TweetUrinary - Kidney support
Introduction
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