Wednesday, February 20, 2008

Kidney Disease-3

Polycystic kidney disease may occur at birth, during childhood, or in adults. Congenital polycystic disease can be detected at birth and may affect all or only small parts of one or both kidneys. Childhood polycystic kidney disease can cause death after a few years because of liver and kidney failure. In some adults, the disease may actually be present at birth, but not manifest any symptoms until young adulthood or middle age. In adults, it can affect either one or both kidneys (Glanze 1996). Polycystic kidney disease is characterized by autonomous cellular proliferation, pockets of fluid accumulation within the cysts, and intraparenchymal fibrosis of the kidney. Other clinical observations include renal failure, liver cysts, and cardiac valve abnormalities (Bacallao et al. 1997).

The traditional method of detecting ADPKD has been by using ultrasound, computed tomography (CT), or magnetic resonance imaging (MRI) of the kidneys to look for the presence of renal cysts. However, the challenge is to detect ADPKD in people who carry the defective gene, but who may not have any symptoms or show any developed cysts and therefore be undiagnosed as having ADPKD. Newer methods of DNA testing can now identify individuals who carry the defective gene, but are not symptomatic. For example, every member of four Chinese families with a known history of ADPKD showed unique DNA patterns (Yuan 1997). DNA diagnostic testing methods have value for patients with existing ADPKD as well as for presymptomatic patients.

ADPKD progresses to end-stage renal insufficiency before the age of 73 in about 50% of affected patients (Grantham 1997). Some patients are affected by numerous cysts that form inside the proximal and distal tubules, while other patients are spared. Why this is the case remains a mystery. The formation of cysts begins in early childhood, affecting less than 1% of tubules as a consequence of mutated DNA. The risk factors associated with polycystic kidney disease include gender (males progress more quickly than females), race (black patients progress more rapidly than whites), and other contributing factors such as hypertension and proteinuria. These factors can aggravate and accelerate polycystic kidney disease through to end term (Grantham 1997).

Because hypertension is a common and serious factor of ADPKD that usually occurs early in the disease before renal function begins to decrease, Doppler ultrasonography has been used to assess renal vascular resistance (RVR) by measuring resistive and pulsatility indices. In a study of 42 patients with ADPKD and 65 control subjects, Brkljacic et al. (1997) found that Doppler indices do reflect increased RVR in those patients with ADPKD and that renal function disturbance did manifest systemic arterial hypertension. The abnormality of the kidneys in these patients was easily observed using ultrasound. However, this method did not show ADPKD potential for patients if renal cysts were not present. DNA testing is required to determine whether a patient carries the PDK1 and PDK2 chromosomes.

The occurrence of cardiovascular complications is a very common cause of death for persons with ADPKD. Chapman et al. (1997) examined the relationship of known cardiovascular risk factors, hypertension, and ADPKD. According to the researchers, left ventricular hypertrophy (LVH) is an important risk factor for premature cardiovascular death in persons with essential hypertension. Hypertension occurs frequently and early in ADPKD patients. In 116 adult ADPKD patients and 77 healthy controls, Chapman et al. (1997) found a higher frequency of LVH in ADPKD men (46% versus 20%) and women (37% versus 12%) compared to the control subjects. LVH in ADKPD patients was associated with higher systolic and diastolic blood pressure. According to the researchers, the role of blood pressure as a contributing factor to LVH in ADPKD patients may be partly due to early onset and inadequate treatment.

The possibility is being explored that ADPKD may have an emerging infectious disease component as well. Research has shown fungal DNA in kidney tissue and cyst fluids of ADPKD patients, but not in healthy kidneys of persons without ADPKD (Miller-Hjelle et al. 1997). In a differential activation protocol assay, the researchers showed bacterial endotoxin and fungal beta-D-glucans in cyst fluids from human kidneys with PKD. Tissue and cyst fluids were examined for fungal components, and the serological tests showed Fusarium, Aspergillus, and Candida antigens. Miller-Hjelle et al. (1977) concluded that "endotoxin and fungal components, sphingolipid biology in PKD, the structure of PKD gene products, infection, and integrity of gut function [will establish a mechanism] for microbial provocation of human cystic disease."


TREATMENT FOR KIDNEY DISEASES

1)Conventional

2)Natural and Adjuvant

Treatment of kidney disease is a complex issue and depends on the type of disease, the underlying cause, and the duration of the disease. Treatment usually starts with addressing the original cause such as inflammation. Inflammation from infection is treated with antibiotics. Inflammation caused by an immune reaction is more difficult to treat. In this case, immunosuppressant drugs (corticosteroids) are used in an attempt to control the immune reaction.

In the case of acute kidney failure, treating the underlying cause may return the kidneys to normal function. Sometimes dietary restrictions (less salt and protein) are required until the kidneys are better able to handle these substances. Diuretic medicines help the body to excrete more water and salt. However, with chronic kidney failure, medicines are used to stop progression of the disease so it does not reach ESRD.

When kidney disease does not respond to treatment with dietary restrictions and medicines, dialysis or kidney transplantation are the next treatments to consider (Glanze 1996). Dialysis is a technique used to remove waste products from the blood and excess fluid from the body in the case of renal failure. Kidney transplantation is a surgical procedure in which the diseased kidney (sometimes both kidneys) is removed and replaced with a healthy kidney from a donor (NIDDK 1999).


Conventional Medical Treatment

1)Medicine and Drugs

2)Kidney Dialysis

3)Transplantation


Medicine and Drugs

In the United States, 4% of the population is at risk for kidney disease. As part of an annual physical checkup, we should have three important tests: blood levels of creatinine, blood urea nitrogen, and urine levels of protein. Small elevations of creatinine can be an early sign of kidney disease. According to the National Kidney Foundation (2001a), 11 million Americans have elevated blood levels of creatinine. Healthy kidneys remove creatinine, but when kidney function diminishes, creatinine levels in the blood go up. Early detection leads to early treatment, which can occur at a stage when treatment can help prevent kidney disease from advancing to a more serious stage. Diabetes is the leading cause of chronic kidney disease, followed by hypertension. See your physician regularly and follow prescribed dietary and drug treatment to control blood sugar levels and blood pressure (National Kidney Foundation 2001a). Treatments for conditions which can lead to kidney disease include numerous prescription drugs and treatment protocols. (See the Life Extension protocols on Diabetes, Immune Enhancement, Cardiovascular Disease [sections on Homocysteine and Hypertension], Thyroid Deficiency, and Urinary Tract Infection for additional information on specific conditions and treatment.)


Kidney Dialysis

Kidney dialysis is a medical treatment used to filter out waste products from the blood. Dialysis has been proven to be an effective technique for removing wastes and extra fluid from the body. According to the annual report of the U.S. Renal Data System (2001), over 243,000 persons in the United States were using dialysis treatment in 1999. Dialysis treatment permits these people to live relatively normal lives within the limitations of their disease.

There are two types of dialysis methods: hemodialysis and peritoneal dialysis. The most common technique is hemodialysis, accounting for slightly over 85% of dialysis treatment. The remaining 15% of patients use peritoneal dialysis (NIDDK 2001b). Neither hemodialysis nor peritoneal dialysis is uncomfortable and both are equally effective in removing wastes and extra fluids from the body. The choice is usually one of preference or level of convenience desired by the patient in consultation with appropriate medical professionals.

Even for patients who use dialysis, kidney failure can cause other health-related problems over time, including high blood pressure (including a latent nocturnal factor), bone disease, anemia, and nerve damage. As kidney function declines past the minimum threshold, kidney transplant becomes the only hope for patients with advanced ESRD.

Studies on human dialysis patients indicate that a high number of free radicals are formed in response to dialysis and that antioxidant dietary supplements can protect against this damage (Saionji 1999; Wratten 1999; Clermont et al. 2000).


Transplantation
Statistical surveys are made of medical facilities yearly. The most recent statistics available indicate that kidney transplantation accounted for 13,483 transplant operations in 1999 (NIDDK 2001b). In the United States, many people live with a functioning kidney as a result of transplantation. However, it is very difficult to obtain accurate statistics on the number of persons who live with a functioning kidney transplant at any given time. Unfortunately, each year patients die while awaiting a matching donor kidney. According to the NIDDK (2001b), as of November 2, 2001, there were 50,305 people waiting for kidney transplants. To be a potential candidate for kidney transplantation, a person must have kidney function estimated to be below 15% and must not be positive for certain diseases, such as unstable coronary artery disease, infection, or glomerulonephritis. (Glomerulonephritis is inflammation of the tiny blood vessels in the nephrons where blood is filtered in the kidneys. It is usually caused by an autoimmune disease, but can also be caused by infection.)

Can Renal Replacement Be Deferred? A study was conducted to determine if a very low-protein diet could defer renal replacement therapy (RRT) in patients with chronic renal failure. High protein intake is known to be stressful for the kidneys and over time can be a contributing factor to a slow, pervasive decline in kidney function. Two groups of patients (23 and 53 patients, respectively) were put on a very low-protein diet (0.3 g/kg) combined with supplemental amino acids. The patients in these groups were well-motivated RRT candidates who were closely monitored for nearly 1 year. During the course of the study, indications of malnutrition did not occur, and the patients were able to maintain acceptable kidney function (glomerular filtration rate or GFR < 10 mL/min or < 15/mL/min for diabetic patients) (Walser 1999).

Note: Since 1973, Medicare has picked up 80% of ESRD treatment costs, including the costs of dialysis and transplantation and of some medications. To qualify for benefits, a patient must be insured or eligible for benefits under Social Security or be a spouse or child of an eligible American. Private insurance and state Medicaid programs often cover the remaining 20% of treatment costs.

Natural and Adjuvant Treatment

1)Dietary Management

2)Inflammation

3)Dietary Supplements

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

1)Phosphorus is especially high in dairy products (milk, cheese, ice cream); dried beans and peas; nuts and peanut butter; some salt substitutes; and cocoa, beer and cola soft drinks.

2)Sodium is especially high in table salt, canned soup, processed cheese, snack foods, prepared and "fast foods," pickles, olives, sauerkraut, and smoked and cured food (ham, bacon, luncheon meat).

3)Protein is found in large amounts in food from animal sources (poultry, meat, seafood, eggs, dairy products). Protein is found in smaller amounts in food from plant sources (bread, cereal, grain, vegetables, fruit).
However, a certain amount of phosphorus, sodium, and protein is necessary for good health. To keep yourself healthy, it is important to learn to read labels and make better choices. For example, non-dairy creamers and milk substitutes are a good way to lower dietary phosphorus.

Avoid losing too much weight. It is important to maintain a good level of calories because calories give you energy. If you are limiting protein, you will need to get more calories from other foods. Good ways to increase calories are to:

1)Increase unsaturated fats from vegetable oils (corn, cottonseed, safflower, soybean, sunflower), olive oil, and mayonnaise salad dressings.

2)Use sugar from gum drops, jelly beans, marshmallows, honey, jam, and jelly.

3)Use canned or frozen fruits in heavy syrup.

Note: The recommendations for using sugar may not be appropriate for diabetics or overweight individuals. If you are diabetic, consult your physician or dietitian for alternative recommendations.

Protecting Kidneys Against Inflammatory Attack

Pentoxifylline (PTX) is a prescription drug approved by the FDA to treat peripheral vascular disease. The standard dose is 1200 mg a day to improve circulation. To suppress proinflammatory cytokines often involved in age-related renal impairment, a lower dose of 400 mg twice a day can be used. (Refer to pentoxifylline precautions in the summary section before using this drug.)

A controlled study on human diabetics with advanced renal failure showed that 400 mg a day of PTX reduced tumor necrosis factor-alpha (TNF-alpha) levels by approximately 35%. In the pentoxiphylline group, a measurement of kidney impairment was reduced 59%. There were no changes in those given placebo. The researchers noted that inflammatory cytokines such as TNF-alpha have long been implicated in the development and progression of diabetic kidney failure (Navarro et al. 1999a). Organ failure induced by TNF-alpha has been confirmed by other studies (Boldt et al. 2001).

In advanced kidney failure, anemia can be induced by an inflammatory cytokine attack on erythropoietin, the major natural hormone responsible for red blood cell (RBC) production. In a group of 7 anemic patients with advanced renal failure, PTX suppressed TNF-alpha and reversed the anemic state (Navarro et al. 1999b).


Dietary Supplements

Dietary supplements are often recommended by physicians and renal dietitians (National Kidney Foundation 2001e). Their recommendations are guided by the results of blood tests that you will be required to take regularly as part of monitoring your condition and treatment results. Always speak with your physician or renal dietitian before using or adding any supplements or herbal products.

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

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

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