% made in kidney, 10% in liver), renin, kinins, prostaglandins

Involved with gluconeogenesis: kidney forms glucose from amino acids and other precursors during prolonged fasting

Regulation of acid-base balance: bicarbonate reabsorption and hydrogen ion secretion Maintenance of calcium and phosphorus balance: hydroxylation of vitamin D to l-25 dihydroxycholecalciferol, filtration and reabsorption of phosphate and calcium (dependant on PTH)

Maintenance of hematocrit/hemoglobin: synthesis of erythropoietin.

About 21% of the cardiac output flows to the kidneys. Each kidney has about one million nephrons (functional unit of the kidney). The nephron consists of the glomerulus, where fluid and some solutes are filtered from the blood, and the tubule, which converts the fluid into urine through reabsorption of solutes and fluid, as well as secretion of solutes and fluid into the tubules. Most plasma substances pass freely into the glomerular filtrate with the exception of proteins. Once in the tubule, water and specific solutes are reabsorbed as well as secreted via the peritubular capillaries. Waste products such as urea, creatinine, uric acid and urates are poorly reabsorbed. Foreign substances and chemicals are also poorly reabsorbed. Some waste products such as creatinine and BUN are additionally secreted from the blood into the tubules. Electrolytes, such as sodium ions, chloride ions, and bicarbonate ions are highly reabsorbed, so little appear in the urine. Nutritional substances, such as amino acids and glucose, are completely reabsorbed. In a healthy individual, they do not appear in the urine even though filtered by the glomerular capillaries.

The kidney can’t regenerate new nephrons. Renal injury, disease and aging will decrease the number of nephrons. After age 40, the functional nephrons begin to decrease by 10% each year due to benign nephrosclerosis. The remaining nephrons adapt to take on the increased work load. 70% of the functional nephrons can be lost before clinical symptoms appear. When kidney function fails, the resulting kidney failure, if untreated, is lethal within a few days. Death is due to a combination of acidosis, a high concentration of potassium and accumulation of fluid.

Kidney Failure

When there is complete kidney failure, the only options available are dialysis and a kidney transplant. Currently, there are 250,000 US citizens undergoing dialysis. There are 35,000-40,000 new dialysis patients annually. Of the people currently being dialyzed, 31.4% have kidney failure due to diabetes mellitus, 24.8% due to hypertension, 18.2% due to glomerulopathies and 4.9% due to cystic kidneys.

There are two types of dialysis available, peritoneal and hemodialysis. Peritoneal involves an umbilical shunt into the peritoneum whereby dialysate can be filtered through the peritoneum multiple times throughout the day. This type of dialysis can be done in the convenience of your own home or at work. It does have a liability of possible peritoneal infection. Hemodialysis is undertaken in a dialysis unit where the person spends 3-4 hours, 3-4 days per week. It requires a fake shunt to be placed in the person’s arm connecting a vein and artery, or a vein is expanded to a larger size so it can receive the large needles necessary in hemodialysis. Neither peritoneal dialysis or hemodialysis is pleasurable. In acute kidney failure, emergency dialysis is via the carotid artery. Acute failure is generally hard to prevent due to the suddenness and rapidity of the event. In some cases, such as postinfectious nephritis, it can often be prevented. Additionally important, it is necessary to support the kidneys through the acute crisis and make sure it does not become chronic kidney failure. Preventing chronic kidney failure is a better goal than treating chronic kidney failure. If the progression of chronic renal failure is fairly far along, anything you can do to slow down complete kidney failure and stave off the eventuality of dialysis will allow the person more time without this stressful process. Prevention of kidney failure can best be accomplished by high- risk groups for kidney failure. Insulin-dependent diabetics, hypertensive individuals, and persons with genetic susceptibility would all be high risk groups. Insulin dependent diabetics have all been found to have histological evidence of glomerulosclerosis when renal biopsies have been undertaken. 35% will develop clinical nephropathy, usually about 15-20 years after diagnosis. All insulin-dependent diabetics, patients with severe hypertension and patients with genetic susceptibility to kidney disease should have yearly exams and blood chemistry screens as well as a urinalysis twice per year. Any evidence of severely high cholesterol or microalbuminuria may be the first clue to nephron damage. If you wait for clinical symptoms to manifest, your patient will have lost at least 70% of their kidney function already. 

Common Causes of Kidney Failure

There are two main categories of kidney failure: acute renal failure and chronic renal failure.

Acute Renal Failure (ARF)

1. Prerenal ARF due to heart failure with reduced cardiac output and low blood pressure, or conditions associated with diminished blood volume and low blood pressure, such as severe hemorrhage.

As long as renal blood flow does not fall below 20% of normal, acute renal failure can usually be reversed if the cause is corrected before renal cell damage occurs. When the blood flow to the kidneys decreases, the glomerular filtration rate (GFR) also decreases. This decreases the kidney’s work load, and therefore decreases the kidney’s requirement for energy and oxygen. Ischemia can not persist for more than a few hours at below 20% blood flow, or the kidney will experience intrarenal ARF.

2. Intrarenal ARF due to abnormalities of the kidney itself, including those affecting the blood vessels, glomeruli or tubules. Examples follow below.

2. a. Acute Nephritic Syndrome (Acute Glomerulonephritis; Postinfectious Glomerulonephritis) - A common cause of acute glomerular capillary damage. 95% of patients with acute glomerulonephritis had damage occur to the glomeruli 1-3 weeks after an infection elsewhere in the body. Antigen-antibody complexes are deposited in the glomeruli. Glomeruli become blocked by inflammation.

2. b.Tubular necrosis due to severe renal ischemia - The epithelium is destroyed due to severe ischemia (prerenal ARF causing intrarenal failure) and inadequate supply of nutrients and oxygen to the tubular epithelial cells. Tubular cells slough off and plug up the nephrons. This blocks urine outflow. Most common cause is a prerenal occurrence of ARF, such as circulatory shock.

2. c. Tubular necrosis due to poisons, toxins or medications which destroy the tubular epithelial cells. Examples are carbon tetrachloride, heavy metals, ethylene glycol, insecticides and medications such as tetracyclines and cis-platinum.

2. d. Interstitial nephritis is due to vascular, glomerular or tubular damage that destroys individual nephrons or involves primary damage to the renal interstitium. Conditions that cause primary interstitial damage are acute pyelonephritis and acute allergic interstitial nephritis. Pyelonephritis can be due to bacterial infections from the bladder (most commonly due to Escherichia coli, from fecal contamination of the urinary tract) or via the blood steam. Drugs or poisons can also induce primary damage to the renal interstitium.

3. Postrenal ARF due to bilateral obstruction of the urinary collecting system anywhere from the calices to the urethra. The most common cause being kidney stones caused by precipitation of calcium, urate or cystine. With moderate acute renal failure, there is retention of water, waste products of metabolism, and electrolytes. This causes edema and hypertension. Excessive retention of potassium can be fatal. Another possibly fatal problem is metabolic acidosis due to inability to excrete sufficient hydrogen ions. The person will die within 8-14 days without restoration of kidney function or dialysis.

Acute renal failure may be treated and the person may never have another problem or it can be the instigating factor for chronic renal failure. Chronic renal failure may show up immediately or many years down the road.

Chronic Renal Failure

Chronic renal failure is due to irreversible loss of large numbers of functioning nephrons. Clinical symptoms occur when there are less than 30% normal functioning nephrons. In general, chronic renal failure occurs due to the same reasons acute renal failure occurs, but the progression is slower. Often the initial insult to the kidney leads to progressive deterioration of kidney function and increased loss of nephrons over time until the person reaches end-stage renal failure and is placed on dialysis or receives a kidney transplant. When nephrons are lost, other nephrons take on a larger load. They adapt and excrete normal amounts of water and solutes until the kidney is reduced to 20-30% normal nephron mass. Over the years, the glomeruli are injured. It is thought this injury is caused by the increased pressure and stretch from the increased blood pressure on the glomeruli. This eventually causes sclerosis and further destruction of the kidneys. The only method known by conventional medicine to slow the glomerular damage down is to lower blood pressure and glomerular hydrostatic pressure by using drugs such as angiotensin-converting enzyme inhibitors to block formation of angiotensin II.

Causes of Chronic Renal Failure

The most common causes of end stage renal failure are diabetes mellitus, hypertension and glomerulonephritis.

Diabetic nephropathy is the most common cause of renal failure. Almost all insulin-dependant diabetics have histological evidence of glomerulosclerosis. 35% will develop clinical nephropathy, usually about 15-20 years after diagnosis. The younger the age of onset of IDDM, the longer the duration, and the more frequent the episodes of ketoacidosis, the more likely the diabetic is to have diabetic nephropathy. Renal failure accounts for 48% of the diabetic deaths in those who acquire IDDM before age 20.

Hypertension and atherocsclerosis can be a primary cause of renal damage. However, renal failure can also induce hypertension and lead to increased renal damage. Even in “normal” people benign nephrosclerosis takes place which diminishes normal kidney function to 40 or 50% by age 80. Benign nephrosclerosis in association with severe hypertension can lead to rapidly progressing malignant nephrosclerosis.

Chronic glomerulonephritis is a slowly progressive disease often leading to irreversible renal failure. It can be a primary disease following acute glomerulonephritis or secondary to systemic diseases, such as diabetes or lupus erythematosus. It usually begins with precipitated antigen-antibody complexes in the glomerular membrane. There is inflammation, thickening, and eventually, fibrous tissue.

Issues and Treatment of Renal Failure

Following are general issues which need to be considered in acute renal failure, chronic renal failure, dialysis and renal transplantation. Treatments listed are for renal health support, treatment of complicating factors surrounding renal failure, and treatment of the side effects resulting from conventional treatments. Only those treatments which appear to be beneficial and safe to use for prevention, as well as treatment of kidney failure, are included. There are methods for treating some of these conditions which have purposely been left out, since they may harm kidney function, or their effects on kidney function are unknown.

Acute Renal Failure

Chinese data suggests that patients with acute renal failure who are treated right away, have an 89.6% - 92.1% chance of recovering normal kidney function. There are many causes of acute kidney failure but a common cause which can be prevented, or treated in conjunction with dialysis, is acute failure due to acute nephritic syndrome (acute glomerulonephritis; postinfectious glomerulo-nephritis). 95% of patients with acute glomerulonephritis have damage occur to the glomeruli 1-3 weeks after an infection elsewhere in the body. Antigen-antibody complexes are deposited in the glomeruli. The glomeruli become blocked by the inflammation.

Give the kidney supportive and protective herbs and supplements.

Chronic Renal Failure - Prevention

The most important tool you have for prevention of renal failure is recognition of the leading causes of renal failure. You can prevent or slow down renal failure only if you treat in the early stages. Clinical symptoms show up when there is 70% destruction of functional nephrons.

#1 cause of renal failure - IDDM (31.4%)

#2 cause of renal failure - Hypertension (24.8%)

#3 cause of renal failure - Glomerulopathies (18.2%)

#4 cause of renal failure - Cystic kidneys (4.9%)

Look for early signs of renal failure in lab work. Abnormal blood cholesterol may be the first and only sign for a few years. High cholesterol levels are seen in renal failure. The levels may be as high as 400 or 500. Watch for microalbuminuria. Yearly physicals and a twice yearly blood chemistry screen and urinalysis is necessary in the high-risk groups mentioned previously.

Early stage chronic kidney failure - Diagnosis is not usually known until much of function is lost. If you have high-risk individuals, such as insulin-dependent diabetics, chronically hypertensive individuals, and individuals with a family history of kidney failure, they can be treated preventatively or at a minimum should be monitored for a rise in uremic indices with the use of a blood chemistry screen and urinalysis twice per year. They should be treated at the first sign of renal damage. The key factor is treating these individuals in the early stages while there is inflammation as opposed to waiting for extensive sclerosis and loss of functional nephrons. For all insulin-dependent diabetics, I suggest preventative treatment. Research has shown all insulin dependent diabetics have histological evidence of glomerulosclerosis when renal biopsies have been undertaken and 35% will develop clinical nephropathy; usually about 15-20 years after diagnosis of diabetes.

Prevention can be undertaken by attending to the causative factors via treatment of hypertension, diabetes, or other causative factors. Additionally, the herbs and food supplements that follow can be used to support kidney function.

Chronic Renal Failure – Treatment

Chinese data suggests 10.9%-13.2% of patients with chronic renal failure are able to fully recover normal kidney function.

Once a person has been diagnosed with chronic renal failure, they generally have less than 30% of nephron function left. At this stage, you attempt to prolong kidney function as long as possible as well as treat life-threatening or irritating symptoms which are a part of the disease process.

Control hypertension

Hypertension is a major problem and neither herbs nor drugs control renal induced hypertension very well. Herbal diuretics, such as Taraxacum leaf, can be helpful. Zea mays is another herb which benefits inflamed kidneys and acts as a diuretic.

Dr. D’Adamo’s “blood type diet” (see Eat Right for Your Type by Dr. Peter D’Adamo) or other methods to remove food allergens is absolutely necessary.

Use herbs such as Crataegus spp., Salvia miltiorrhiza and Allium sativa. I have used viscum and veratrum. Veratrum has to be given in small doses every four hours for best results. Although I have used them both in renal hypertension, the results were moderate.

Control hypercholesterolemia

Hypercholesterolemia is a sign of chronic renal failure but is also thought to be a causative factor of additional kidney damage.

Dietary fiber, exercise, nutritional supplements that are usually given for hypertensive individuals: Polygonum multiflorum, Taraxacum officinalis, Allium sativa, Panax ginseng, Rheum officinalis, Curcuma longa are all herbs which lower cholesterol. Panax and Rheum additionally support normal kidney function. Polygonum is used in Chinese herbal formulas for kidney support, and these formulas have been shown to be beneficial in research experiments, but when used by itself it has had a negative effect on kidney function in research animals. Therefore, do not use this herb alone, only in conjunction with balanced Chinese formulas.

Control hyperglycemia, if diabetic

Diet, exercise, nutritional supplements as appropriate in diabetes, Allium sativa, Polygonum multiflorum (see contraindication under control of hypercholesterolemia), Vaccinium myrtillus.., Panax ginseng, Rheum officinalis. Panax and Rhaum are both additionally useful in lowering the uremic index. Gymnema sylvestre is the best herb I know for hyperglycemia; however, I am unsure of it’s safety in renal failure since there is no history of use during renal failure. I still mention it here due to it’s often astounding results, apparent lack of toxicity and unfortunate lack of use by most health care practitioners. See case history # 3.

Support blood vessel integrity, including glomerular capillaries and peritubular capillaries.

    Uremic bruising or bruising from prednisone use can be treated with Vaccinium myrtillus.

    Capillary damage is also a problem in hypertension where glomerular sclerosis takes place. In theory, herbs such as Crataegus can be used for both the hypertension as well as support of capillary integrity in the glomerulus. See case history #4.

Support diuresis

    Taraxacum officinalis leaf - one teaspoon BID-TID, Zea mays (fresh), Petroselinum crispum root. Petroselinum was used as a diuretic in one case of renal failure without any apparent irritation of the kidneys; however, I’m concerned that it could irritate the kidneys, so this diuretic should be used cautiously. The other herbs appear to be safe diuretics.

Decrease or eradicate renal inflammation and uremia

Appropriate Chinese herbal formulas are used to cleanse blood and protect kidney function.

Fish oil and herbal support is used for nephron function. Ginkgo, Salvia, Panax, Rheum.

Decrease work load on the kidney

Restrict protein – Protein consumption increases metabolic wastes which the kidney must remove from the body.

    Use enemas with charcoal. Use plain hot water at 104 -110 degrees Fahrenheit. Dissolve one to five tablespoons of charcoal in two quarts of water. For a retention enema use one tablespoon per one cup of lukewarm water. Use once to twice per day.

Keep the skin pores open and assist the skin in removal of metabolic wastes:

    1) Fever treatment of 100-101 degrees Fahrenheit for edema, to induce water loss through diaphoresis. Monitor blood pressure during this process.

    2) Hot mud packs. Daily packs for two weeks showed considerable amounts of uric acid excretion through the skin. Sometimes the percentage of uric acid in the sweat reached a value equal to or exceeding that in the blood.

Maintain hematocrit

Erythropoietin is primarily made by the kidney. The liver makes 10% of the body’s erythropoietin. When the kidneys fail, the red blood cell count falls severely. Erythropoietin treatment is used to maintain hematocrit; may be able to substitute Cervi cornu verum (unossified horns of stags) for part of erythropoietin.

Maintain energy

Panax ginseng, mild to moderate exercise, keep hematocrit as normal as possible.

Maintain calcium and iron levels

Muscle spasms are a painful problem for the person with chronic kidney failure. It appears to be at least partially due to low calcium levels due to the lack of 1- 25 di-hydroxycholecalciferol. This leads to decreased intestinal absorption of calcium and decreased availability of calcium. Calcium and 1-25 di-hydroxycholecalciferol both need to be supplemented as well as using hot water bottles for acute spasms.

Restless legs can be treated with calcium and vitamin B.

Iron supplementation is usually necessary.

Emotional support

Homeopathy for mental, emotional support as well as to decrease the progression of the disease.

Counseling is often necessary.

Supporting the Person on Dialysis

Use the same regime as listed under treatment of chronic renal failure, with these additions:

Control dialysis-induced itching (also for renal-failure-induced itching)

Capsaicin, a constituent in Capsicum has been effective for dialysis-induced itching. Whole Capsicum extracts can be used also. Creams or salves are used externally.

Ginkgo cautions

Ginkgo will increase bleeding time so be wary since the anticoagulant heparin is given during dialysis. If your patient has trouble clotting after dialysis, the heparin level will need to be decreased or eradicated except for the amount in the dialysate fluid which can’t be decreased. The Ginkgo may also need to be decreased if decreasing the heparin is not enough.

Dialysis side effects

Length of time during each dialysis session is important. Longer sessions will decrease the possibility of sudden electrolyte changes and sudden loss of water, inducing consequent muscle spasms, headaches and a general sick feeling.

Salt cravings are common after dialysis, especially when shorter dialysis runs are given.

Keep phosphorus and potassium blood levels in normal range.

Avoid phosphorus and potassium-containing foods and liquids (increased potassium due to decreased GFR, use of ACE inhibitors or due to destruction of distal tubules and cortical collecting tubules). Note that Dandelion, which is used as a diuretic by many herbalists, contains a large amount of potassium and you may think it would be cause for alarm. Mineral content is highest in capsules, lower in decocted teas, while liquid extracts contain minimal amount of minerals. Use of the liquid extract in two cases made no difference in potassium serum levels. I suggest use of the liquid extract only.

Post Renal Transplant

The general issues which need to be considered are:

Control hypertension - see above information.

Control hypercholesterolemia - see above information.

Control hyperglycemia if diabetic - see above information.

Decrease renal inflammation to new kidney if causative factor still exists - see above information.

Support blood vessels, including glomerular capillaries - see above information.

Decrease prednisone bruising - see above information.

Treat cyclosporin-induced gout.

1 teaspoon Flaxseed oil BID or 1 tablespoon ground flax seeds BID, 1 teaspoon Evening primrose oil BID or other oils high in linolenic acid. Urtica dioica is quite beneficial with gout, but must be used long term for one month or more. Can use one cup of tea TID, if there is no edema or 1/2 teaspoon 1:1 fresh liquid extract BID, if there is edema. Never use Urtica which has been harvested after it goes into bud stage. This can irritate the kidneys and cause nephritis.

Decrease the chance of rejection and protect the kidney & liver from cyclosporin

Research shows Ginkgo biloba may decrease the chance of delayed graft function and rejection.

Research has shown Ginkgo and fish oil to effectively protect the transplanted kidney from damage due to cyclosporin Silybum marianum may also protect the kidney from cyclosporin damage.

Silybum and Ginkgo are used for liver protection from cyclosporin damage.

Treat diseases, such as hepatitis B and C, from transplant.

Glycyrrhiza is usually used for hepatitis but is contraindicated with severe hypertension. Other herbs used in hepatitis which appear to be safe to use for the renal transplant patient are Silybum, Phyllanthus spp. and Bupluerum chinense/falcatum. See case history #5.

Watch for herb interactions with drugs, since they may affect the half life of the drug, and for herbs which can be harmful.

Herbs or drugs which can alter the cytochrome p450 system will alter the half lives of immune-suppressive drugs. This means all herbs with hepatoprotective action should be suspect and the immunosuppressive drugs should be monitored closely while these herbs are being used. Examples are the liver herbs listed above for hepatitis, such as Silybum.

One research article (16) showed Ginkgo may increase the level of cyclosporin in graft recipients.

Chronic Glycyrrhiza use mimics aldosteronism by increasing sodium reabsorption and potassium excretion by the kidney. Long term use can induce hypertension in normotensive persons. Hypertension is something the person with a kidney transplant already has to deal with, you don’t want to add to it.

Caution with all treatments which may affect the immune system since the person is using immunosuppressive drugs. Increasing the activity of her/his immune system may cause rejection of the transplant.

Other helpful suggestions

Emotional support

Be aware of mood fluctuations from OKT3 (a drug given immediately after transplant surgery) and steroids and counsel the patient about these drugs and their psychological side effects.

Nurture self through massage and other supportive methods.

Energy work such as Qi Gong can be helpful.

Rest is absolutely necessary.

Constipation after surgery

After surgery, get the bowels moving with rheum and acupuncture.

Weight gain

Expect an average 35 lb. weight gain from surgery and steroids. Healthy diet, eradicate allergenic foods, exercise when appropriate.

Platelet Activating Factor (PAF) And its Role in Renal Failure

Platelet activating factor or PAF (a glycero-phospholipid) is an inflammatory mediator that plays an important role in allergic and inflammatory processes, including ischemic renal failure. Evidence for involvement of PAF in renal immune injury has been provided by the observations that PAF is released during kidney hyperacute allograft rejection. It has been proposed that PAF participates in glomerular immune complex deposition in experimental serum sickness and also in systemic lupus erythematosus. Research shows it is released by isolated perfused kidneys and glomeruli as well as by suspensions of medullary cells, although not by tubules. The mesangial cells are thought to be the major source of PAF in the glomerulus. PAF has been shown to cause renal vasoconstriction and release of inflammatory agents, such as prostaglandins and thromboxane B2 in the kidney. There are specific binding sites for PAF.

Platelet Activating Factor Antagonists

PAF antagonists interfere with the binding of PAF to its cellular receptors. Ginkgolides from Ginkgo biloba, kadsurenone and other lignans isolated from Piper futokadsurae, and gliotoxin-related compounds from various fungi and bacteria constitute three groups of naturally occurring platelet-activating factor antagonists. Of the 3 naturally occurring PAF antagonists, Ginkgo is the most available and most researched.

Ginkgo biloba: A mixture of Ginkgolides ABC in 2:2:1 ratio inhibit most of the biologic effects induced by PAF. Ginkgolide BN 52021 (Ginkgolide B), has been shown to be a receptor antagonist for PAF. (16) One research article shows Ginkgolides A, B, and C inhibiting cyclosporin damage to the kidney. Cyclosporin is a fungal cyclic polypeptide (multiamino acid compound from a fungus) which suppresses both humoral and cell-mediated immunity and is therefore used in organ transplantation. Ginkgo reduces tubular and interstitial damage without affecting cyclosporin’s immune-suppressive effects (7). Ginkgolides inhibit PAF-induced release of thromboxane B2 and prostaglandins from primary cultures of human and rat glomerular mesangial cells. BN 52021 also inhibits PAF-induced formation of reactive oxygen species from cultured mesangial cells and destruction of the glomeruli. (Ginkgo is known to be an antioxidant which is important since free radical production is implicated in progressive kidney disorders.) In addition, this antagonist inhibits PAF-induced decreases in renalblood flow, glomerular filtration and urinary sodium excretion (10). The use of BN 52021 reduces proteinuria and the hi~itopathological lesions in nephrotoxic rabbits. Given preventively, or even curatively, BN 52021 abolishes the adriamycin-induced lethality and proteinuria in rats. This protection is associated with a significant reversal of the glomerular alterations induced by the drug. BN 52021 also prevents acute rat renal failure induced by glycerol injection. BN 52021 given intravenously prior to renal graft surgery and for 4 days after surgery has been shown to increase the chance of graft survival and decrease the number of acute rejection episodes after surgery. (16)

Effects of herbs

Salvia miltiorrhiza - A traditional Chinese medicinal herb used for treatment of hemorrhage, menstrual disorders, swelling, and coronary heart disease. Salvia’s active ingredients include diterpenoids, polyphenolic acids, and a flavanone. The crude extract as well as its diterpenoids and flavanone have shown antimicrobial activity, inhibit blood platelet aggregation, dilate coronary arteries, and increase coronary blood flow without affecting heart rate in vitro and in vive. They also have preventive effects on development of respiratory distress syndrome. The crude extract and polyphenolic acid have been found to improve renal function in vitro and in vivo. (13)

Salvia miltiorrhiza reduces accumulation of methylguanidine and guanidinosuccinic acid levels in uremia. Methylguanidine and guanidinosuccinic acid (oxidation products) have been reported to cause platelet dysfunction, hemolytic activity, glucose-metabolism disturbance and inhibition of lymphocyte transformation. This demostrates protection of the body in uremic situations, and also indicates Salvia ‘s action as a possible free radical scavenger (8). (Active oxygen has been shown to be involved with proliferation of mesangial cells.)

The constituent, magnesium lithospermate B, a tetramer of caffeic acid, has been shown to decrease blood urea nitrogen, serum creatinine, methylguanidine, guanidinosuccinic acid and inorganic phosphate in uremic rats whose uremic state had been induced by an adenine diet. It activates the kallikrein-kinin system in the rat kidney to promote the production and secretion of prostaglandin E2, inducing dilation of the renal vascular system, and increasing the renal blood flow and glomerular filtration rate. PGE2 also inhibits proliferation of mesangial cells (in glomeruli) and acts antagonistically against vasoconstriction brought about from Thromboxane A2. PGE2 has been found to inhibit tubular reabsorption of sodium in one study. PGE2 has been demonstrated to have a protective role in the maintenance of hypertension which accompanies renal disease. Magnesium lithospermate B may therefore ameliorate the development of hypertension through excretion of urinary sodium and by improving renal hemodynamics. (5)

Ginkgo biloba - See above, under Effects of PAF

Panax ginseng - Oral Ginseng has been shown to decrease uremic toxins such as creatinine, methylguanidine, and guanidinosuccinic acid. One study found oral ginseng suppressed uremic toxins, decreased urinary excretion of protein and inhibited mesangial proliferation, demonstrating the arrest of progressive renal disorder from subtotal nephrectomy. In experiments using cultured mesangial cells, there was considerable suppression of mesangial cell proliferation. This suggests ginseng has a role as a free radicalscavenger. Another study shows Ginseng saponin protecting the kidney from oxidative stress. Ginseng’s action as a free radical scavenger is important since free radical production is implicated in progressive kidney disorders. (2, 3)

Rheum officinalis - Increases glomerular filtration, and decreases cholesterol and triglyceride levels. Interactions of lipids with advanced glycosylation have been implicated in the genesis of diabetic microangiopathy in the kidney. Rheum may relieve diabetic nephropathy by improving lipid metabolism. Experimental research with aqueous extract has shown lowered blood glucose levels. Aqueous extract also increases urinary excretion of urea nitrogen and creatinine, probably due to increased glomerular filtration. (1, 2)

Ephedra distachya, Terminalia chebula, Geranium thunbergii - Like Rheum these are tannin-containing herbs. In one experiment, these herbs showed benefits in reducing uremic indices in animals. Animal research indicates many condensed or non-hydrolysable tannin-containing herbs seem to improve uremic indices. (15)

Astragalus membranaceous - Acts as a diuretic when the kidneys are weak. It provides support for the kidneys and has been used in Chinese medicine for treatment of chronic nephritis. Astragalus is thought to increase renal blood flow. It is anti-inflammatory, hepatoprotective and an antioxidant. It helps restore normal tissue tone and function.

Zea mays - A soothing diuretic and antiseptic. It supports normal kidney anatomy and physiology. Glycoproteins in corn silk produce interferon, inhibit IgE formation and enhance IgG and IgM formation. They also have antiviral and antitumor activities.

Evodia rutecarpa - Reduced uremic state in rats. (2)

Peonia lactiflora - Reduced uremic state in rats. (2)

Stevia rebaudiana - May induce nephrotoxicity, specifically, at the proximal convoluted tubules. This herb should be avoided or used with caution by all persons with renal disorders.(l4)

Case Histories

Case #1 from Dr. Kruzel in Portland, OR.

Case of dialysis sepsis, food poisoning in person with renal failure.

20 yo female presenting with chronic kidney failure d/t Post strep GN. On home dialysis 3-4 times per day. Presented with fever, edema, has severe HA following dialysis, swollen red L leg, hot to touch. LV swollen, no palpable nodes.

DX: post dialysis sepsis

TX:     1) Echinacea 2, Astragalus 1, Hydrastis .5, Ligusticum .5, Phytolacca .5, Belladonna .5

Sig: 1 teaspoon every 4 hours

    2) Homeopathic Pyrogenum 30C BID

24 hours later: temp. decreased, feeling better - continuing meds. Follow up: feels better, normal temp, no swelling, BP 168/118 - on allopathic med but takes infrequently- told to take it.

TX: Salvia milt. 3 oz, Chimaphila 1 oz, @ 1 t BID. Sepsis formula taken 1 t QD, renal protomorphogen and Rhus tox 12C TID and dietary changes based on blood type. Will return in 4 weeks after seeing nephrologist. Called in 2 weeks to say something she ate on holiday gave her diarrhea and abdominal discomfort. Nausea and vomiting, can’t keep fluids down, light headed, craving salt water. Charcoal tabs did not help.

Assessment: food poisoning and prolonged dehydration coupled with dialysis led to electrolyte imbalance.In a household where they have some herbs available - put together concoction with what was available - Capsules of Althea 1, Hydrastis .5, Echinacea .5, Viburnum .5, Taraxacum .5. 2 caps with mint tea every 2-4 hours and contact Doc next day.

Next day diarrhea almost gone, can keep fluids down. Appetite returned. Eating chicken soup. - Keep taking caps, 1 TID for several days and other medicines as soon as able. 3 weeks later, recovered, gained 10 pounds, feeling more energy. Urinary output the same, but higher specific gravity (Signifying a greater concentrating ability of kidneys). Analysis of peritoneal dialysate showed higher concentration of solutes which meant dialysis more efficient. No return of sepsis. BP still high at 190/108.

Presently she is being maintained on dietary changes, formula of Salvia and Chimaphila and Rhus tox. Unclear if there will be any return of kidney function. Goal now is to keep her from developing sepsis from dialysis and decrease the number of times per day she needs to undergo procedure. Working nutritionally to decrease long term effects of renal failure and constant dialysis.

Case #2 from Dr. Tilgner in Eugene, Oregon.

45 yo male, 170# presents with sore throat of 2 weeks duration, sore throat getting better, back pain, fatigue, edema (not pitting), dark urine.

Dx: Postinfectious Glomerulonephritis - Strep antigen-antibody reaction causing acute glomerulonephritis

Strep Tx: Given Usnea 2, Echinacea 3, Hydrastis (Goldenseal) 2.5, Phytolacca (Poke) .5, for possible strep infection.

Sig: 2 droppers or 60 drops every 2 hours (waking hours) for first 24 hours, then 2 droppers 5 times per day for 24 hours, then 2 droppers 4 times per day for 5 days then dosage will be adjusted as necessary. Call Dr. at end of first 24 hours. Family also had strep and were additionally treated.

Renal Tx: 1) Zea mays (Corn silk) 2, Salvia miltiorrhiza 3, Ginkgo biloba 3, for kidney support. Take 2 droppers 3 times per day. 2) 24% 40 mg Ginkgo, 2 capsules BID - which he never took. 3) Althea tea for kidney - use one heaping tablespoon per cup water. Drink 3 cups per day.

He recovered and felt no need for follow up, although I felt he should continue kidney support for at least 6 months.

Case #3 from Dr. Mariana Markell in Brooklyn NY

40 yo male with type 2 diabetes and a two yo kidney transplant. He had erratic blood glucose and was still not feeling well after two years post transplant.

Tx: 100 mg Panax ginseng extract BID, 30 mg Ginkgo biloba extract BID. Blood glucose improved with glycosylated hemoglobin dropping from 8.6% to 7.9%. When he ran out of herbs, and did not replenish them, his blood glucose became worse. He reinstated his tx and it improved again.

Case #4 from Dr. Mariana Markell

61 yo female with Addison’s disease, Type 1 diabetes, hx of MI, 15 year old kidney transplant. Had severe bruising secondary to+ corticosteroid use and low dose aspirin.

Tx: 250 mg bilberry extract BID - In 3 weeks she noticed decreased bruising. In 6 months there was minimal bruising.

Case #5 from Dr. Mariana Markell

36 yo female who developed fulminant hepatitis C from a cadaveric kidney transplant.

Tx: Given interferon - did not tolerate it well. Recovered liver function with bilirubins in 2.5-3.5 mgl dl range, transaminases remained elevated. Eleven months post transplant she was given 175 mg Silybum BID (standardized to 80% silymarin). In nine months her transaminases normalized and her albumin increased from 2.9 to 3.4 mg/dl. At one year her bilirubins and transaminases were within normal limits and hepatitis C was no longer detectable in her serum.


1. Takako Yokozawa, et al., “Effects of Rhubarb Extract in Rats with Diabetic Nephropathy”. Phytotherapy Research, 97;11:73-75.

2. Takako Yokozawa, et al., “A Study on the Action of a Modified Wen-Pi-Tang Prescription, Using Uremic Toxins in Blood as Indices”. Phytotherapy Research, 94;8:456-460.

3. Takako Yokozawa, et al., “Increase of Active Oxygen in Rats after Nephrectomy is Suppressed by Ginseng Saponin”. Phytotherapy Research, 96;10:569-572.

4. Takako Yokozawa, et al., “The Ethanol-insoluble Fraction of an Aqueous Cervi Cornu Vemum Extract Improves the Condition of Renal Anemia in Rats Fed an Adenine Diet.” Phytotherapy Research, 94; 8:276-280.

5. Takako Yokozawa, et al., “Renal Responses to Magnesium Lithospermate B (MLB) in Rats with Adenine-induced Renal Failure”. Phytotherapy Research, 93;7:235-239.

6. Ye Guoji, et. al., “Effects of Polysaccharides Purified from Salvia miltiorrhiza radix on Experimental Nephrosis in Rats”. Phytotherapy Research, 94;8:237-341.

7. E. Pirotzky, et. al., “Cyclosporin-Induced Nephrotoxicity: Preventive Effect of a PAF-Acether Antagonist, BN 52063". Transplantation Proceedings, 88;XX33(3)665-669.

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9. Stoof, et al., “Does Fish Oil Protect Penal Function in Cyclosporin-Treated Psoriasis Patients?” Journal of Internal Medicine, 89;226:437-41.

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14. Chaivat Toskulkao, Deechakawan, et. al., “The Low Calorie Natural Sweetener Stevioside: Nephrotoxicity and its Relationship to Urinary Enzyme Excretion in the Rat”. Phytotherpy Research, 94;8:281-286.

15. Yokozawa, Fujioka and Oura, “Confirmation that Tannin-containing Crude Drugs Have a Uremic Toxin- decreasing Action”. Phytotherapy Research, 1995;9:1-5

16. Grino, T., “BN 52021: A Platelet Activating Factor Antagonist for Preventing Post-Transplant Renal Failure - A Double-Blind, Randomized Study”. Ann. Intern. Med., 1994;121:345-347.

17. Inselmann, Blohmer, Kottny, et. al., “Modification of Cisplatin-Induced Renal p-Aminohippurate Uptake Alteration and Lipid

Peroxidation by Thiols, Ginkgo biloba Extract, Deferoxamine and Torbafylline". Nephron, 1995;70:425-429.

18. Leishi, L. “Rheum officinale: A New Lead in Preventing Progression of Chronic Renal Failure”. Chin. Med. I., 1996;109(1):35-37.

19. Hase, Kasimu, et. al., “Preventive Effect of Lithospermate B from Salvia miIfiorvhiza on Experimental Hepatitis Induced by Carbon Tetrachloride or D-Galactosamine/ Liposaccharide”. Planta Medica, 1997;63:22-26.

20. Bokemeyer, C., et. al., “Silibinin Protects Against Cisplatin-induced Nephrotoxicity without Compromising Cisplatin or Ifosfamide Anti-Tumor Activity”. Br. I. Canccu, 1996;74(12): 2036-2041.

21. Gaedeke, J. et. al., “Cisplatin Nephrotoxicity and Protection by Silibinin”. Nephrol. Dial. Transplant. 1996; Tan; 11(1):55-62.
  Copyright 2001 Paul Bergner

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