Alternative names: Chronic Kidney Disease, CKD.
Unlike acute renal failure with its sudden (but reversible) failure of kidney function, chronic renal failure is slowly progressive. It most often results from some disease that causes gradual destruction of the kidneys and can range from mild dysfunction to severe kidney failure; progression may continue to end-stage renal disease (ESRD). Chronic renal failure usually occurs over a number of years as the internal structures of the kidney are slowly destroyed.
Chronic renal failure occurs in approximately 2 out of every 10,000 people.
Causative diseases include glomerulonephritis of any type (one of the most common causes), polycystic kidney disease, hypertension, Alport syndrome, reflux nephropathy, obstruction, kidney stones, infection, and analgesic toxicity. Diabetes mellitus is a major cause of chronic renal failure.
Chronic renal failure results in the accumulation of fluid and waste products in the body, causing low urine output and waste accumulation. These may occur without symptoms. Most bodily systems are affected by chronic renal failure.
In the early stages, there may be no symptoms. Progression may be so gradual that symptoms do not occur until kidney function is less than one-tenth of normal.
Treatment of the underlying disorders may help prevent or delay development of chronic renal failure. Treatment focuses on controlling the symptoms, minimizing complications, and slowing the progression of the disease.
Associated diseases that cause or result from chronic renal failure must be controlled. Hypertension, congestive heart failure, urinary tract infections, kidney stones, obstructions of the urinary tract, glomerulonephritis, and other disorders should be treated as appropriate. Blood transfusions or medications such as iron and erythropoietin supplements may be needed to control anemia.
Fluid intake may be restricted, often to an amount equal to the volume of urine produced. Dietary restrictions may slow the build-up of wastes in the bloodstream and control associated symptoms such as nausea and vomiting. Salt, potassium, phosphorus, and other electrolytes may be restricted.
There are steps that can be taken, but must be taken early, to reduce the complications and symptoms as much as possible. Some ways to help prevent or slow down the onset of chronic renal failure include:
There is no cure for chronic renal failure. Untreated, it usually progresses to end-stage renal disease. Lifelong treatment may control the symptoms of chronic renal failure. Dialysis or kidney transplant may eventually be required.
Leukonychia (partial or completely white nails) is a sign of renal failure.
High levels of magnesium can develop in patients with kidney failure and in elderly people whose kidney functions are reduced. This is especially true when supplementing with magnesium. Kidney disease, rather than diet, is the usual cause of magnesium overload, because the kidneys lose the ability to remove excess magnesium.
The common medical complications of being severely underweight include kidney damage.
With about a million glomeruli in each kidney, there is an ample reserve of kidney function, and a person can go many years or even decades without feeling the effects of renal failure. However, once a glomerulus is damaged, it cannot be repaired. IgAN progressively destroys these glomeruli. As more and more glomeruli become scarred and non-functional, the remaining ones start working harder (a process called hyperfiltration), and eventually, as more and more of them fail at an increasingly faster rate, the kidneys no longer have enough function left to perform their task of filtering waste products from the blood.
Diabetes mellitus is a major cause of chronic renal failure. In Singapore, statistics have shown that out of the 500 newly diagnosed kidney failure patients each year, 50% were caused by diabetes and 9% were caused by hypertension. When sugar levels rise enough to spill into the urine, as in diabetes, blood vessels in the kidneys are damaged. This condition is known as diabetic nephropathy. Symptoms related to kidney failure usually occur only in late stages of the disease, when kidney function has diminished to less than 25% of normal capacity. For many years before that point, kidney disease of diabetes exists as a silent process.
Anemia is almost always present in cases of chronic renal failure, and can occur through any of the basic mechanisms (blood loss, excessive destruction of red blood cells, or low production of red blood cells.) However, the typical anemia associated with CRF results from decreased production of red blood cells by the bone marrow: failing kidneys no longer produce sufficient erythropoietin, a hormone that stimulates the production of oxygen-carrying red blood cells (RBCs). In addition to decreased levels of RBCs, patients often begin to accumulate toxic metabolites, which shorten the lifespan of existing RBCs.
Homocysteine levels in patients suffering from chronic renal failure are significantly elevated at an early stage. The kidney plays a very significant role in homocysteine metabolism but this does not occur during chronic renal failure. In addition, there is a decreased extra-renal catabolism, which contributes to the hyperhomocysteinemia state. [Hyperhomocysteinemia: A Role in The Accelerated Atherogenesis of Chronic Renal Failure?, Netherlands Journal of Medicine, 1995;46: pp.244-251]
Patients with impaired renal function filter and excrete less uric acid and therefore become hyperuricemic. Interestingly, patients with renal failure do not develop gout as frequently as expected, despite their high plasma urate levels. The explanation for this phenomenon may be that they have not incurred sustained hyperuricemia levels long enough to develop gout. Only 1% of renal failure patients develop gout but nearly 30% of patients with adult polycystic kidney disease do.
In a study of patients with chronic renal failure undergoing long-term hemodialysis 450mg of chitosan 3 times a day for 12 weeks produced multiple benefits. Mean serum cholesterol went down 43% and mean serum hemoglobin increased from 5.8 to 6.8 g/dl in those patients who received the chitosan. Mean urea (from 75 to 45 mM) and creatinine (from 1. 001 to 0.875 mM) levels in serum showed significant reductions after 12 weeks of chitosan treatment. Compared with the control group, the treatment group reported significantly improved appetite, sleep and feeling of physical strength. No significant side effects were seen. (Jing SB. et al. J Pharm Pharmacol 1997;49:72 1-723.)
Reported in Natural News, August 26, 2009: Researchers in the United Kingdom have made a breakthrough in the treatment of advanced CKD – using a daily dose of sodium bicarbonate (baking soda). Baking soda has been shown to slow the decline of kidney function in CKD, according to a study set for publication in the Journal of the American Society of Nephrology (JASN). "This cheap and simple strategy also improves patients' nutritional status, and has the potential of translating into significant economic, quality of life, and clinical outcome benefits," said researcher Magdi Yaqoob, MD, of the Royal London Hospital.
Dr. Yaqoob studied 134 patients with advanced CKD and low bicarbonate levels, a condition known as metabolic acidosis. One group of these patients was treated with a small daily dose of sodium bicarbonate in tablet form, in addition to their usual care. The results? The rate of decline in kidney function was dramatically reduced in these patients. Overall, the decline was about two-thirds slower than in patients not given sodium bicarbonate. "In fact, in patients taking sodium bicarbonate, the rate of decline in kidney function was similar to the normal age-related decline," Dr. Yaqoob stated.
A low protein diet is important in reducing the processing responsibilities of compromised kidneys.
Lengthy fasting should generally be avoided by people with renal failure. Short-term fasts may be helpful, but must be done under an experienced doctor's supervision.
Reports by doctors using homeopathy say that patient response is better in those who have not yet started with dialysis. Long-term constitutional therapy as well as therapy aimed at improving kidney function helps to keep the patient relatively free of symptoms and complications. Remedies such as Serum Anguillar Ichthyotoxin, Solidago and Urea have been found useful in dealing with chronic renal failure and its complications. Hipuric acid has been found to be useful for the itching of skin arising from chronic renal failure.
If you have kidney problems, taking magnesium supplements may make you accumulate the mineral too quickly, which could be toxic. In this case you should check with your doctor before taking magnesium supplements.
There have been a variety of trials of omega-3 fatty acid supplementation in patients with a variety of renal disorders. These trials suggest that such therapy may be of use in the treatment of IgA nephropathy and chronic renal failure. Dietary polyunsaturated fatty acid manipulation results in an anti-inflammatory. [Polyunsaturated Fatty Acids and Renal Disease, Proceedings of the Society For Experimental Biology and Medicine, 1996;213: pp.13-23]
Fish oil supplementation is promising and does not produce the risks associated with corticosteroid and immunosuppressive drug use.
Patients with chronic renal failure have homocysteine levels that are significantly elevated at an early stage. Taking 5mg of folic acid daily can significantly lower these homocysteine levels. [Hyperhomocysteinemia: A Role in The Accelerated Atherogenesis of Chronic Renal Failure?, Netherlands Journal of Medicine, 1995;46: pp.244-251]
The authors of the following study believe it shows that vitamin C supplementation leads to a significant increase in serum oxalate levels in dialysis patients. In renal insufficiency, vitamin C levels were elevated, but not oxalate levels. Caution is advised with regard to vitamin C and renal insufficiency.
"Relationship Between the Serum Concentration of Oxalic Acid and Ascorbic Acid in Chronic Renal Insufficiency", Gerold, M., et al, Nieren-Und Hochdruckkrankheiten, May 1992;21(Suppl. 1): pp.58-61. (Address: Dr. G. Stein, Erlanger Allee 101, O-6902 Jena-Lobeda, Germany)
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